Anatomy & Physiology for Midwives 3: Third Edition

Chapter 15. The transition to neonatal life

Learning objectives

• To identify the key steps in the transition to successful neonatal life.

• To describe the vulnerability of the neonate, with particular reference to the potential risk of respiratory problems, hypoglycaemia and jaundice.

• To outline the principles of thermoregulation in the newborn.

• To compare the fetal and neonatal circulatory and respiratory systems, describing the transition stages.

• To describe factors relating to the neonatal gastrointestinal, renal and nervous systems that make breast milk the ideal food.

• To describe normal physiological fetal to neonatal transition and to recognise signs of a neonate experiencing compromised transition.


During fetal life, the placenta carries out the crucial physiological roles of gas exchange, nutrition, elimination of waste products and additional aspects of circulation. Within minutes of birth, the placental support ceases so the baby's own cardiovascular, respiratory, gastrointestinal, renal and metabolic systems must function independently. The transition from fetal to neonatal life needs to be smooth, swift and successful; the majority of infant deaths occur within the neonatal period (first 28 days) and these are linked to inadequate progression to neonatal physiological functions. Millennium Development Goal 4, set by UNICEF in 2000, is to reduce child mortality (deaths under 5 years of age) by two-thirds between 1990 and 2015. Although under-5 mortality rates have improved, neonatal rates have increased (Lawn et al., 2010). The leading cause of neonatal mortality is complications of preterm birth and compromised transition to neonatal life.

The transition to extrauterine life depends on the degree of maturation in late gestation, the process of delivery itself and establishment of independent physiological processes for regulating homeostasis after placental separation. These physiological processes include establishing continuous respiration, changing from a parallel to a serial circulatory organization and ceasing the right-to-left shunting across the heart so oxygenated blood can be delivered to the tissues, establishing oral intermittent feeding and independent thermoregulation and glucose homeostasis. These complex physiological changes must occur within a relatively short time frame. Monitoring and assessing neonatal transition are important in order to recognise delayed or compromised adaptation or the warning signs of more serious conditions such as birth injury, congenital abnormality or disease (Askin, 2009a).

Chapter case study

The midwife officially recorded Zak as having an Apgar score of 9 at approximately 1 min of age. Following the delivery James was surprised how alert his son Zak was, that he seemed to be aware of his surroundings and appeared to be actively looking around.

• What factors could have contributed to Zak's behaviour and what are the possible explanations for Zak being so alert following his delivery?

Zara asks the midwife if she can attempt to breastfeed.

• What could the midwife do to encourage Zak to suckle?

The process of birth is physiologically stressful with fluctuations in placental blood flow resulting in a degree of hypoxia and respiratory acidosis. Increased secretion of adrenal catecholamines, stimulation of the sympathetic nervous system and the subsequent mobilization of glycogen and lipid stores are fundamental in the activation of essential physiological mechanisms that result in an alert and active baby at birth. However, a prolonged or difficult delivery and marked hypoxia/anoxia and acidosis can result in an overstressed or seriously asphyxiated baby (Box 15.1).

Box 15.1

Fetal asphyxia

Fetal asphyxia is due to a significant reduction in the amount of oxygen available via the placenta and the maternal circulation. There are many possible causes for example placental abruption, rapid deterioration in the maternal condition, such as eclampsia, uterine hyperstimulation in response to syntocinon augmentation. Whatever the reason, prolonged fetal hypoxia will result in asphyxia (low oxygen levels and raised carbon dioxide levels). Fetal hypoxia, if suspected during labour, can be assessed by obtaining a small sample of blood from the fetal scalp, from which the pH and base excess can be measured. Acidaemia is diagnosed if the pH of the fetal blood is below 7.2, however many babies can tolerate moderate acidaemia without long term problems. A base excess above 12 mmol indicates chronic or prolonged acidaemia. The risk of asphyxia rises with lower pH and higher base excess. Babies born with asphyxia require active resuscitation to restore pH and base excess. In extreme cases, severe asphyxia results in irreversible brain damage.

Both the fetus and the neonate can tolerate degrees of hypoxia and anoxia that would result in serious morbidity or mortality in an adult. The neonate retains the capability to divert a considerate proportion of its cardiac output to the brain thus protecting it. Although the brain is vulnerable to hypoxia, the compensatory mechanisms can increase tolerance to hypoxic states (Parer, 1998). However, severe asphyxia can cause cerebral microhaemorrhages resulting in a spectrum of damage from impaired intellectual development to spasticity and irreversible brain damage (Box 15.2). Neonates are also vulnerable to infection.

Box 15.2

Neonatal head cooling

In extreme cases of neonatal asphyxia, brain cell distruction triggers apotosis in surrounding cells. The number of apoptotic neural cells can be reduced by neonatal head cooling thus potentially reducing the severity of brain damage (Wyatt et al., 2007 and Polderman, 2008).

Although there is usually a good correlation between gestational length and degree of maturity, infants affected by intrauterine growth retardation (IUGR) may have precocious organ development because undernutrition and the resulting fetal stress promote increased fetal cortisol secretion thus enhancing fetal organ maturation. In humans, fetal cortisol appears not to have a role in inducing labour as has been demonstrated in other species (see Chapter 13). The major problems of premature infants can be attributed to a shorter duration of glucocorticoid exposure (even though fetal stress results in actual levels being higher); this results in an increased risk of persistent fetal circulation, increased likelihood of lung immaturity and respiratory diseases syndrome and immaturity of thermoregulatory responses, the gastrointestinal system and enzymes involved in maintaining glucose homeostasis.

Fetal preparation for birth includes storing glycogen, producing catecholamines and laying brown and white fat. The glucocorticoid system is pivotal in the fetal preparation for birth. Fetal cortisol levels rise from about 35 weeks. Glucocorticoids cause the natural decrease in growth that occurs towards term and are also thought to be responsible for the growth retardation associated with physiological stress in utero such as that due to hypoxia and undernutrition. Glucocorticoids bring about functional and morphological changes in many biochemical pathways and fetal tissues including lungs, liver, gut, adipose tissue and skeletal muscle (Fowden and Forhead, 2009). Glucocorticoids influence surfactant production and maturation of the alveoli and other respiratory tissues thus promoting lung maturation. They stimulate glycogen deposition in the fetal liver and skeletal muscle and also induce hepatic gluconeogenesis enzymes by promoting adrenaline synthesis (and potential effective response to stress), inducing hormone receptors and affecting thyroid hormone synthesis. They also enhance proteolysis so fetal protein accretion is reduced. Fetal corticotrophin-releasing factor (CRF) and antidiuretic hormone (ADH) and placental CRF orchestrate the increase in fetal cortisol production, which influence adrenocorticotrophin (ACTH) production by the maturing fetal pituitary gland; increased ACTH stimulates cortisol production.

At birth, there are also changes in the regulation of growth. Fetal growth is substrate-limited and actively constrained to optimize successful delivery (see Chapter 9). The rise in glucocorticoids towards term suppresses growth and is responsible for the natural decrease in growth that occurs at this time (Fowden and Forhead, 2009); the increase in glucocorticoids also induces growth hormone receptors and changes in expression of insulin-like growth factor I (IGF-I).

The cardiovascular system


Before birth

Fetal blood (Table 15.1) is structurally and functionally different to adult blood; it contains larger and more numerous erythrocytes (red blood cells) with a higher haemoglobin content which maximizes their uptake of oxygen (Palis and Segel, 1998). Fetal haemoglobin with its two α-chains and two γ-chains has a higher affinity for oxygen in the slightly more acid fetal environment. Less-effective binding of 2,3-bisphosphoglycerate (or 2,3-diphosphoglycerate) to the γ-chains means that the oxygen–haemoglobin dissociation curve of the fetus and neonate is shifted to the left (Fig. 15.1). Shifts of pH in the placenta further increase both dissociation of oxygen from maternal haemoglobin and its uptake by fetal haemoglobin. This means that, although fetal haemoglobin has an increased oxygen uptake, it is less efficient at releasing oxygen to the tissues.

Table 15.1 Fetal and adult blood

Note: the theoretical value is the amount of oxygen the blood can be saturated with whereas, in practice, the blood is saturated to a lesser degree because the transfer of oxygen across the placenta is less efficient than the transfer of oxygen across the alveoli.




Blood volume

80–100 mL/kg

75 mL/kg

90–105 mL/kg (preterm)

Red blood cell number

6–7 ∞ 106/mL

Female: 4.8 ∞ 106/mL

Male: 5.4 ∞ 106/mL

Haemoglobin content

20.7 g/dL

Female: 14 g/dL

Male: 16 g/dL

Oxygen content of 100 mL saturated blood

21 mL (theory)

16 mL (theory)

13 mL (practice)

15.7 mL (practice)

Red blood cell lifespan

80–100 days

120 days

60–80 days (preterm)

Haemoglobin type

HbF: α2γ2

HbA: α2β2

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Fig. 15.1

The maternal and fetal oxyhaemoglobin dissociation curves.

At term, the ratio of fetal haemoglobin to adult haemoglobin (HbF:HbA) is 80:20; by 6 months production of the β-chain replaces the γ-chain so the ratio is 1:99 (Fig. 15.2). Preterm infants tend to have an even higher HbF level and a decreased 2,3-bisphosphoglycerate concentration therefore oxygen unloading at the tissue level is even less efficient. The raised levels of HbF in the neonate mean that haemoglobinopathies caused by altered synthesis of β-chains (such as β-thalassaemia) or altered structure of β-chains (such as sickle-cell anaemia) are not evident immediately at birth but become evident when the infant is at least 2 months old. It is possible to detect fetal blood cells in the maternal circulation, an observation that is utilized in the management of Rhesus incompatibility (see Chapter 10) (Lamvu and Kuller, 1997).

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Fig. 15.2

Changes in fetal:adult haemoglobin (HbF:HbA) ratios in fetal and infant blood.

(Reproduced with permission from Begley et al., 1978.)

After birth

At birth, fetal blood has an increased population of nucleated erythrocytes (even more so if the baby has been subjected to increased stress, is immature or has Down's syndrome). For the first 3 months of life, the erythrocytes are more fragile, have an increased metabolism and a shorter half-life and erythropoietin production is suppressed (Box 15.3). Once respiration in the neonate is established, the excess red blood cells compensating for the lower oxygen saturation within the uterine environment are no longer needed. These red blood cells are broken down and physiological jaundice may result, usually around day 3 of life as the neonatal liver is immature and initially cannot keep up with the rate of bilirubin production from red blood cell breakdown.

