Supporting the newborn infant

Chapter 30 Supporting the newborn infant

Chapter overview

This chapter provides an overview of neonatal physiology and the transition to extrauterine life. It explains the knowledge and skills that midwives need for assessing neonatal wellbeing, including puerperal assessment. It concludes with an overview of the most common minor complications that affect the neonate’s health.


The neonatal (or newborn) period lasts from birth until 28 days of age (London et al 2006). Midwives care for women and their new babies for up to six weeks postpartum. In Australia, the period of postnatal midwifery care varies between states and between urban and remote settings. In New Zealand, women and babies are generally discharged from midwifery care at six weeks postpartum. Initial and ongoing monitoring of the health and wellbeing of the newborn infant is one of the primary purposes of ongoing midwifery care.

While much midwifery care for newborn infants involves information-sharing, maternal support and day-to-day observations of normal growth and development, there are times when individual babies show behaviours or signs that are not quite as expected. At these times, midwives must use professional knowledge and judgement to assess the baby and to implement care that may include continued observation, midwifery intervention and/or referral to a medical practitioner. Women and their families expect that the midwife’s practice and the information they receive is current and supported by available evidence.

Midwives are part of families’ lives for a very short period. One of their major roles is to support and enable women to be confident mothers. Knowledge of her baby’s behaviour and development, understanding how to care for her baby, and reinforcement that she is a capable mother, all engender the mother’s confidence in her ability to mother her baby.

Caring for newborn babies is not always part of young women’s experiences before they have their own children, and therefore midwives are often in the position of supporting and guiding women as they learn to care for their new infant. In these circumstances, it is tempting for professionals to regard the baby as ‘theirs’ and to give women information in an instructional fashion that relegates the baby’s mother to the role of ‘outside’ caregiver, afraid to use her own common sense or to do things for her baby without permission from the ‘expert’. At all times the midwife’s client is the woman. The woman is the baby’s mother; most know whether their baby is doing well or not. Midwifery care is provided in partnership with the baby’s mother, and therefore all midwifery observation, care, treatment and referral are undertaken only in consultation and agreement with her.1


This section explores neonatal physiology and the transition to neonatal life, in sections related to body systems.

Respiratory system

While functional at birth, the alveoli continue to mature until about eight years of age (London et al 2006; Michaelides 2004a). A term baby has approximately 8% of the adult number of alveoli. Pulmonary, vascular and lymphatic structures differentiate during the first 20 weeks of gestation. Alveolar ducts have begun to develop by 24 weeks of pregnancy and primitive alveoli appear by 28 weeks gestation. There are two types of alveolar cells: type I cells necessary for gas exchange, and type II cells for the synthesis and storage of surfactant (London et al 2006).


Surfactant is produced in the lungs in increasing amounts from 32 weeks gestation. It comprises phospholipids and specialised protein molecules that reduce the surface tension of the alveolar fluid at the air/alveolar interface, and contributes to the elasticity of lung tissue (London et al 2006; Varney et al 2004). As gestation increases, the lining of the alveoli becomes thinner, increasing the surface area for eventual gas exchange and effectively fusing the capillary endothelium and alveolar basement membranes (Michaelides 2004a; Novak 2005a). At term, the alveoli are lined with surfactant. Because surfactant reduces the surface tension in the alveoli, it reduces the tendency of the alveoli to collapse with each breath due to the elastic recoil of the lungs, providing the lung stability for effective gas exchange. Surfactant increases lung compliance and thus reduces the pressure required to inflate the lungs for inspiration (Michaelides 2004a; Novak 2005a; Ricci & Kyle 2009; Varney et al 2004). Synthesis of surfactant is thought to be affected by acidosis and/or hypothermia (Michaelides 2004a).

Fetal breathing movements

Respiration after birth is a continuation of an intrauterine process. From as early as 11 weeks gestation, fetal breathing movements occur in order to develop the chest muscles and diaphragm (London et al 2006). As the fetus grows, the frequency and strength of breathing movements increases, until they reach 30–70 breath movements per minute and are present 40%–80% of the time (Davis & Bureau 1987, cited in Michaelides 2004a, p 530).

Lung fluid

Lung fluid is not surfactant. It is a clear fluid that facilitates cell proliferation and differentiation. Prior to labour, production of lung fluid is reduced. At birth the lungs’ primary function changes from secretion of fluid to the absorption of gases. It is possible that the catecholamine surge at birth is the final trigger for this change (Ricci & Kyle 2009). Lung perfusion, commenced in late labour and continued after birth, facilitates the absorption of lung fluid from the alveoli by osmosis (Mercer & Skovgaard 2002, cited in Davies & Richards 2008). At birth, the remaining lung fluid (approx 80–100 mL) is either expelled through the upper airways or absorbed through temporarily more permeable alveolar epithelium into the interstitial tissue (Michaelides 2004a; Ricci & Kyle 2009). Within two hours of the birth of a healthy term neonate, about 80% of the fluid has been reabsorbed and is completely absorbed from the alveoli within 12–24 hours. The fluid is absorbed from the interstitial tissue into the pulmonary vasculature and lymphatic drainage over the next few days (Novak 2005a; Ricci & Kyle 2009).

First active breath

The respiratory and cardiovascular changes that occur immediately after birth happen simultaneously and are mutually dependent (Davies & Richards 2008). while much is known about the initiation of respiration, the precise mechanism that triggers the first actine breath is not get fully understood. Research continues to identify the precise process involved (Rieci & Kyle 2009). Most babies take their first extrauterine breath at the time of birth.

In short, factors initiating the first breath and lung expansion are thought to be the result of a combination of some or all of the following factors:

uterine contractions in the second stage of labour may result in enhanced perfusion that begins to fill the fetal pulmonary capillary bed (Mercer & Skovgaard 2002, cited in Davies and Richards 2008, p 110)

compression of the chest wall during birth and the recoil of the chest wall immediately after birth. Chest compression and recoil expand intrathoracic capacity, stimulating the baby to take a breath. Lung fluid is displaced through the nose and mouth or across the alveolar walls into the interstitial space, and the mechanism essential for effective respiration and pulmonary gas exchange is triggered (Novak 2005a). Significant negative intrathoracic pressure of up to 9.8 kPa (100 cm of water) is produced as the lung fluid is emptied and the pulmonary tissue and vasculature expand. Much less pressure is needed for subsequent breaths (Farrell & Sittlington 2003a).

chemoreceptor stimulation by reduction in oxygen and increase in carbon dioxide in the blood. It is possible that normal labour causes mild hypoxia, hypercapnia and acidosis, which play a role in stimulating neonatal respiration. Physiological hypoxia and hypercapnia trigger the establishment of the respiratory drive in the respiratory centre in the medulla oblongata

(Farrell & Sittlington 2003a; Novak 2005a). However, Blackburn (2007) states that chemoreceptors in the neonate are less responsive in the first few days after birth and emphasises the major role of chest recoil and absorption of fluid in facilitating the first breaths. Davies and Richards (2008), in contrast, describe Mercer & Skovgaard’s 2002 model which postulates that increased perfusion and oxygenation from second-stage contractions and delayed cord clamping are the primary factors in the initiation of respiration.

other external stimuli such as cold, light noise and touch are secondary triggers for the baby to take the first breath.

Neonatal breathing patterns

At birth, the respiratory system is immature. Neonates have shallow, irregular breathing and breathe through the nose for the first two to three months. ‘Babies are obligatory nose breathers and do not convert automatically to mouth breathing when nasal obstruction occurs’ (Farrell & Sittlington 2003a, p 729). On auscultation, breathing may sound noisy and wet during the first one to two hours while any remaining fluid is cleared from the lungs (Varney et al 2004) (see Clinical point on wet lungs, previous page).