Box 15.3

Physiological anaemia of infancy

Haemopoiesis (red blood cell production) is controlled by the hormone erythropoietin, which increases when oxygen delivery to the kidney is reduced; it stimulates red blood cell production by the bone marrow. The increased oxygen levels inhibit erythropoietin levels in the neonate postnatally (Strauss, 1994). Levels remain low for 2–3 months (longer in preterm infants) and then increase, resulting in increased bone marrow activity and red blood cell production. As the neonate appears to tolerate the fall in haemoglobin concentration without ill-effects, it is deemed to be physiological. The haemodilution effects are increased by rapid growth being matched by total blood volume, which precedes any change in red blood cell number.


Neonates, particularly those born prematurely but those who are healthy as well, have an increased risk of haemostatic problems because they are born with a deficiency of plasma coagulation factors, inhibitors of haemostasis and other components of the fibrinolytic system (Aronis-Vournas, 2006). However, despite this, because the deficiencies in components of the coagulation and fibrinolytic system tend to be balanced, the healthy term neonate does not usually have thrombotic or haemorrhagic problems. The most common example of neonatal haemostatic problem is (Kuehl, 1997) disseminated intravascular coagulation (DIC) due to accelerated and inappropriate coagulation, which depletes the body's supply of platelets and clotting factors and paradoxically increases the risk of haemorrhage. Susceptibility is increased because, first, the immature neonatal reticuloendothelial system has a decreased capacity to remove intermediary products of coagulation so they can further stimulate coagulation and consumption of clotting factors, and, second, synthesis of clotting factors by the immature liver is inefficient. Vitamin K levels in the neonate are about 50% of adult values, which affect the efficiency of the clotting cascade. Vitamin K levels are low because placental transport of the vitamin is poor and colonization of the gut by bacteria that synthesize vitamin K is not immediate. The consequent reduced level of all vitamin K-dependent clotting factors is associated with an increased bleeding tendency, which can predispose to haemorrhagic disease of the newborn (HDNB) (Box 15.4). Neonatal platelets exhibit decreased aggregation and adhesiveness because their production of thromboxane A2 (TxA2) is impaired. This appears to protect the term neonate against thrombosis but to increase the vulnerability to bleeding of the preterm or sick baby. Placental transfer of maternal drugs such as aspirin can affect coagulation in the neonate.

Box 15.4

Haemorrhagic disease of the newborn (HDNB)

• Bleeding from the gut, umbilicus, circumcision wounds and oozing from puncture sites

• Evident 2–3 days after birth

• Associated with antibiotics, which affect colonization of the gut with vitamin K-synthesizing bacteria

• Associated with anticonvulsant drugs (e.g. phenobarbital, diphenylhydantoin), which concentrate in the fetal liver and antagonize the effect of vitamin K

• Associated with maternal warfarin treatment, which decreases levels of vitamin K-dependent clotting factors and prolongs prolonged clotting times

• Prophylactic vitamin K is routinely administered to all babies born in the UK (Paediatric Formulary Committee, 2010)

• Term babies respond well to vitamin K therapy but synthesis of clotting factors is further limited in preterm babies by inadequate hepatic synthesis of precursor proteins

The circulation

Before birth

As the fetal oxygen source is the placenta rather than the lungs, blood in the fetal circulation flows in a circuit that perfuses the placenta and largely bypasses the lungs (Fig. 15.3). In order to do this, the fetal circulation has several additional structures: the umbilical vein, which carries blood rich in oxygen and nutrients to the underside of the liver, the ductus venosus (a venosus is a shunt that connects a vein to a vein), which bypasses the liver taking blood from the umbilical vein to the inferior umbilical vein en route to the right side of the heart. With increasing gestational age, more blood goes to the liver rather than bypassing it (Askin, 2009a). The hypogastric arteries, which branch off the internal iliac arteries, are contiguous with the umbilical arteries of the umbilical cord, returning blood to the placenta. The lungs are bypassed by two structures: the foramen ovale, which allows blood to move directly from the right atrium to the left atrium, and the ductus arteriosus, which connects the pulmonary arterial trunk to the descending aorta (an arteriosus is a vascular shunt that connects an artery to an artery).

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Fig. 15.3

The fetal circulation.

(Reproduced with permission from Goodwin, 1997.)

The oxygenated and nutrient-enriched blood is taken from the placenta in the umbilical vein that goes through the abdominal wall to the underside of the liver. This is the only unmixed blood and is about 80% saturated with oxygen; the blood goes through the ductus venosus to the inferior vena cava where it mixes with oxygen-depleted blood returning to the heart from the lower body (Fig. 15.4 A). The inflows of blood from the inferior and superior venae cavae do not mix thoroughly because of their angle of entry and the shape of the right atrium. Because the entry of the inferior vena cava is aligned with the foramen ovale, most (about 60%) of the blood from the inferior vena cava travels from the right atrium through the foramen ovale into the left atrium and thence to the left ventricle and the ascending aorta. The foramen ovale is kept open because the high pulmonary vascular resistance (PVR) means that the pressure in the right atrium is also high.

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Fig. 15.4

Changes in circulation at birth: (A) fetal circulation showing oxygen saturation of blood; (B) neonatal circulation.

(Reproduced with permission from Chamberlain et al., 1991.)

Most blood entering the right atrium from the superior vena cava passes through the tricuspid valve into the right ventricle and to the pulmonary arterial trunk. The ductus arteriosus is inserted into the vessel at the bifurcation of the right and left pulmonary artery (taking blood to the right and left lung, respectively); it shunts blood from the pulmonary arterial route into the descending aorta. The pulmonary circulation is vasoconstricted and has a high PVR, because the pulmonary environment is relatively hypoxic. Systemic vascular resistance (SVR) is low. Only about 10% of the output of the right ventricle continues into the pulmonary circulation for the growth and metabolic needs of the lungs; the rest is diverted through the ductus arteriosus which has a low resistance; its patency is maintained by the low fetal PO2 and by high levels of prostaglandins produced by the placenta. Towards the end of gestation, the proportion of blood perfusing the lungs tends to increase. From the descending aorta, the blood supplies the remaining organs and the lower body. The hypogastric arteries branch off the internal iliac arteries and return to the placenta via the umbilical arteries.

The upper body and head are fed from arteries which branch off from the aortic arch before the insertion of the ductus arteriosus and the subsequent mixing of slightly less-well-oxygenated blood. The early branching of the coronary and carotid arteries means the heart and brain receive slightly better oxygenated blood. The advantages conferred by the early branching of the subclavian arteries which supply the upper limbs can be illustrated by the enhanced development of arms compared to the legs.

After birth

One of the most important transitional stages in the adaptation to extrauterine life is the establishment of the neonatal circulation. In fetal life, the source of oxygen is the placenta so most of the blood flow bypasses the fetal lungs. At birth, blood fully perfuses the lungs and flow through the fetal vascular structures ceases. At birth, these changes that mark the transfer of the fetal into adult-type circulation (see Fig. 15.4B) are not rapid or immediate. They are initiated within 60 s of delivery but may not be fully completed for a few weeks. The two determining events that initiate the closure of the fetal shunts are the arrest of the umbilical circulation, and therefore placental perfusion, and lung inflation and expansion, which results in increased pulmonary blood flow. The first breath results in lung expansion and vasodilatation of the pulmonary vessels in response to increased partial pressure of oxygen so blood flow to the lungs increases. The tortuosity of the capillaries is reduced and the pulmonary circulation changes from a high-resistance to a low-resistance pathway so 90% of the blood flows through the pulmonary vascular bed. There is a brief reversal of flow through the ductus arteriosus, which vasoconstricts in response to the change in oxygen level, mediated by prostaglandins, especially decreased prostaglandin PGE2 (Thorburn, 1992). The placenta no longer contributes to prostaglandin production and prostaglandin breakdown is increased because more blood flows to the lungs where significant prostaglandin metabolism and breakdown occur.

The smooth muscle of the umbilical artery walls is not innervated but is irritable. Vasoconstriction is stimulated by stretching and handling the cord, by cooling and in response to stress-related catecholamine release. The thicker walls of the umbilical arteries are able to generate high intraluminal pressure, which arrests the placental circulation, preventing flow from the infant to the placenta. This is augmented by the increased synthesis of prostaglandins and thromboxanes in response to the raised oxygen level due to breathing, which increases vessel irritability and vasoconstriction. The umbilical vein remains dilated; blood flow from the placenta to the infant can continue via gravity. Thus, initial neonatal blood volume is affected by the timing of clamping of the umbilical cord and by the relative positions of the infant and placenta at the time of clamping. The usual practice is to clamp the umbilical cord earlier if the baby is subject to fluid overload (hydropic), or if the baby is polycythaemic (e.g. infants of diabetic mothers or growth retarded), to limit the transfer of maternal analgesic agents or antibodies or to avoid possible baby-to-baby transfusions in the cases of multiple births (Kinmond et al., 1993).

The flap of the foramen ovale (Fig. 15.5) is pushed closed because the decreased umbilical flow results in a decreased venous return from the inferior vena cava so the pressure in the right atrium and PVR falls in response to changes in oxygenation. The increased pulmonary blood flow results in an increased return to the left atrium and consequent increase in pressure. Thus, the pressure gradient across the foramen ovale is reversed. So at birth, PVR falls and SVR increases. The relatively thick layer of smooth muscle in the pulmonary blood vessels begins to thin from birth.

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Fig. 15.5

Initiation of neonatal circulation and closure of the foramen ovale between the right atrium (RA) and left atrium (LA).

The closure of the fetal structures may not be immediate or permanent and may never be completed. The closure of the foramen ovale is reversible at first; interruption of ventilation or a drop in alveolar oxygenation results in constriction of the pulmonary capillaries and consequent reversal of pressure across the atria and reversion to fetal circulation. The incomplete closure can result in intermittent and reversible cyanotic episodes. After a few days of functional closure, the tissue associated with the foramen ovale fuses and closure becomes permanent. In many adults, a patent foramen ovale can be demonstrated (a probe can be passed through) although the pressure gradient maintains effective functional closure. Intermittent flow through the ductus arteriosus may initially occur during each cardiac cycle when aortic pressure is maximal following ventricular contraction. Bradykinin released from the newly inflated lungs mediates the constriction of the ductus arteriosus. Production of prostaglandins, which had maintained the open ductus arteriosus in the fetus, is decreased as oxygenation increases. Most neonates have some degree of patency of the ductus arteriosus in the first 8 h of life but it becomes functionally closed within the first or second day (Askin, 2009a). Fibrolysis and obliteration of the lumen of the ductus arteriosus are usually complete within 3 weeks; continued patency is very serious and can result in left ventricular failure. The ductus venosus constricts when umbilical flow is halted. The obliterated vessels remain as anatomical ligaments; the slow closure of the umbilical vein and its degeneration into ligamentum teres are utilized as a route for neonatal blood transfusions if required.

The nervous control of the cardiovascular system is well developed in the neonate with mature physiological control of blood pressure and cardiac output demonstrable. The systemic arterial blood pressure is relatively low in the first few weeks as vascular tone develops which increases vascular resistance. Pulmonary arterial blood pressure is initially high but falls to mature values as pulmonary resistance falls. The neonate's heart rate is fast, as in the fetus. As in the fetus, control of cardiac output is largely achieved by changing heart rate because the heart is small and non-compliant and has a relatively thick wall. At birth, the wall of the right ventricle is thicker than the left, which hypertrophies in response to the changed postnatal circulation.

The respiratory system

The primitive air sacs are developed by the 20th week of gestation, and by 26 weeks respiratory bronchioles with a rich capillary supply are evident. Although the enzymes for synthesis of phospholipid/lipoprotein components of surfactant are present from week 18, the type II pneumocytes secrete surfactant only from week 26 with a surge in production after week 30. Surfactant, a detergent-like wetting agent, allows increased compliance, so the force required to inflate the alveoli is reduced thus increasing compliance. A lack of surfactant causes respiratory distress syndrome (RDS) (see below). The lecithin:sphingomyelin (L:S) ratio of the surfactant can be determined by amniocentesis indicating the maturity of the respiratory system (Fig. 15.6). By week 35, the L:S ratio in a healthily developing fetus is 2:1. This ratio is decreased in pre-eclampsia, prematurity, narcotic addiction, maternal diabetes and other problems in pregnancy. Administration of cortisol (dexamethasone) to the mother prior to delivery of a baby born from 24 to 34 weeks' gestation increases fetal surfactant production within 24 h and can be used to decrease the risk of RDS (Hutchison, 1994).Variations (polymorphisms) in the genes for components of surfactant are associated with a range of inherited neonatal respiratory problems including bronchopulmonary dysplasia (BPD), (RDS) and respiratory syncytial virus (RSV) bronchiolitis and may influence susceptibility to influenza virus (Hallman and Haataja, 2006). Premature infants, particularly those born before 28 weeks, have immature alveoli with fewer type II cells and may require instillation of exogenous surfactant down endotracheal tubes to alleviate respiratory distress. Poor ventilation suppresses surfactant secretion so the severity of hypoxia, hypercapnia and acidosis is worsened and respiratory muscle activity is compromised which further compromises surfactant production.

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Fig. 15.6

Lecithin:sphingomyelin (L:S) concentration in the amniotic fluid; the concentration rises very sharply after 30 weeks' gestation.

(Reproduced with permission from Chamberlain et al., 1991.)

The lungs

Before birth

In fetal life, the lungs are filled by fluid secreted by the lung epithelium; the lung fluid is essential for growth and development of the lungs and this fluid exchanges with amniotic fluid. At birth, the neonate has to rapidly clear fluid from its air-spaces; 10–25 mL/kg fluid will be expelled or resorbed. Fetal breathing movements (FBM) are observed on ultrasound from the first trimester. Initially, they are intermittent, rapid and irregular. As gestation progresses, FBM increase in strength and frequency, occurring up to 80% of the time in an organized episodic pattern (Nijhuis, 2003). The lung fluid is ‘breathed’ out by the fetus into the amniotic fluid. Patterns of FBM dominate during the daytime and are correlated with fetal behavioural states. Fetal wakefulness and arousal are associated with sustained vigorous respiratory patterns. Quiet sleep is associated with an absence of FBM. Adrenergic and cholinergic compounds, prostaglandin synthesis inhibitors and raised maternal carbon dioxide levels stimulate FBM. They are inhibited by hypoglycaemia, cigarette smoking, alcohol consumption and accelerated labour. Despite the relatively low partial pressure of oxygen and high partial pressure of carbon dioxide, the fetus makes only shallow respiratory movements although severe hypoxia and acidosis may stimulate gasping. Mild hypoxia leads to quiet sleep and reduced energy expenditure and oxygen consumption, which may be protective. The movement of the diaphragm generates about 25 mmHg pressure for between 1 and 4 h per day in a pattern that coincides with rapid eye movement (REM) sleep but not during slow-wave sleep or fetal ‘wakefulness’. FBM are important in lung development (Harding and Hooper, 1996), promoting growth and allowing rehearsal of the respiratory actions. Lung development is retarded in conditions where FBM are limited such as congenital disorders of the diaphragm or nervous system. The fluid volume in the fetal airways correlates with the functional residual capacity in postnatal life (Strang, 1991).

After birth

The most urgent need after delivery is the initiation of ventilation; the neonate has to clear its lungs of fluid, establish regular breathing and increase pulmonary blood flow to match pulmonary perfusion to ventilation. Many factors interact to stimulate the first breath, including changes in temperature and state. The mild asphyxia (decreased oxygen concentration, raised carbon dioxide concentration) and acidosis (decreased pH) due to flow in the cord ceasing sensitize the fetal aortic, carotid and central (medullary) chemoreceptors that increase ventilatory drive. Tactile stimulation, such as that which occurs during delivery, also promotes respiration. In additional, it is thought that the placental prostaglandins may inhibit breathing (decreased oxygen concentration, raised carbon dioxide concentration). The surge of endogenous steroids and catecholamines associated with labour also contributes; infants who do not experience labour are more likely to retain residual fluid in their lungs and have less efficient respiratory performance.

The fluid-filled lung with collapsed alveoli and undispersed surfactant proffers a high resistance to inflation and the first breath requires considerable effort. The diaphragm contracts strongly and the complaint flexible ribs and sternum of the newborn baby are pulled concave in the effort of the first breath. Once the lungs are inflated, the lung fluid is forced into the alveoli where it aids dispersal of surfactant and is rapidly resorbed into the pulmonary lymphatic vessels. Subsequent breaths require fewer changes in pressure and less mechanical work. The thoracic compression of a vaginal delivery contributes to fluid loss from the upper respiratory tract; the compression of the chest (known as the ‘vaginal squeeze’) creates negative pressure which draws air into the lungs and they re-expand. Most of the fluid clearance is due to a change in the lung epithelium from being a predominantly chloride-secreting membrane at birth to being predominantly a sodium absorbing membrane after birth (Jain and Eaton, 2006).

Most babies gasp within 6 s and have patterns of normal breathing and gas exchange within 15 min. Initially the newborn infant has metabolic and respiratory acidosis due to decreased oxygen concentrations (resulting in increased lactic acid) and increased carbon dioxide levels, respectively; this acid–base imbalance is corrected as ventilation improves. The risk of transient tachypnoea of the newborn (TTN) is increased in babies who are delivered by caesarean section or those who experience perinatal hypoxia. It is thought that TTN is due to immaturity of the sodium transport mechanisms of the lung epithelium (Jain and Eaton, 2006).

The rate of ventilation of the newborn is high compared with an adult but is similar when relative size is taken into account. Ventilation is often irregular with the baby exhibiting periods of fetal-like shallow breathing. The reflexes associated with lung inflation also appear to be different. As well as the Hering–Breuer Reflex (where filling of the lungs increases expiratory centre activity), the newborn infant demonstrates Paradoxical Reflex of Head (where filling the lungs excites the inspiratory centre thus stimulating further inspiration) (Givan, 2003). For the first few weeks, babies breathe via the nose and suck via the mouth. Control of ventilation by chemoreceptors is functional but qualitatively different in that hypoxia tends to increase depth of respiration (rather than respiratory rate) and that the response is temperature-dependent and is abolished in cold temperatures. The chemoreceptors seem to be more sensitive to raised carbon dioxide levels.

Babies have a relatively large oxygen consumption, which reflects their heat generation and that their more metabolically active tissues (e.g. liver and brain) are proportionately larger. The high airway resistance means that the energy cost of respiration is higher. PVR drops 6–8 weeks after birth when the diameter of the small arterioles increases. The relatively high requirement for oxygen means that neonates are more susceptible to asphyxia than other age groups. Neonatal resuscitation aims to prevent mortality and morbidity. Hypothermic neonates are predisposed to hypoglycaemia and acidosis. Acidosis compromises respiration because it increases PVR and suppresses both respiratory drive and surfactant production. The aims of neonatal resuscitation are to promote and maintain adequate ventilation and oxygenation, to initiate and maintain adequate cardiac output and perfusion and to maintain body temperature and adequate blood glucose levels.

Respiratory distress syndrome

RDS is caused by a deficiency in surfactant, which results in alveolar collapse and increased airway resistance. Surfactant deficiency is usually inversely related to gestational age and lung maturity. Abnormal pH, stress and inadequate pulmonary perfusion also inhibit surfactant synthesis and recycling. RDS is worsened by asphyxia and is the most common cause of respiratory failure in the preterm infant. The reduced surface tension affects alveoli expansion. Small alveoli tend to collapse and normal alveoli are overdistended. Segments of the lung close and hypoxaemia and carbon dioxide retention progressively increase. The resulting metabolic and respiratory acidosis further limits the production of surfactant from the type II pneumocytes. Hypoxaemia causes vasoconstriction of the pulmonary arteries thus compromising pulmonary perfusion and increasing the likelihood of right-to-left shunting through the foramen ovale and ductus arteriosus. Local ischaemic damage affects the alveolar tissue and capillary endothelium. Changes in pulmonary pressure brought about by the infant attempting to maintain adequate air flow, together with the low plasma protein level common in preterm infants, tend to cause displacement of fluid into the alveoli. Fibrinogen in the exudate is converted into fibrin and lines the alveoli thickening the membrane. The thickened membrane and excess fluid increase the diffusion distance and impair gas transfer.