The normal baby has an average respiratory rate of 40 breaths/minute (range is 30–60 breaths/minute; see Table 30.1), although the rate may be elevated in the first two hours after birth (Davies & Richards 2008; London et al 2006). Breathing is diaphragmatic—the chest and abdomen rise and fall together. Such symmetry confirms that the lungs and diaphragm are functioning correctly. Newborn babies commonly have periods of irregular breathing, particularly during random-eye-movement (REM) sleep. The irregular pauses between breaths usually last 5–15 seconds. These pauses are not associated with changes to the baby’s colour or heart rate. Pauses of less than 20 seconds are not usually of clinical concern (London et al 2006; Ricci & Kyle 2009).

Table 30.1 Neonatal breathing patterns

  Normal variations Outside normal variations (any or all of these)
More than 60 breaths/minute (sleeping or in quiet alert state)

Chest/abdominal movement Synchronised diaphragm and abdominal movement Subcostal and/or intercostal in-drawing
Nose Breathes through the nose, no nasal flaring Flaring of nostrils
Sound Silent Expiratory ‘grunt’
Colour Pink Pale/cyanosis

(See Ch 39 for respiratory distress syndrome.)

While an elevated respiratory rate is a sign that the baby is unwell, tachypnoea cannot be assessed without taking the baby’s other behaviours into account, such as recent crying, feeding or sleeping (Farrell & Sittlington 2003a; Michaelides 2004a). A baby’s cry is loud and of medium pitch. Over time, mothers learn to distinguish variations in crying and to attach meaning to them (e.g. hungry, wet, in pain).

Cardiovascular system

The fetal circulation is completely different to that of postnatal circulation (see Fig 30.2) and is discussed in detail in chapters 20. Blood oxygenated in the placenta reaches the fetus via the umbilical vein. About 50% perfuses the liver, and the remainder enters the inferior vena cava by way of the ductus venosus. This blood mixes with the venous return from the liver and the lower half of the fetal body, and then flows to the right atrium via the inferior vena cava. Streaming of the blood through

the right atrium causes it to cross to the left atrium via the foramen ovale. This blood is more highly oxygenated than blood returning by the superior vena cava, and constitutes the left ventricular output supplying the first part of the aorta. Thus the coronary and carotid arteries receive the most oxygenated blood available. Blood returning to the right atrium through the superior vena cava flows into the right ventricle. Only a small proportion of the right ventricular blood enters the pulmonary circulation; most passes through the ductus arteriosus into the arch of the aorta. The remainder flows to the lower parts of the fetal body. Changes from fetal to post-birth circulation are dealt with in more detail in the following sections.

Post-birth respiratory and cardiovascular changes occur simultaneously and are mutually dependent (Davies & Richards 2008; Farrell & Sittlington 2003a).

Closure of the ductus arteriosus

In fetal life, the ductus arteriosus is nearly as wide as the aorta. Blood is shunted directly from the pulmonary artery to the aorta via the ductus

arteriosus, thereby avoiding the lungs. At birth, the pulmonary vascular resistance falls and the amount of blood being shunted to the aorta via the ductus arteriosus is substantially decreased. Constriction of the muscular walls of the ductus arteriosus occurs almost immediately after birth. Decreasing levels of maternal prostaglandins (previously supplied by the placenta) and rising arterial oxygen tension trigger vasoconstriction. The ductus arteriosus is usually functionally closed by 8–10 hours after birth, but will not anatomically close for several more months. Indeed, before pressures stabilise, a temporary reverse shunt through the ductus arteriosus may persist for a few hours. Moreover in some babies the ductus has been shown to be intermittently patent up to three days after birth (Blackburn 2007; Farrell & Sittlington 2003a; Michaelides 2004a; Novak 2005a).