The infant responds to the respiratory difficulties by increasing respiratory rate and effort. The clinical signs appear early and increase in severity over 2 or 3 days. The infant may grunt and exhibit oedema and cyanosis. Cyanosis tends to be progressive and is due to high levels of deoxygenated haemoglobin in the capillaries. It is enhanced by right-to-left shunting, alveolar hypoventilation and impaired gas diffusion across the alveolar membranes. The baby grunts because expiration is against a partially closed glottis, which increases pressure and retards expiratory flow, therefore increasing gas exchange. RDS risk is increased in prematurity, babies of diabetic mothers (because insulin is antagonistic to cortisol), antepartum haemorrhage and second-born twins. Male babies are twice as susceptible to RDS. Chronic hypertension, maternal heroin addiction, pre-eclampsia and growth retardation appear to protect against RDS.

Temperature regulation

Before birth

In utero, the fetus depends on its mother for temperature regulation. It loses heat via the placenta and via conduction (from skin to amniotic fluid to uterus). The fetus is a net heat producer although raised maternal temperature may compromise it (Edwards et al., 1997). Brown fat is actively inhibited and fetal oxygen consumption is about 30% of postnatal levels. Fetal temperature is maintained at about 0.5°C above maternal temperature and the fetus does not expend energy in keeping warm. Research has focused on raised maternal temperature due to fever, exercise and external raised temperature (such as hot baths and saunas). The results are inconclusive. However, maternal fever has effects not only on temperature gradients but also on oxygen consumption and haemodynamics and may be associated with teratogenesis and preterm labour.

After birth

The infant is usually born into a wet and relatively cold environment. As environmental temperature is usually lower than maternal temperature, the baby will experience a temperature loss at birth. Heat transfer is affected by two gradients: the internal gradient involving transfer from the core to the surface of the baby and the external gradient involving heat transfer from the body surface to the environment. Cooling is usually rapid at a rate of 0.2–1.0°C per minute depending on the environmental factors and the gestational age of the infant (which affects body composition). Transfer of heat through the internal gradient depends on insulation and blood flow. Neonates are predisposed to heat loss; they have less subcutaneous fat than adults do (about 16% body fat compared with 30%), a higher surface area:mass ratio (about three times the relative surface area of an adult) and a lower ability to shiver. Should the baby be born small, it will not only have an even larger surface area:mass ratio but also the insulation provided by its subcutaneous fat will also be further compromised and skin permeability will be increased. Small-for-dates babies have proportionately bigger heads and higher metabolism and are disadvantaged in that their heat losses are higher. Changes in peripheral circulation affect heat loss via conduction.

Heat loss across the external gradient depends on the temperature difference between the body and the environment. Conduction, convection, evaporation and radiation transfer heat from the baby. Warming objects that will come into contact with the neonate, and increasing insulation by wrapping, limit heat loss by conduction. Evaporation offers the greatest route for heat loss immediately after delivery but drying the baby, especially the head, immediately after delivery is effective at reducing the loss. Skin keratinization is inadequate in immature infants so evaporative heat losses are higher. Evaporative insensible heat loss increases with respiratory problems, activity, the use of radiant heaters or phototherapy and low relative humidity. Convective losses are related to draughts and are affected by ambient temperature and humidity. Higher air temperatures, minimal air circulation, swaddling and baby hats reduce heat loss by convection. Radiation is the major form of heat loss from babies in incubators. It involves the transfer of radiant energy to surrounding objects not directly in contact with the baby. Consideration therefore has to be given to the temperature of objects in the local environment including the incubator, walls and windows. Skin-to-skin contact with the mother immediately following birth is a very efficient way of reducing heat loss from the neonate. The large skin area and the softness of the breasts enable a large amount of maternal skin to come into direct contact with the baby's skin surface.

The mechanisms of heat conservation and generation mediated by the peripheral nervous system are insufficient in the neonate (Okken, 1991). Infants can produce heat from metabolic processes and by increasing activity. Postural changes are also important in conserving heat. Shivering is not so important in infants but heat generation by non-shivering thermogenesis (NST) is important. NST takes place in brown adipose tissue (BAT), a specialized type of adipose tissue that is well vascularized, particularly by sympathetic nerves, and has cells densely packed with mitochondria (Fig. 15.7). In humans, BAT is mostly replaced by white adipose tissue (WAT); adults have very few BAT cells which are interspersed with WAT (Wolf, 2009). However, BAT has a major role in heat production in the neonate. BAT is formed from about 30 weeks' gestation until about 4 weeks' postbirth. Fat mass is significantly altered by maternal nutrition and gestational length; stores of BAT (and white fat) are lower in preterm infants. BAT comprises about 2–7% of birth weight and is predominantly located around the core organs (Fig. 15.8). It generates heat by uncoupling electron transport from oxidative phosphorylation in the mitochondria so the energy released by electron transport will not be used to synthesize ATP but will be liberated as heat instead (Fig. 15.9). Fifty percentage of cellular respiration is uncoupled from ATP formation in BAT (Wolf, 2009). The unique uncoupling protein (UCP1) is a proton transporter located in the inner mitochondrial membrane. UCP1 causes protons to leak across the inner mitochondrial membrane so the electrochemical gradient, that usually drives ATP production, is lost and heat is produced. When UCP1 is maximally activated, it allows the production of at least 100 times as much heat from BAT compared to other tissue. UCP1 is synthesized during the maturation of fetal fat (Symonds et al., 2003). At birth, the activation of BAT is accompanied by mobilization of fat and a marked increase in lipolysis. Thermogenesis by BAT is inhibited in the fetus by PGE2 and prostacyclin (PGI2) produced by the placenta. The placenta also suppresses formation of active T3 (tri-iodothyronine) from T4(thyroxine) (see below).

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Fig. 15.7

Structures and development of white and brown adipose tissue.

(Reproduced with permission from Hull, 1966.)

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Fig. 15.8

Location of brown adipose tissue in the human infant.

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Fig. 15.9

Metabolic pathways in brown adipose tissue: triglycerides break down to yield useful heat (about 160 kcal/mol are produced during each turn of the cycle).

(Reproduced with permission from Begley et al., 1978.)

Heat production per unit mass of the neonate is higher than that of an adult; thermogenesis begins when a critical temperature difference of 12 °C between the environment and the skin is exceeded. The drop in temperature stimulates release of noradrenaline from sympathetic nerve endings that stimulate the brown adipose cells (Gunn et al., 1991). At birth, catecholamines from the adrenal medulla and rise in T3production by the thyroid gland augment the effect of noradrenaline. Inhibition of BAT by the placenta ceases. Oxygen consumption and metabolic rate increase markedly in response to a drop in temperature. Heat generation involves lipolysis of BAT, which depends on the availability of oxygen, ATP and glucose. There is a strong interrelationship between ventilation, feeding and temperature regulation, which means that hypoglycaemia, hypoxia or acidosis can affect the ability of the neonate to produce heat (Fig. 15.10). Persistent hypothermia can therefore result in metabolic acidosis (due to increased lactic acid production), decreased surfactant production and, if it is chronic, compromised growth. Cold stress or hypothermia will increase metabolic rate and peripheral and pulmonary vasoconstriction. The increased metabolic rate will increase oxygen demand. Peripheral and pulmonary vasoconstriction can compromise oxygenation and perfusion efficiency. Tissue hypoxia may increase acidosis because anaerobic metabolism increases lactic acid production. Hypoxia inhibits metabolic rate and compromises the thermal response; it also affects surfactant production.

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Fig. 15.10

Interrelationship between temperature regulation, glucose concentration and respiration.

Mechanisms for losing heat are not well developed in the neonate (Power, 1992). The neonate can lose some heat by sweating (which increases evaporation) but peripheral vasodilatation is the main source of heat loss. Although the density of neonatal sweat glands is high in some areas, they are less responsive and less efficient at sweat production. Phototherapy increases water loss. Sweating is more inefficient in preterm babies and those with central nervous system dysfunction. As the baby gets older and can rely on physical methods of generating heat, NST becomes less important. BAT gradually diminishes in the first year.

WAT provides both insulation and an energy reserve. Development of body fat in the fetus is under nutritional constraint whereas postnatal growth is controlled by genetic potential. Compared to other mammals, human infants are not only extremely fat at birth but also they continue to increase in adiposity during early postnatal life. Although it has been suggested that the role of the fat is insulation required as compensation for human hairlessness, evidence to support this is weak. A more likely explanation is that the adipose tissue acts as an energy reserve both to support the demands of a large brain and to protect the infant from nutritional disruption at birth and weaning or during infection (Kuzawa, 1998).

The neonatal liver


The functions of the neonatal liver are similar to those of an adult but are relatively immature. The ability to synthesize plasma proteins such as albumin and to metabolize foreign substances is inefficient. Neonates produce more bilirubin because the red blood cells have a higher turnover and shorter lifespan. These factors, together with immature intestinal processes, means the neonate is at increased risk of developing hyperbilirubinaemia. Before birth, bilirubin is cleared by the placenta and then handled by maternal metabolism. If bilirubin accumulates in the serum of the neonate, jaundice (or icterus) can occur; yellow staining of the skin and sclera. Neonatal jaundice is common affecting up to 60% of term and up to 80% of preterm infants (Juretschke, 2005). However, markedly elevated levels of bilirubin can cause severe jaundice and potentially cause brain damage. As the blood–brain barrier of the neonate is more permeable, free bilirubin can access the brain easily and in sufficient concentrations can deposit in the basal ganglia causing kernicterus (brain tissue is heavily stained with bilirubin). Bilirubin encephalopathy, damage to the brain by bilirubin deposits, results in a range of symptoms from convulsions and abnormal behaviour such as lethargy, hypotonia and poor suck to cerebral palsy, deafness or death.

Physiological jaundice is due to normal breakdown of red blood cells and neonatal immaturity; it is usually mild and resolves relatively quickly. Severe jaundice may result from increased production of bilirubin and/or decreased excretion. Risk factors include sepsis (which compromises the liver's ability to breakdown excess haemoglobin), excessive trauma and interstitial bleeding (e.g. haematomas, excess bruising, etc), polycythaemia, AB rhesus incompatibility (neonatal blood cells are destroyed by maternal antibodies) and liver abnormalities. In such cases, kernicterus is more likely to occur and so careful monitoring of serum bilirubin levels is required.

Bilirubin is a breakdown product of haemoglobin from red blood cells (Fig. 15.11). Iron from red blood cells is recycled. Haem, the pigment, is degraded by macrophages of the reticuloendothelial system to biliverdin and then to bilirubin. Unconjugated (indirect) bilirubin is insoluble and cannot be excreted. It is transported bound to plasma albumin to the liver to be metabolized into conjugated (direct) bilirubin, which is soluble. Conjugation involves binding of glucuronide sugars to bilirubin forming bilirubin diglucuronate. Conjugated bilirubin is excreted into bile and so into the duodenum. It is a major component of bile and faeces. In the intestine, conjugated bilirubin is further metabolized by bacterial flora to produce urobilin and stercobilin (which give the characteristic colour of faeces). Some of the breakdown products of bacterial metabolism of bilirubin are deconjugated and absorbed across the gut wall to be recirculated. Small amounts of bilirubin are also excreted via the kidneys.

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Fig. 15.11

Breakdown of haemoglobin to form bilirubin.

Decreased production of plasma proteins can result in raised unconjugated bilirubin levels. The pathways in the liver that deconjugate bilirubin to its water soluble, and therefore excretable, metabolite may also be compromised. As meconium is rich in bilirubin, delayed passage of meconium increases the possibility that bilirubin will be deconjugated, absorbed and re-enter the circulating pool. Production of bilirubin in neonates is inversely correlated to gestational age and remains high for a few weeks (Lockitch, 1994). This is partly due to high circulating levels of blood cells, which are then removed, and also to having more fragile red blood cells with a shorter lifespan (see Table 15.1). The risk of hyperbilirubinaemia is further increased by other conditions that stress this pathway such as excess blood cell breakdown (as in excessive trauma at birth or due to infection) or increased red blood cell breakdown (as in polycythaemia due to maternal diabetes).

Infants are vulnerable to a number of diseases which are associated with oxidative injury including retinopathy of prematurity, necrotising enterocolitis, intraventricular haemorrhage and BPD. It has been suggested that as bilirubin has antioxidant properties, there may be a potential benefit of raised levels of bilirubin in early infancy to help protect infants from oxidative damage (Juretschke, 2005).

Fuel storage

Fetal metabolism is dominated by anabolic pathways, whereas the neonate has to catabolize fuel stores to provide nutrients between periodic neonatal feeds (Hay, 1994). The last weeks of gestation are an important time for laying down lipids and glycogen. During fetal life, glycogen is stored in the liver and skeletal muscle. Hepatic glycogen provides the substrate for energy metabolism during delivery and the first few hours of postnatal life (Nelson, 1994). Fat stores serve as an alternative energy source; the neonate markedly increases fatty acid oxidation and uses ketone bodies for energy production. In the first few days of life, the respiratory quotient falls from 1.0 (as glucose sources are exhausted) to about 0.7 (a value similar to that seen in adult diabetics) as fat and protein are mobilized until adequate milk is consumed.

Glucose regulation

Thyroxine (T4) is relatively inactive and is usually converted to active tri-iodothyronine (T3). Fetal T3 levels are low because fetal liver levels of outer-ring deiodinase are low and placental levels of inner-ring deiodinase are high, both of which drive preferential production of inactive reverse T3. The resulting low level of the active thyroid hormone T3 can support brain development but suppresses oxygen consumption by non-neural tissues and inhibits thermogenesis. In late gestation, the rise in glucocorticoids induces expression of outer-ring deiodinase in the fetal liver so production of fetal T3 increases markedly. The rise in T3 plays a role not only in hepatic enzyme activity but also in tissue maturation and lung and bone development. At birth, the T3 levels increase further as the inner-ring deiodinase is reduced on placental separation, and evaporative cooling induces a rise in thyroid-stimulating hormone (TSH, thyrotrophin), which further stimulates hormone production by the thyroid gland. Adipose tissue significantly contributes to the conversion of T4 to T3 after delivery; smaller fat depots result in less thyroid hormone production, potentially further compromising thermogenesis in premature infants.

Blood glucose levels in the neonate tend to fall after delivery because the immature liver is better at promoting glycogen synthesis than glycogenolysis, and because the baby has increased activity and metabolism at birth. At birth, neonatal glucose concentrations are about 70% of maternal levels (Aylott, 2006) and falls to its lowest point 1–2 h later. The neonate has a high requirement for glucose because it has a relatively large brain and more and larger red blood cells. The stress of delivery and cooling at birth stimulate the release of catecholamines, which stimulate glucagon release and suppress insulin release and are important in activating the metabolic pathways in the liver. The neonate is unable to regulate blood glucose efficiently (Smith, 1995) and is usually hypoglycaemic (glucose levels are about 2 mmol/L) (Box 15.5). The enzymes involving glucose metabolism do not reach optimal levels in the liver for 2–3 weeks, so glycogenolysis (mobilization of glycogen stores) and gluconeogenesis (hepatic synthesis of glucose from substrates) are relatively slow in correcting falls in blood glucose. Lipolysis generates ketones which are used as alternative sources of energy for brain metabolism. If the delivery is protracted, the neonate may deplete its glycogen stores. Also the response to raised levels of glucose is slow; although adequate concentrations of insulin are present in the pancreas, the β-cells initially lack sensitivity to glucose, responding better to amino acids. Thus, neonatal blood glucose levels fluctuate and hypoglycaemia may occur because hepatic glucose production is inadequate or there is excess insulin secretion (common in the infants of mothers with gestational diabetes). Hypoxia and hypothermia can exacerbate hypoglycaemia because of the energetic costs of respiration and heat production, respectively. Blood glucose values as low as 1.0 mmol/L have been recorded. In an adult, such a level of hypoglycaemia would cause convulsions, hypoglycaemic coma and probable neurological damage, whereas in the newborn they might cause an apnoeic attack. The central nervous system of the neonate exhibits a degree of plasticity and is partially protected as it can utilize fatty acids and ketones efficiently. Physiological responses to hypoglycaemia activate the sympathetic nervous system and cause neuroglycopenia. Clinical signs of hypoglycaemia can include changes in level of consciousness (such as lethargy and drowsiness), changes in behaviour (such as irritability and jitteriness, hypotonia and poor feeding) and changes in vital signs (such as apnoea, hypothermia, bradycardia, bounding pulse and sweating).

Box 15.5

Risk factors and symptoms of hypoglycaemia

Risk factors

• Hypothermia, evaporation, draughts, cold room

• Babies who do not feed or have a poor response to feeding in the early postnatal period

• Intrauterine growth retardation (IUGR)

• Prematurity

• Maternal diabetes

• Stress


• Lethargy: ‘floppy baby’ (normal muscle tone is reduced to conserve glucose usage of skeletal muscle)

• Drowsiness: difficult to rouse, indicating neurological function is impaired by lack of glucose

• Jitteriness: an adverse tremor in response to stimulation such as loud noise or touch, indicating neurological inhibition of reflexes is affected

• Coldness: may be a cause or consequence of hypoglycaemia

Note: many babies may be hypoglycaemic without clinical symptoms, indicating that they are maintaining normal neurological function by other metabolic pathways. The clinical symptoms indicate these pathways are failing and the infant is at risk. Hypoglycaemic screening of the neonate involves measuring the level of glucose in the infant's blood by analysis of a small amount obtained from a heel prick.

The gastrointestinal system at birth

The gut completes anatomical development by week 24 and the term neonate is able to digest and absorb milk from birth. The fetus swallows amniotic fluid which passes through the gut. Water, electrolytes and glucose are absorbed in the small intestine. Species-specific growth factors in milk are important in promoting postnatal development of the gut. The neonatal gut has immature digestive and absorptive capacities but there are a number of compensatory mechanisms, particularly for babies who are breastfed who receive both digestive enzymes and growth factors that stimulate gut development in the milk (Lonnerdal, 2003).

Feeding reflexes

From birth, a normal infant can suck from the breast, convey milk to the back of the mouth and swallow it for a period of 5–10 min while breathing normally. There is an innate programme of reflexes and behaviour, which become evident within an hour or so following delivery, including the ability to move from the mother's abdomen to her breast, coordinated hand–mouth activity, rooting for the nipple, attaching to the breast and feeding vigorously before falling asleep. Touching the palate triggers the sucking reflex. The neonate exhibits rhythmic jaw action, which creates a negative pressure, and the peristaltic action of the tongue and jaw strips milk from the breast and moves it to the throat thus triggering the swallowing reflex. These breastfeeding reflexes are strong at birth in the normal neonate and are evident in preterm babies from about 32 weeks (about 1200 g). Extremely preterm babies and those that are sick or have a very low birth weight have markedly decreased or absent reflexes. Other babies who experience feeding problems include those with physical problems such as cleft lip or palate and those subjected to obstetric sedation, analgesia or extreme stress at birth.

The sucking and swallowing reflexes are aided by the particular morphological configuration of the neonate's mouth, which has a proportionately longer soft palate. The neonate also has an extrusion reflex in response to the presence of solid or semisolid material in the mouth. This reflex is lost at 4–6 months and is replaced by a pattern of rhythmic biting movements coinciding with the development of the first teeth at 7–9 months.

Hormone and enzyme production

Gastric secretion is developed but low; responses to gut regulatory hormones appear also to be low. The effect is that the gastric juice has a pH close to neutral (compared with a pH of 2 in an adult's stomach). The high gastric pH means that salivary amylase is not inactivated in the stomach so starch digestion can continue. Reflux of gastric contents is common, as the lower oesophageal sphincter is immature in both musculature and neurological control. Less-acidic gastric juice does not cause painful tissue damage to the oesophageal mucosa but also it is less effective at denaturing proteins including microorganisms. It has been suggested that a reflux of human milk is advantageous as very small amounts of milk may reach the upper part of the respiratory tract conferring an immunological benefit there. Breastfed babies have a lower incidence of respiratory problems. Decreased acid production in the stomach means that the activation of pepsinogen to pepsin is restricted, limiting protein digestion in the stomach. The decreased acidity and protein digestion may enhance the defence mechanism promoting the activity of immunoglobulins and antigen recognition in the gastrointestinal tract as these proteins survive the gentler gastric environment.

Pancreatic amylase levels are low in the newborn but breast milk contains mammary amylase, which can augment starch digestion. Colostrum is particularly rich in mammary amylase. Lactase activity is relatively late in developing, reaching adequate levels after 36 weeks' gestation. However, many preterm babies can digest lactose satisfactorily as unabsorbed lactose can be metabolized by colonic bacteria to short-chain fatty acids, which can then be absorbed thus salvaging the energy. The low pancreatic lipase levels are compensated for by lingual and gastric lipase produced by the neonate (stimulated by suckling) and by bile salt-stimulated lipase in human milk. Bile acid formation is low but human milk is rich in taurine, which is used for neonatal conjugation of bile salts.