Characteristics of neonatal cardiac function

Heart rate—in the first week after birth the average heart rate is 110–150 beats per minute in a quiet, healthy term neonate. However, wide fluctuations occur deplending on whether the baby is active, feeding or asleep (Farrell & Sittlington 2003a; London et al 2006).

Peripheral circulation—the healthy term baby’s hands and feet are mildly cyanosed (acrocyanosis) for several hours after birth until peripheral perfusion is complete.

Blood volume and blood pressure—systolic blood pressure varies with gestation, birthweight and neonatal activity such as crying. It is not usually assessed in healthy term infants (London et al 2006). At birth, the total circulating blood volume is 80 mL/kg of bodyweight (i.e. 280 mL for a 3.5 kg baby) (Blackburn 2007). The relatively low total circulating blood volume means that quite small quantities of blood represent a large blood loss for the neonate (e.g. 10% of adult blood volume is 800 mL; 10% of a 3.5 kg baby’s blood volume is 28 mL). Attentive concern is required when assessing blood loss from the umbilical cord or the amount of blood taken for laboratory analysis.

Heart murmurs

Heart murmurs are sounds that may be heard as: blood flow is disturbed as it crosses an abnormal valve; as it flows under pressure through a defect in either the atrial or ventricular septum; or sometimes when there is increased flow as it crosses a normal valve. The murmur reflects turbulent blood flow, typically from the pressure difference between adjacent cardiac structures.

Cardiac murmurs in the neonate may be normal (physiological, benign, flow, transitional, etc.) or abnormal (pathological). Most neonates (90%) will have ‘soft’ murmurs which are transient and not associated with anomalies (London et al 2006). Murmurs can be classified according to their:

Temperature regulation

Newborn babies sustain life within a narrow range of core (internal) body temperatures, generally 36.5–37.5oC (Blackburn 2007). The body uses a number of mechanisms to balance heat loss and heat production in order to maintain the core temperature within this range despite a wide range of environmental temperatures. Balancing heat loss and gain is known as thermoregulation. The range of ambient temperatures that maintains a baby’s core body temperature using minimum oxygen consumption at a minimum metabolic rate is called the thermoneutral range (Blackburn 2007; London et al 2006; Ricci & Kyle 2009).

At birth, babies’ thermoregulatory mechanisms are not fully developed, although these become progressively more efficient. Limited response to temperature changes in the first 24 hours of life results in babies being particularly susceptible to chilling during this time. By 24–48 hours of age, healthy term neonates are able to increase their heat production up to 2.5 times in response to cold; however, they remain susceptible to environmental temperature changes. Until the mechanisms controlling thermoregulation (and heat loss in particular) stabilise, the thermoneutral range of babies is at a higher environmental temperature than older children and adults. During the first weeks of life, warmed rooms, or extra clothing and blankets if babies are taken outside, are often required (Blackburn 2007; London et al 2006; Michaelides 2004b).

Neonatal heat loss

Heat is very easily lost at birth, when autonomic thermoregulation is at its least efficient and the baby is wet. Hypothermia (a temperature less than 36.5°C) can occur rapidly unless active steps are taken to prevent heat loss.

There are four ways in which babies can lose heat from their body surface (Blackburn 2007; London et al 2006; Michaelides 2004b; Novak 2005b):

Neonatal thermogenesis

Neonates rarely shiver. They generate heat by increasing their metabolic rate using muscular activity such as moving limbs and suckling, and by chemical thermogenesis (heat production), also called non-shivering thermogenesis (Blackburn 2007).

Thermogenesis and brown adipose tissue

Heat production by chemical means involves the metabolism of brown adipose tissue (BAT). Brown fat is of particular importance in human neonates because it has the ability to dissipate stored energy as heat. In contrast to other cells, including white adipocytes, brown adipocytes express mitochondrial uncoupling protein 1 (UCP1), which gives the cells’ mitochondria an ability to uncouple oxidative phosphorylation and utilise substrates to generate heat, rather than via adenosine-5’-triphosphate (ATP). Exposure to cold leads to sympathetic stimulation of brown adipocyte via norepinephrine binding to beta-adrenergic receptors.

Approximately 2%–7% of neonatal bodyweight is thought to be BAT or brown fat. It begins to be deposited in the fetus from 26 weeks gestation, steadily increasing in amount until two to five weeks after birth. Recently, substantial quantities of BAT have been detected in adult humans using positron-emission tomography, especially when the individuals are exposed to cold temperatures.

At term, BAT is deposited around the nape of the neck and mid-scapular area, under the clavicles and in the axillae, around the kidneys, adrenal glands and large vessels in the neck and in the mediastinum (London et al 2006; Novak 2005b). Maternal prostaglandins and adenosine prevent non-shivering thermogenesis in utero. BAT is only activated after birth. Brown fat stores are not renewable once they have been used (Michaelides 2004b).

Brown adipose tissue is so-named because of the colour that results from the tissue containing a more extensive blood supply and greater numbers of intracellular organelles such as mitochondria than in white adipose tissue. Neonatal cooling causes noradrenaline, other catecholamines and thyroid hormones to be released so that rapid lipolysis of BAT and consequent heat production is induced. Oxygen and glucose are required in the metabolism of brown fat. Brown fat lipolysis uses up to three times more oxygen than other tissues. Normal oxygen consumption, conservation of brown fat stores and maintenance of core body temperature are promoted by keeping babies in a thermoneutral range (Blackburn 2007; Farrell & Sittlington 2003a; London et al 2006; Novak 2005b).

Maintaining temperature after birth

At birth, healthy term babies are placed against their mother’s body skin-to-skin, dried and covered with a warm blanket to maintain their temperature. A mother’s body conducts direct warmth to the baby, and the blanket traps a layer of warm, insulating air around the baby (Blackburn 2007; Michaelides 2004b). Studies of preterm babies in Colombia and England showed that skin-to-skin contact between the mother’s breasts satisfactorily maintains body heat (Sleath 1985; Whitelaw et al 1988). More recent studies have suggested that the maternal body temperature fluctuates in response to the baby’s temperature so that a stable temperature is maintained. Furthermore, skin-to-skin contact appears to stabilise and support cardiorespiratory function (Davies & Richards 2008).

The following methods are commonly used to conserve heat in newborn infants (McHugh 2004).

Bathing and temperature maintenance

Babies are no longer bathed immediately after birth unless there is a risk of vertical transmission of an infection from the mother, such as hepatitis B or HIV. Bathing soon after birth increases the risk of hypothermia, and therefore it should not be undertaken until the baby’s temperature has stabilised (Leveno et al 2003). Breastfeeding is more important, both to initiate feeding and provide fuel for the baby’s metabolic processes, including temperature maintenance, and to enhance the mother–baby relationship. Skin-to-skin contact seems to influence neurobehavioural responses so that rooting and latching are easier (Ferber & Makhoul 2004).

Although babies’ thermoregulatory mechanisms become more efficient as the days pass, bathing remains a time when they can be easily chilled. The following precautions should always be taken (London et al 2006; Michaelides 2004b; Varney et al 2004).

Clinical point

Neonatal temperature measurement

Axillary temperatureThis is the preferred site.

Note: In a hypothermic baby, the reading will be higher than the core as the area contains large areas of brown fat (Bliss-Holtz 1991). As this may make recognition of hypothermia more difficult, behavioural and other physiological signs should also be assessed when the temperature is taken.

Rectal temperature—It is considered preferable to routinely measure the temperature via the axilla; however, core temperature may be required in individual situations. The rectal temperature measures the core temperature and is the most accurate. It is used when the axillary temperature is abnormal; e.g. check rectal temperature if axillary temperature is <36.5°C.