Bowel movements

Passage of meconium, a mix of mucus, epithelial and gut cells, larger molecules and skin cell debris from the amniotic fluid, fatty acids and bile pigments (which gives it the characteristic greenish-black colour) confirms that the lower bowel is patent. (Usually defaecation does not occur in utero unless the fetus is stressed.) Passage of a changing stool (meconium and food residue), usually within 24 h, indicates the whole gut is patent. Slow (more than 48 h after birth) or absent passage of meconium can indicate Hirschsprung's disease, impaired motility of the colon due to the absence of ganglion cells; diagnosis is usually made following biopsy of the bowel wall. At birth, the stomach capacity is 10–20 mL, which rapidly increases to 200 mL by 1 year.

The kidneys

Before birth

In utero, from 9 to 10 weeks' gestation, the fetus produces large volumes of hypotonic (dilute) urine, which is an important contributor to amniotic fluid (Box 15.6). However, the regulatory and excretory functions of the kidneys are minimal before birth (Guillery, 1997). The placenta corrects any osmotic imbalance. Mature kidney function is not developed until about 1 month; until then the urine is fetal-like. The neonatal kidneys, weighing about 12.5 g each, have a low glomerular filtration rate (GFR) and relatively low surface area. The ability to reabsorb or excrete sodium (Na+) is poor so the urine produced is of low specific gravity and hypotonic, reaching 1.5 times plasma concentration (700–800 mOsm) compared to adult values of three to five times plasma concentration (1200–1400 mOsm).

Box 15.6

Clinical symptoms of Potter's syndrome

• Bilateral renal agenesis (absence of kidneys)

• Urine is not excreted into amniotic fluid

• Results in oligohydramnios (defined as less than 500 mL of amniotic fluid at term)

• Incidence: about one in 3000 live births

• Incompatible with postnatal life; most affected babies die within a few hours of birth

• Causes: pulmonary hypoplasia because of restricted space for thoracic expansion and an imbalance of fluid for filling the lungs; musculoskeletal abnormalities because fetal movement is constrained; abnormal facies because face is moulded by compression; cord compression in labour and fetal distress (Scott and Goodburn, 1995)

After birth

At birth, the normal obligatory water loss means the baby loses 5–10% of its birth weight in the first 4 days as a result of the loss of water and Na+. Neonatal renal function can efficiently prevent dehydration and eliminate the lower level of metabolic waste products of the breastfed infant. Because the newborn infant does not retain Na+ efficiently, it is vulnerable to dehydration. Changing fluid intake (or increasing the solute load) can result in osmotic imbalance, acidosis or dehydration. The risks are lower if the baby is feeding on demand; however, the very immature renal function of preterm babies requires careful calculation of fluid and electrolyte balance as Na+-rich urine may be produced despite low plasma Na+ levels. This can be crucial if there is high extrarenal water loss, for instance in the presence of fever or high ambient temperature.

The ability to excrete protons or hydrogen ions (H+) is also limited, thus increasing the neonate's susceptibility to acidosis. Elimination of drugs such as antibiotics cleared by the renal system is decreased so the half-life of the drug in the circulation is increased necessitating a requirement for decreased frequency of dose. The neonate should urinate within 24 h of delivery. Initially, 15–30 mL/kg of urine is produced per day increasing to 100–200 mL/kg by day 7 as the fluid intake increases. Mature renal function is not achieved until 12 months to 2 years.

The nervous system

Before birth

The fetus responds to noises, intense light, noxious stimulation of the skin and decreased temperature by changing autonomic responses such as heart rate and by moving. Fetal movements can be felt from about week 14; the ‘exercise’ is thought to aid muscle growth and limb development. By term, the nervous system is prepared to process and receive information. Human cortical function is relatively immature compared with that of some other mammalian species. Complete myelination of the long motor pathways occurs after birth, therefore fine movements of the fingers, for instance, are not evident until several months after birth.

After birth

After birth, the nervous system undergoes accelerated development in response to increased sensory input. Reflexes may be slightly depressed for the first 24 h, particularly if there has been transplacental transfer of narcotic analgesia, after which several reflexes can be elicited. In cases of severe asphyxia, low Apgar scores (see p. 399) or neurological damage, reflexes are depressed, abnormal and may take longer to appear. The grasping reflex and the Moro embrace are used to assess the reflex ability of the newborn. Babies also demonstrate a strong palmar grasp and a rhythmic stepping movement. Many reflexes common to the neonate disappear unless there is pathological interference, in which case they may be exhibited in the adult, for example Babinski's reflex. The baby exhibits general awareness to its surroundings and reacts to sound and light.

Babies are born with active sensory pathways. Studies have demonstrated that neonates can recognize the smell of their mother's milk. They can differentiate between tastes and appear to have a preference for sweet tastes. Although babies can see at birth, there are big postnatal developments in visual capability, particularly in the first 6 months. The neonate has limited visual acuity but appears to focus at a distance of 20 cm. From birth, babies can discriminate between contrast and contours and can follow movement. The neonate is able to hear and discriminate between sounds particularly those of low- to middle-range frequency. Studies have demonstrated a neonate's ability to recognize the characteristics of their mother's voice and to demonstrate a preference for rhythmic sing-song intonation. Neonates are reassured by the rhythmic sounds of breathing, heartbeat and gut peristalsis, which they hear, for instance, while being held. Newborn infants can be trained to activate a tape recorder by sucking non-nutritively on a modified nipple; they demonstrate that they recognize not only their mother's voice but also particular passages of a book that they were read in utero (Lipsitt and Rovee-Collier, 2001). The development of motor function is described by the ‘Jacksonian principle’, a hierarchical model whereby the last reflexes to develop are the first to be lost when the organism degenerates and dies. This pattern occurs because the first reflexes to develop are well rehearsed and require less oxygen to be initiated than more recent reflexes. The order of sensory development (tactile, vestibular, thermal, chemical, auditory and visual) is also reversed during injury, disease or ageing.

Sleep and behavioural states

The fetus exhibits slow-wave and REM sleep between patterns of wakefulness. The neonate sleeps about 16 h per day, 40% in REM sleep, compared with a total of 12 h asleep at 2 years of age (20% in REM sleep). Sleep patterns are not diurnal and do not follow a light–dark cycle. Six sleep–wake states are recognized: quiet (deep) sleep, active (light) sleep, drowsy state, awake (quiet) alert, active alert and crying (Wolff, 1966). The proportion of time in each state varies with postconceptual age. Quiet deep sleep is restful and the baby is in an anabolic state when growth hormone secretion is high, mitotic rate is high, oxygen consumption is low and there is little movement. In active sleep, the eyes are closed but the baby moves its face and extremities. Respiration and heart rate are irregular. The baby exhibits ‘paradoxical’ REM sleep, in which the brain activity is similar to awake states. This state is associated with learning and synapse development. The drowsy state is transitional between being awake and asleep. The eyes are open and the baby is alert but has little movement. The baby appears to focus on visual stimuli and appears to be processing sensory information. In the active alert state, respiration rate is increased and is irregular. There are skin colour changes, much activity and the baby has increased sensitivity to stimuli. Crying is the method of communication usually in response to unpleasant stimuli. Characteristically, neonates close their eyes, grimace and make sounds. However, preterm infants may not be capable of making a noise.

At one time, it was believed that the immature degree of myelination and lack of experience meant that neonates were unable to perceive pain. In fact, not only do the anatomical and functional requirements for pain perception develop early and the fetus, preterm and term infant demonstrate similar physiological responses to the adult, but there is also evidence that pain perception is more intense and that early experience of pain has long-term developmental and behavioural consequences (Taddio and Katz, 2004). Abundant sensory fibres, a functional spinal reflex, connections to the thalamus and connections to subplate neurons are evident by 20 weeks of fetal development but mature thalamocortical projections are not present until about 30 weeks (Lowery et al., 2007). It is obviously difficult to measure and interpret pain in the fetus during gestation but many countries are introducing legislation to require consideration of possible fetal pain during intentional termination of pregnancy. In the neonate, procedures likely to cause pain cause catecholamine and cortisol release to increase, heart rate and respiration rates to change, metabolic rate and oxygen consumption to increase and blood glucose levels to rise. The rate of transmission may be slower but a probable shorter distance between the pain receptor and brain compensates for this. Assessment of pain can be difficult as pain may be expressed differently in neonates; facial expressions may be used but some babies tend to withdraw and increase passivity and sleep more in response to pain.

The skin and immune system

The skin of a neonate appears relatively transparent and soft and velvety. It is important in temperature regulation, as a barrier and as a sensory organ. Part of the appearance is due to the lack of large skin folds and localized oedema. Melanin production and pigmentation are low in the newborn so the skin is vulnerable to damage by ultraviolet rays. However, residual levels of maternal and placental hormones can produce transient pigmentation of certain skin areas. During delivery, the skin is subject to changes in blood flow and mechanical stress from the pressure of contractions and from maternal structures which can result in abrasions and ischaemia. Obstetric interventions, for example, fetal monitoring, scalp sampling and use of amnio-hooks, forceps and vacuum extraction, also compromise the integrity of the skin. Immediately after birth, most fair-skinned babies have characteristic pink coloration with blue but warm extremities.

Vernix caseosa is a superficial fatty substance that coats the fetal skin from the middle of gestation and subsequently decreases as gestation progresses. Lanugo is the first generation of downy body hair that is fine and unpigmented; it appears from the 12th week and is mostly shed before birth. Vernix caseosa tends to accumulate at the sites of dense lanugo growth and is evident on the preterm baby on the face, ears and shoulders and in folds. At term, traces of vernix are present on the brow, ears and in the skin creases. Vernix caseosa is composed of sebaceous gland secretion and skin cells and is rich in triacylglycerides, cholesterol and fats. Its role is to protect the fetus from the amniotic fluid and to prevent loss of water and electrolytes. It provides insulation for the skin and helps to reduce friction at delivery; it may also have antibacterial properties.

The barrier properties of the stratum corneum of the skin increase with increased gestational age, especially after 24 weeks (Rutter, 1996). The epidermis of a preterm baby might be only five layers thick compared with about 15 layers in a term infant. A thinner epidermal layer results in increased transepidermal water loss, decreased ability to cope with friction, thermal instability because of the increased blood supply to the surface and increased permeability to microorganisms and chemicals (such as topically applied substances and reagents on clothes). Premature babies have translucent shiny red skin that becomes pinker through to the white thick skin of term infants. Drying out of the skin is a normal maturation process. Substances that interfere with the keratinization process, such as emollients, can delay the development of the skin becoming effective as a barrier. The transepidermal water loss can be limited by use of a thermal blanket, altering the air flow and maintaining an insulating layer of saturated air in contact with the skin.