1 Measuring a newborn’s rectal temperature: The well-lubricated thermometer should be gently inserted no more than 3 cm into the rectum of the term baby and no more than 2 cm in the preterm baby (Blackburn 2007; Fleming et al 1983). The baby’s legs need to be held still during this procedure and great care taken to ensure that the rectum is not damaged. For this reason, many institutions prohibit this procedure.

Tympanic temperature—As the reading is often affected by environmental temperature, this site is less accurate for newborn babies and should not normally be used. Wells et al (1995) showed that readings were 0.5–1.0°C higher than the core temperature when the environmental temperature was >30°C, and 0.5–1.0°C lower when the environmental temperature was <30°C.

Skin sites—For a rapid general assessment of temperature, skin sites can be useful.

Commercial ‘spots’ or ‘tapes’—Used on the skin, these are a non-invasive method for taking the temperature that parents may find useful as the baby grows older.

Impaired thermoregulatory control

Neonatal hypothermia

If the neonate’s temperature falls below 36.5°C, the baby is at risk of hypothermia. Prevention is the best treatment. A mildly hypothermic baby (36–36.5°C) can generally be warmed without difficulty by nestling the baby against the mother skin-to-skin (and covering with a blanket) in a warm (>25°C) room if the neonate’s other assessments are stable, or by placing in an incubator set at 35–36°C. In the latter situation the baby should be clothed but not under a blanket (Blackburn 2007; London et al 2006; Michaelides 2004b; Novak 2005b).

Untreated hypothermia can result in generalised vasoconstriction that includes the pulmonary vessels. Pulmonary vasoconstriction results in decreased pulmonary perfusion that affects pH, PaO2 and PaCO2 levels. Increased PaCO2, and decreased PaO2 and pH levels result in respiratory acidosis. Consequently the baby will exhibit signs of respiratory distress (Farrell & Sittlington 2008).

Underscoring the need for active steps to prevent heat loss is the fact that in newborn babies there is an interrelationship between thermoregulation, oxygenation and normal glycaemia. Normal function/levels in each of these metabolic processes support normal function/levels in the others. Therefore, the development of hypothermia, hypoxia or hypoglycaemia puts the baby at risk for development of the other two conditions.

Neonatal hyperthermia

Hyperthermia is a temperature above 37.5°C and is much less common than neonatal cooling. It can be as harmful as hypothermia if it is ignored. The most common cause of neonatal hyperthermia is underestimation of the effect of the environmental temperature on the baby (e.g. putting the bassinet next to a heater). Babies can develop hyperthermia in response to an infection, environmental overheating or occasionally an underlying medical condition. Recent research has reported a possible association between sudden unexpected death in infancy (SUDI) and the presence of Staphylococcus aureus (Blackwell 2008; Weber et al 2008). Blackwell’s study notes that hyperthermia is one of the symptoms associated with the presence of staphylococcal endotoxins.

Clinically discriminating between environmental factors and an infection can be extremely difficult, as babies with an infection can have a temperature below 37.5°C, while a temperature above 37.5°C can be the result of environmental factors. It is important to assess the whole clinical picture rather than rely solely on temperature as a guide.

Medical consultation is warranted when the baby’s temperature is above 37.5°C without an obvious environmental cause, such as direct sunlight in a well-heated room, or when the baby has a lower temperature but is exhibiting other signs of unwellness, such as not feeding. Similar consultation would be made if the temperature has not returned to normal within an hour of correcting an environmental cause (Farrell & Sittlington 2003a; Michaelides 2004b).

In the case of overheating due to an environmental cause, the baby should be slowly cooled by removing bootees and hat, exposing hands to the air and leaving the baby under a single blanket or sheet. Extremes such as removing all covers or cool bathing must be avoided, as rapid cooling can precipitate excessive heat loss and shock (Michaelides 2004b).

Haemopoietic system

Clotting factors

Colonisation of the intestine by the bacteria that synthesise vitamin K does not occur until milk feeding is established. Therefore, blood clotting is impaired in the first week postpartum while levels of vitamin-K-dependent clotting factors II (prothrombin), VII, IX and X are low. Adult levels of platelets are present, but their capacity for adhesion and aggregation is reduced (Blackburn 2007; Michaelides 2004a).

Vitamin K prophylaxis

It is unclear why newborn infants have reduced levels of vitamin-K-dependent clotting factors; it has been postulated that this may be related to fetal growth regulation (Blackburn 2007). If vitamin K is not administered parenterally, the natural course is for the vitamin K levels to initially decrease as maternally acquired vitamin K is used. Neonatal vitamin K stores then increases gradually over the first month (Blackburn 2007).

Routine vitamin K prophylaxis

The need for routine prophylaxis for all babies has been questioned since Golding et al (1990, 1992) published the results of a study that linked administration of intramuscular (IM) vitamin K to increased risk of childhood cancer. Several later reports have not demonstrated the same relationship (McKinney et al 1998; Olsen et al 1994; Passmore et al 1998; Zipursky 1996). While some methodological criticisms have been made of some of these later studies, in places where routine use of IM vitamin K was stopped or replaced by oral doses subsequent to the Golding et al study, the incidence of VKDB increased (Passmore et al 1998; Zipursky 1996). It is probable that vitamin K prophylaxis is not needed at birth by every baby; nevertheless, because it is not possible to identify those who do need vitamin K with any certainty, prophylaxis is policy in most maternity services. The New Zealand College of Midwives Consensus Statement (2001) supports vitamin K prophylaxis. In Australia, most babies are given vitamin K prophylaxis (NHMRC 2000). A selective policy of vitamin K administration after screening is not appropriate, because without prophylaxis a relatively high incidence of late VKDB occurs.


After the Golding et al report, several studies were carried out comparing different dosage regimens (Cornelissen et al 1992; Greer et al 1998). The conclusions drawn from these studies and other studies are as follows:

IM or oral vitamin K improves the neonate’s coagulation status in the first week (Farrell & Sittlington 2003a).

A single dose (1 mg) of IM vitamin K at birth effectively prevents classic VKDB (Medsafe 2006).

The effectiveness of IM vitamin K in the prevention of late VKDB has been established (Loughnan et al 1999, cited in NZCOM 2001). A Cochrane review (2000) compared IM with oral routes of administration of vitamin K (Puckett & Offringa 2000). Evaluation of 11 randomised controlled trials (RCTs) identified that if administered soon after birth, a single dose of IM vitamin K, compared with a single oral dose, provided higher plasma levels of vitamin K in the first few weeks of life when the risk of VKDB is highest. However, multiple doses of oral vitamin K resulted in higher plasma levels at two weeks and two months than a single IM dose.

Local policies relating to the administration of oral vitamin K may differ. The three-dose regimen is common. The doses are usually spread across the first six weeks of life (e.g. at birth, one week and six weeks) (Ministry of Health 2004).

Immunological adaptations

Functional immaturity of the immune system and lack of exposure to common microorganisms at birth means that babies are very vulnerable to infections, particularly respiratory and gastrointestinal infections. Antibody-mediated and cell-mediated immunity, the inflammatory response and complement factors are different in newborn infants. Neonates cannot localise infections very well, and so an infection is more likely to become systemic. The immaturity of the gut defence mechanism increases the likelihood of both gastrointestinal infection and later development of allergies (Blackburn 2007; Novak 2005b; Varney et al 2004). Both commensal and pathogenic microorganisms begin to colonise the baby during birth. Colonisation occurs first from the maternal genital tract, then from the mother’s skin, and finally from other people and the general environment (Novak 2005b).

Specific immune responses

Antibody-mediated immunity

At birth the neonate has 55%–80% of the adult total immunoglobulin values (IgG, IgA and IgM) (Blackburn 2007).