The neonate is a compromised host, vulnerable to nocosomial (cross) infection. Host defence mechanisms are immature, partly because of lack of previous exposure to common organisms and partly because the neonate has limited cellular responses (see Chapter 10). Breaks in the delicate mucosa and skin from delivery and invasive obstetric procedures provide opportunities for the entry of pathogenic bacteria. In relation to artificial feeding, neonates are at increased risk of developing gastrointestinal infections, which may be associated with later development of allergies. Preterm infants, especially those of less than 34 weeks' gestation, are very vulnerable as they have less maternal IgG transfer. At birth, the neonate leaves the sterile fetal environment for one loaded with microorganisms (Jarvis, 1996). Ingestion and inhalation provide routes for bacterial colonization after birth, initially with organisms derived from the maternal genital tract. The neonate's skin, umbilical cord and genitalia are colonized first, followed by the face, respiratory system and gut. Skin flora is increased in infants with little vernix caseosa and is limited by antiseptic agents and alkaline soaps. The use of detergents may affect the integrity of the skin and cause dermatitis by interfering with the pH mantle; therefore, the use of only water to clean neonatal skin is advocated. If heavy soiling is present, then the use of pH neutral products may minimize skin irritation (Cork et al., 2009). There seems to be no differences to the effects on the skin whether the infant is bathed or washed using a cloth (Blume-Peytavi et al., 2009).

Initially, gut colonization is with organisms that the infant comes into contact with at and immediately after delivery. The profile of organisms is affected by the diet; breastfed babies have optimal conditions for the growth of the protective lactobacilli and bifidobacterium. Different patterns are seen in babies of very low birth weight and those who require feeding or ventilatory assistance. Meconium in vivo is usually sterile but when excreted provides rich culture conditions for microorganisms. The use of antibiotics changes the pattern of bacterial colonization of the neonate and can encourage the growth of resistant bacteria.

Case study 15.1 gives an example of neonatal infection.

Case study 15.1

During a routine visit, the midwife examines Tracy, a 3-day-old baby, who was delivered in hospital and discharged the day before. Her umbilicus appears moist and sticky so the midwife takes a swab for culture and sensitivity. Two days later it is revealed that Tracy's umbilicus has been colonized with methicillin-resistant Staphylococcus aureus (MRSA). The infant appears well, has been exclusively breastfed and has regained her birth weight.

• What treatment, if any, would Tracy require and what reasons could be applied to argue against the use of antibiotic therapy?

• Do you think it is necessary to try to identify the source of the infection?

• What should the midwife do to ensure that further cross-infections do not occur?

• What factors may put other individuals at risk?

Normal neonatal transition

Much of the physiological adaptation to extrauterine life takes place during the first few hours following birth but final cardiovascular changes may not take up to 6 weeks. During the first few hours, most of the fetal lung fluid is absorbed, normal lung function is established and the normal neonatal blood flow to the lungs and tissues is initiated. This results in a pattern of predictable changes which can be monitored as changes in heart rate, respiratory pattern, gastrointestinal function and body temperature. Three discrete phases of neonatal transition were identified (Askin, 2009a). The first phase (0–30 min) is a period of reactivity; heart rate increases, respiration is irregular and fine crackles in the chest are accompanied by nasal flaring and grunting. This is followed by a phase of decreased responsiveness (30 min to 3 h) in which respiration is more shallow, heart rate decreases and muscle activity is decreased but jerks, twitches and sleep may occur. The third phase is another phase of reactivity (3–8 h after birth) in which tachycardia and a labile heart rate are common, tone and colour may change and aging and vomiting are not uncommon. Healthy infants may continue to exhibit normal signs of transition in the first 24 h of life; these may include lung crackles, a soft heart murmur (due to turbulent blood flow following the closure of fetal vascular shunts), tachypnoea, tachycardia and acrocyanosis. Some infants may also exhibit mild-to-moderate respiratory distress, slight temperature instability and slightly low blood sugar levels. Immediately following delivery, it is considered normal for infants to exhibit transient acrocyanosis during episodes of crying.

Delayed or complicated adaptation or increased signs of distress are important to identify quickly to ensure appropriate interventions. Risk factors for abnormal transition include maternal factors such as diabetes, hypertension, anaemia and shock, prenatal factors such as growth restriction, placental problems, multiple gestation, mal-presentation and drug exposure, intrapartum factors such as infection, instrumental delivery, meconium-stained amniotic fluid and fetal distress or factors affecting the neonate directly such as prematurity or postmaturity, birth trauma and congenital malformations. Moderate to severe respiratory distress is indicated by intermittent grunting, nasal flaring, marked retractions, tachypnoea (respiratory rates of 100–120 breaths per minute) and prolonged need for supplemental oxygen. Persistent pulmonary hypertension of the newborn (PPHN) is due to the normal drop in PVR not occurring so there is continued shunting of blood away from the lungs in a fetal circulatory pattern. The resulting hypoxia causes further constriction of the pulmonary vessels and on-going shunting. Mild respiratory problems such as TTN may result in acrocyanosis whereas more severe problems can be evident as central cyanosis, pallor or greyness. Cyanosis is due to the presence of desaturated (unoxygenated) haemoglobin so hypoxia can be masked by anaemia and polycythaemic babies can look cyanotic at higher oxygen saturation levels because they have more haemoglobin. Pallor might indicate anaemia. Although a soft heart murmur is common in the first 24 h after birth, a cardiac murmur accompanied by respiratory distress, cyanosis or signs of congestive heart failure needs further investigation. Abnormal heart rate and rhythm might indicate compromised cardiovascular function. Persistent bradycardia (heart rate less than 80 bpm) can be due to heart block associated with maternal SLE and bradycardia during rest and sleep can indicate hypoxia and sepsis.

Initial examination of the newborn

After delivery, the baby is always examined by a midwife who, in accordance with professional legislative requirements, must refer any deviation from the normal to a medical practitioner. There is a statutory requirement to document findings.

The Apgar score

The baby's condition, including mental and physical development and level of alertness, is assessed using the Apgar score (Table 15.2). Although ‘Apgar’ is named after Virginia Apgar, the doctor who developed the scoring system, the mnemonic Appearance, Pulse, Grimace, Activity and Respiration can be useful.

Table 15.2 Apgar score





Heart rate


Slow (<100 beats per minute)

Fast (>100 beats per minute)

Respiratory effort


Irregular, slow

Regular, cry

Muscle tone


Some flexion in limbs

Well-flexed limbs

Reflex irritability



Cough, cry


White, blue

Body pink, extremities blue

Completely pink

Although the interpretative value of the Apgar score has been questioned, it is a means of assessing a baby for the absence or presence and degree of birth asphyxia. It is quick and simple and no other test has been routinely adopted. The Apgar test scores the baby's heart rate, respiratory effort, colour (of the skin in pale-skinned infants and of the mucous membrane in dark-skinned babies), muscle tone and reflex responses at 1 and 5 min following birth. It is repeated at 5-min intervals when active resuscitation measures are undertaken. The 1-min score may be low as the baby has been subjected to physical stress including a drop in temperature. Measurement of heart rate can be done by listening to the heart with a stethoscope or palpating the heart via the anterior chest wall. A heart rate of 110–150 beats per minute is considered normal. A heart rate persistently above 160 may be due to respiratory problems or sepsis. A heart rate of 90 or less may be indicative of congenital heart block, for example, associated with antiphospholipid syndrome or maternal SLE. A baby who is crying is obviously breathing in order to produce sound. Breathing can be seen easily, even on quiet babies. The respiratory rate of a healthy newborn baby is about 40–60 breaths per minute and should not be punctuated by grunting. A high-pitched or irritable cry may indicate brain damage or cerebral irritation due to oedema or haemorrhage. Rapid respirations in conjunction with chest retractions should be observed closely – early resolution is common in TTN but if prolonged may indicate sepsis.

The colour of the mucous membranes inside the mouth and the eyelids is assessed. If the blood flow is good, as in a healthy baby, these areas will be pink. If the tissues are being deprived of oxygen, they appear purplish or navy blue if the deprivation is severe. Healthy babies often appear bluish at the extremities but this may be due to cold rather than poor circulation. The face may appear congested if the cord was around the neck or if pressure from the delivery was prolonged. Pale babies may be anaemic, and polycythaemic babies (with an excess of red blood cells) tend to look very red.

The rooting reflex, turning of the head towards a touch on the cheek, is noted. Alternative reflexes include the baby curling the toes if the sole of the foot is stroked or responding with a grabbing movement if the palm of the hand is stroked (palmar grasp reflex). Abnormal responses such as the toes curling upwards (Babinski's sign) are often associated with abnormalities. The Moro reflex is looked for by startling the baby. If the head is allowed to drop back a few centimetres, the baby responds by flinging the arms outwards, usually accompanied by crying.

Muscle tone is more difficult to assess. All newborn babies have poorly developed musculature and seem fairly floppy, but babies who are especially floppy because they have immature coordination do not resist limb movement. Healthy babies have flexed limbs and respond to handling; the normal procedure is to lay the baby on the midwife's hand resting on its stomach and to observe position of the limbs.

A baby that needs urgent resuscitation is pale and floppy has a sluggish pulse and makes no respiratory effort. This is apparent and needs immediate response without having to calculate the Apgar score first. The Apgar score indicates the baby's capability to survive without intervention. If the Apgar score is above 7, little intervention is required, but a baby with an Apgar score of 5–7 will often need cutaneous stimulation and oxygen via a face mask. A score of 3–5 usually requires administration of oxygen via an ‘Ambu’ bag or equipment that allows facial oxygen to be delivered under cycles of positive pressure to inflate the lungs. A lower score requires immediate active treatment usually requiring ventilation via an endotracheal tube.

Case study 15.2 is an example of a baby possibly in need of resuscitation.

Case study 15.2

Paul is only 10 s old. He appears blue, not moving and limp and does not respond to touch. The midwife summons help and a paediatrician is called. The paediatrician arrives 4 min later to find a healthy, well-perfused infant, crying while being held by his mother.