Immunoglobulin G (IgG)—the baby’s levels of IgG are equal to or slightly higher than those of the mother, as maternal IgG is transferred across the placenta. Transfer increases progressively until term. The maternal IgG gives the baby some degree of passive immunity to the diseases to which the mother has antibodies, for approximately six months. After birth, levels fall gradually as the transferred IgG is used. The baby does not develop significant production of IgG until after six months of age. Adult levels are reached over four to six years (Blackburn 2007; Michaelides 2004a; Novak 2005b).

Immunoglobulin A (IgA)—newborn levels of IgA and IgM are low, as the molecules are too large to cross the placenta. IgA is important for localised immunity in the gastrointestinal and respiratory tracts. It is found in saliva, tears, and intestinal mucosa by two to three weeks of age, although adult levels are not reached in the saliva for two months. Maternal secretory IgA is also transferred to the baby in colostrum and breast milk, affording local protection to the gut. IgA levels reach 20% of adult levels by one year (Blackburn 2007; Novak 2005a).

Immunoglobulin M (IgM)—at term the baby’s IgM level is 20% of the adult value, which is not reached for two years. In utero, IgM is able to be formed after 19–20 weeks gestation in response to exposure to certain antigens, such as the TORCH organisms. IgM protects against blood-borne infections and is the main immunoglobulin produced in the first four weeks of life. Half the adult value of IgM is reached by six months of age (Blackburn 2007).

Cell-mediated immunity

Low levels of complement components contribute to decreased opsonisation capability. Serum complement levels increase to adult values by 6–18 months (Blackburn 2007). Nevertheless, Blackburn (2003) reports that neutrophils act normally in neonates when bacterial numbers are not too large and the baby is not stressed (e.g. by perinatal asphyxia). However, significantly reduced bacteriocidal activity for Gram-positive and Gram-negative organisms has been shown in stressed babies (Blackburn 2007).

Gut defence mechanism

In humans the gastrointestinal (GI) tract is part of the natural immune system. Defences in the GI tract include acidity, digestive enzymes that break down large molecules, and secretory IgA that lines the small intestine (Varney et al 2004). At birth, the epithelial lining of the GI tract is immature and relatively permeable. Development of the epithelium and the mucosal surface as an impenetrable barrier against pathogenic microorganisms and other antigens is known as gut closure. Gastric acid, peristalsis and the mechanical barrier properties of the gut mucosal surface are some non-immune factors that contribute to the gut defence mechanism (Blackburn 2007).

Renal system

At birth the kidneys are structurally complete but functionally immature. There are limitations in the glomerular filtration rate capability and the ability to concentrate or dilute urine. Newborn babies have little renal reserve to cope with increased levels of solutes, which may occur in physiologically stressed or ill neonates (Michaelides 2004a; Novak 2005a; Varney et al 2004). The total body water content in newborn babies is a larger proportion of body fluid than in adults. The shift of intracellular fluid into the extracellular compartment after birth results in a diuresis that causes loss of 5%–10% of birthweight over the first week (Novak 2005a).

Urine is first passed within 24 hours of birth. Initially the newborn baby excretes only a small quantity of urine; as little as 30–60 mL is passed in the first 48 hours of life. Volume and frequency increases with rising fluid intake. The urine has a low specific gravity, is straw-coloured and odourless. There should be no protein or blood in the urine. Until fluid intake increases, the urine may be cloudy from the presence of mucus or urates. Urates may cause pink or brick-red staining on the napkin. While common and a normal finding in the first few days of life, the presence of urates in the urine of babies more than a few days old may indicate dehydration

(Michaelides 2004a; Novak 2005a; Varney et al 2004).

When the bladder becomes full it is palpable abdominally. The kidneys may also be palpable. On micturition the direction and force of the stream of urine should be noted (Michaelides 2004a; Novak 2005a; Varney et al 2004).

Gastrointestinal system

Jun 18, 2016 | Posted by in MIDWIFERY | Comments Off on Supporting the newborn infant

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