• Was the midwife justified in being cautious by summoning a paediatrician early?

• How many midwives in practice wait a full minute before their initial assessment of the newborn?

• What actions do you think the midwife took prior to the arrival of the paediatrician?

• What care will Paul require in the first few hours of his life and are there any specific observations that the midwives should be carrying out during this period?

Body measurements and inspection

Once these tests are completed, further examination of the newborn can take place. An initial development check is followed by a fuller examination about 24 h later. It is becoming more common for midwives to undertake this more detailed examination of the newborn which traditionally was always undertaken by a paediatrician or general practitioner. This examination includes screening for common conditions such as congenital cataracts, cardiac and circulatory abnormalities, congenital hip dysplasia (CHD). Minor physical anomalies and variations can be found in 15–20% of newborns but most are not significant; some specific anomalies may indicate an underlying medical condition or genetic syndrome (Askin, 2009b). Major congenital anomalies are structural defects, such as cleft palate, gastroschisis and spina bifida, present at birth that significantly affect function or social acceptability. Minor congenital anomalies, such as birth marks and skin tags, have minimal effect on function but have social significance; they predominantly occur on the face or hands because there are the areas which are complex. Developmental or normal variations are found in about 4% of the population and have no functional or social significance. Chromosomal investigation is recommended if three or more congenital anomalies are present (Askin, 2009b).

The baby's weight, length and head circumference are measured and recorded, however, it is important to note that head circumference and length may change as moulding of the fetal skull and oedema in the scalp resolves. Babies with birth weights above the 90th centile or below the 10th centile have an increased risk of becoming hypoglycaemic.

Examination of the genitalia allows assignation of the sex of the baby. Small genetalia may indicate underlying endocrine disorders or genetic syndromes. In male infants, the scrotum is felt for the presence of both testes and the position of the urethral exit on the penis is checked. In female babies, the vaginal and urethral orifices are inspected. Presence of meconium demonstrates patency of the anus; this may become evident on rectal temperature measurement although rectal temperature recording should be avoided unless the baby is very cold and the core temperature needs assessing due to the increased risk of developing necrotizing enterocolitis.

Moulding of the head, oedema of the scalp and distortion of the face are common at birth because of intrauterine pressure, the pressure imposed by the birth canal (see Chapter 13) and birth trauma. Microcephaly or macrocephaly feature in a number of syndromes and may indicate intrauterine infection. The normal term infant is well endowed with subcutaneous fat and usually has vernix caseosa in the skin folds. Postmature babies may have dry and peeling skin. The fontanelles and suture lines are observed. Bulging fontanelles may indicate an increased pressure and sunken fontanelles that the baby is dehydrated. An abnormal-shaped head indicates abnormal moulding (see Chapter 13). Eyes and ears are checked for abnormalities; the eyes should be clear and free from discharge. Low-set, absent or deformed ears may be associated with chromosomal abnormalities. The baby's mouth is inspected for the presence of teeth, which can be removed, or other extraneous material. Both the soft and hard palate are checked; the baby should demonstrate a sucking reflex. Minor skin blemishes are common. Hypertrophic sebaceous glands or milia present as white spots on about 40% babies. Both these spots and ‘stork marks’ – minor capillary haemangiomas – usually on the nose or eyelids, disappear within a few months of delivery.

The overall morphology of the baby should be symmetrical. The insertion of the umbilicus should be central, and is checked for swellings. The nipples, of either male or female babies, may be swollen and producing milk in response to circulating maternal hormones. Respiratory movement of the chest of a healthy baby is symmetrical and the abdomen is rounded. The limbs are checked for equal length and free movement; short limbs can indicate achondroplasia. A single crease across the hand (Simian crease) is a common variant but occurs with higher incidence in Down's syndrome. The digits are counted; extra digits (polydactyly), a curved fifth finger (clinodactyly), fused fingers (syndactyly) and webbing between the digits are relatively common. The feet and ankles are examined for talipes and other abnormalities.

Visible signs of congenital dislocation of the hips (CDH) also known as CHD are asymmetry of the pelvis, asymmetrical creases in the groin and apparent differences in leg length. Midwives may be discouraged from undertaking manipulative tests of the hips as there is a danger of malpositioning the head of the femur into the acetabular cup, which can trap the femoral blood flow resulting in necrosis of the head of the femur. Midwifery units usually have local policies and protocols for the screening of hips for congenital dislocation.

The neck is observed for shortness, webbing or folds of skin on the back of the neck; these characteristics are associated with chromosomal abnormalities, such as Turner's syndrome. The spine is checked for swellings or defects and for pilonidal dimples or hairy patches, which may indicate occult spina bifida. Before the baby is discharged from the postnatal ward, there should be confirmation that the baby is feeding normally; excretion of urine and meconium normally occurs within 24 and 48 h of delivery, respectively. Early screening is important both to reassure the parents and to detect any abnormality or problem requiring further investigation.

Key points

• Many changes must occur at birth for successful transition to neonatal life, including initiation of breathing, conversion from fetal to neonatal circulation and physiological homeostatic control of thermoregulation and metabolism.

• The transition to neonatal circulation requires closure of the fetal shunts and vasodilatation of the pulmonary circulation; oxygen is a major stimulant.

• Successful breathing requires adequate maturation of the lungs, particularly the presence of adequate surfactant and neuromuscular control, and clearance of lung fluid.

• The relatively large surface area of neonates means they are vulnerable to excessive heat loss; body temperature is maintained by non-shivering thermogenesis. Efforts to reduce heat loss at birth are essential.

• Normal newborn infants are able to maintain adequate blood glucose levels be compromised by a stressful labour, abnormal maternal metabolism, restricted fetal growth and prematurity.

• Human milk and early physiological conditions compensate for the immature development of the neonatal gut.

Application to practice

An understanding of the transition to neonatal life is important for the following reasons. Many infants require some degree of intervention to support establishment of respiration after birth. An infant who does not appear to adapt fully at birth (i.e. is cyanotic) may for example have an underlying cardiac defect or be suffering from sepsis.

The midwife should use her or his assessment of adaptation as part of the neonatal check and not check solely for visible abnormalities therefore assessment of factors such as alertness, movement, muscle tone and vital signs, in the context of maternal, family and antenatal/perinatal history, is an important component of the initial and 24-h detailed examinations.

Many parents are distressed at the appearance of a baby that has just been born and need reassurance that the transition is not always completely spontaneous and that this is quite normal. An understanding of the effects of hypoxia and anoxia during labour are important in the planning the subsequent care of an affected neonate following delivery.

Annotated further reading

Askin, D.F.; Physical, assessment of the newborn: part 1 of 2: preparation through auscultation, Nurs Womens Health 11 (2007) 292–301.

Askin, D.F., Physical assessment of the newborn: part 2 of 2: inspection through palpation, Nurs Womens Health 11 (2007) 304–313.

A comprehensive description, published in two parts, of a thorough and structured approach to undertaking a head-to-toe physical inspection of the newborn using palpation and auscultation. These guides provide a practical and structured approach for practitioners undertaking examination of the newborn.

Askin, D.F., Fetal-to-neonatal transition – what is normal and what is not? Part 2: red Flags, Neonatal Netw 28 (2009) e37–e40.

A clear summary of the signs and symptoms of the common complications of neonatal physiological transition to extrauterine life which warrant further investigation in order to identify infants with underlying disease or abnormalities.

Baston, H.; Durward, H., Examination of the newborn. ed 2 (2010) Routledge, London .

For practitioners wanting to develop their skills in undertaking examination of the newborn this book is a comprehensive text covering all aspects of the physical examination.

Blackburn, S.; Maternal, fetal, & neonatal physiology: a clinical perspective. ed 3 (2007) Saunders .

An in-depth and well-illustrated description of physiological adaptation to pregnancy and development of the fetus and neonate that draws from physiological research studies. The chapters are clearly organized by physiological systems and link physiological concepts to clinical applications, including the assessment and management of low- and high-risk pregnancies.

Burke, C., Perinatal sepsis, J Perinatal Neonatal Nurs 23 (2009) 42–51.

A guide to the risk factors, symptoms, diagnosis, management and physiological effects of sepsis in the neonate. Recognition of sepsis in the neonate is often difficult and this guide is useful in enabling practitioners recognise the early subtle signs of sepsis.

Christensen, R.D.; Henry, E.; Jopling, J.; et al., The CBC: reference ranges for neonates, Semin Perinatol 33 (2009) 3–11.

A review, based on recent research reports, which proposes references ranges for parameters of the complete blood count for neonates of various gestational and postnatal ages and discusses the physiological reasons for the different normal values.

Davies, L.; McDonald, S., Examination of the newborn and neonatal health: a multidimensional approach. (2008) Churchill Livingstone .

This book has chapters that focus on pre-birth influences that should be considered when undertaking the examination of the newborn. It also focuses on the screening elements of the newborn examination.

Di Renzo, G.C.; Simeoni, U., An atlas of the prenate and neonate: the transition to extrauteine life informa. (2006) .

Practitioners undertaking the examination of the newborn will find the diagrams and illustrations in this book useful in developing knowledge to underpin the examination process.

Hansmann, G., Neonatal emergencies. ed 1 (2009) Cambridge University Press, Cambridge .

This book provides a useful and easy to use reference guide to neonatal emergencies common in the first 72 h of life. It provides a multidisciplinary approach in such emergency situations including the role of the midwife.

Johnson, M.H., Essential reproduction. ed 6 (2007) Blackwell, Oxford .

An excellent, well-organized research-based textbook that explores comparative reproductive physiology of mammals including a chapter on the fetus and its preparations for birth.

In: (Editors: Meeks, M.; Hallsworth, M.; Yeo, H.) Nursing the neonate (2009) Wiley-Blackwell.

This book is a useful reference guide for midwives with little or no experience in caring for the sick neonate. It focuses on body systems in a systematic and comprehensive way.

Rennie, J.M., Roberton's textbook of neonatology. ed 4 (2005) Churchill Livingstone .

This book is invaluable for practitioners who require information on congenital disorders and pathological conditions in the neonate. It covers a wide range of conditions but it is especially useful for the rarer conditions not commonly observed in clinical practice.

Williamson, A.; Crozier, K., Neonatal care: a textbook for student midwives and nurses. (2008) Reflect Press Ltd .

This book provides a basic and simple guide which may be useful not only for midwifery and nursing students but for maternity care assistants who require to develop skills in caring for neonates within the maternity services.


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