During fetal life, the alveoli produce fetal lung fluid that expands the alveoli and aids in lung development. As the fetus nears term, production of lung fluid decreases. During labor, the fluid begins to move into the interstitial spaces, where it is absorbed. Absorption is accelerated by the process of labor and may be delayed after cesarean birth that occurs without labor. This continues throughout labor and during the early hours after birth. At birth only about 35% of the original amount of fetal lung fluid remains (Blackburn, 2013).

Surfactant, a slippery detergent-like combination of lipoproteins, is detectable by 24 to 25 weeks of gestation (Blackburn, 2013). It reduces surface tension within the alveoli. Without surfactant, the alveoli collapse as the infant exhales. They must be reexpanded with each breath, greatly increasing the work of breathing. Sufficient surfactant is usually produced beginning at 34 to 36 weeks of gestation to prevent respiratory distress syndrome (Gardner, Enzman-Hines, & Dickey, 2011). Surfactant secretion increases during labor and immediately after birth to enhance the transition from fetal to neonatal life.

Steroids may be given to women in preterm labor to help increase surfactant production and lung maturation. Some complications, such as hypertension, placental insufficiency, maternal infection, and rupture of membranes greater than 48 hours may cause accelerated lung maturity. Diabetes may delay surfactant production (Gardner et al., 2011)

The infant’s first breath at birth must force the remaining fetal lung fluid out of the alveoli and into the interstitial spaces to allow air to enter the lungs. This requires a much larger negative pressure (suction) than subsequent breathing. Breathing is initiated by chemical, mechanical, thermal, and sensory factors that stimulate the respiratory center in the medulla of the brain and trigger respirations (Figure 21-1).

Oxygenated blood from the placenta enters fetal circulation through the umbilical vein. About a third of the blood is directed away from the liver into the ductus venosus (DV) which connects to the inferior vena cava (IVC). The rest of the umbilical vein flow goes through the liver before entering the IVC. Near the end of pregnancy, the liver needs more perfusion, and 70% to 80% of the oxygenated blood from the umbilical vein flows through to the liver (Blackburn, 2013).

As blood from the DV or the portal system enters the IVC, it joins blood from the lower part of the body to travel to the heart in separate streams so that there is little mixing of the blood. When the blood enters the right atrium, the more highly oxygenated blood is directed across the atrium to the foramen ovale (Blackburn, 2013).

The foramen ovale is a flap in the septum between the right and left atria of the fetal heart. About 50% to 60% of the blood from the right atrium moves through the foramen ovale to the left atrium (Blackburn, 2013). The blood flows from the left atrium to the left ventricle and leaves through the ascending aorta. The majority of this better oxygenated blood flows to the heart, brain, head, and upper body.

Blood that does not cross the foramen ovale moves to the right ventricle but flow is restricted to the lungs by the narrow pulmonary artery and pulmonary blood vessels. This elevates the pressure in the right side of the heart. Pressure is low on the left side of the heart because there is little resistance as blood leaves the left ventricle to travel to the rest of the body and into the widely dilated placental vessels. This difference in pressure between the right and left sides of the heart allows blood flow through the foramen ovale.

Blood from the superior vena cava and the less oxygenated blood from the inferior vena cava flow into the right atrium, to the right ventricle, and into the pulmonary artery. Approximately 10% to 12% of the blood goes to the lungs and the rest passes through the ductus arteriosus to the aorta (Blackburn, 2013). Little blood is allowed into the lungs because the pulmonary artery and other blood vessels are constricted, causing high pulmonary vascular resistance. Blood perfusing the lungs returns to the left atrium by the pulmonary veins.

At birth, the shunts close and the pulmonary vessels dilate. These changes occur in response to increases in blood oxygen and shifts in pressure within the heart, pulmonary, and systemic circulations, as well as clamping of the umbilical cord. The changes necessary for transition from fetal to neonatal circulation occur simultaneously within the first few minutes after birth. They are discussed separately here (see Figure 12-9).

As the newborn takes the first breaths at birth, the rise in oxygen level causes the ductus arteriosus to constrict, preventing entry of blood from the pulmonary artery. The pulmonary blood vessels respond to the increased oxygenation by dilating. At the same time, fetal lung fluid begins to shift into the interstitial spaces and is removed by blood and lymph vessels. These changes decrease pulmonary vascular resistance and allow more room for dilation of the pulmonary blood vessels. As a result, the pulmonary vessels can expand to hold the suddenly increased blood flow from the pulmonary artery.

At birth, pressures between the right and left sides of the heart are reversed. The sudden dilation of the vessels of the lungs allows blood to enter freely from the right ventricle and decreases pressure in the right side of the heart. Clamping of the umbilical cord further decreases pressure in the right side of the heart. Increased blood flow from the pulmonary veins into the left atrium causes pressure in the left side of the heart to build. Systemic resistance increases as blood flow to the placenta ends with clamping of the cord, further elevating pressure in the left heart.

Because the foramen ovale opens only from right to left, it closes when the pressure in the left atrium is higher than that in the right atrium. This change forces the blood from the right atrium into the right ventricle and pulmonary artery. Thus blood flow through the heart and lungs changes from fetal to neonatal circulation and is similar to that in the normal adult.

The foramen ovale is functionally closed soon after birth because the unequal pressures between the atria prevent it from opening. Conditions such as asphyxia (insufficient oxygen and excess carbon dioxide in the blood and tissues) and persistent pulmonary hypertension, however, may reverse the pressures in the heart and cause the foramen ovale to reopen. It is permanently closed within several months (Kenney, Hoover, Williams, et al., 2011). The ductus arteriosus closes gradually as oxygenation improves and prostaglandins, which helped keep it open, are metabolized. Functional closure occurs for most term infants at about 72 hours and permanent closure occurs within 1 to 2 weeks (Kenney et al., 2011).

Until closure is complete, the blood that does flow through the ductus arteriosus usually reverses, moving from the aorta to the pulmonary artery and increasing blood flow to the lungs. This sequence occurs because pressure in the aorta is now higher than that in the pulmonary artery. A murmur may be heard as a result of blood flow through the partially open vessel.

Low levels of oxygen in the blood may cause the ductus arteriosus to dilate and the pulmonary vessels to constrict, increasing resistance to blood flow to the lungs. The result may be opening of the foramen ovale to allow a right-to-left shunt of blood and flow from the pulmonary artery through the ductus arteriosus and into the aorta. The ductus venosus closes shortly after birth. Permanent closure occurs by 1 to 2 weeks after birth (Kenney et al., 2011).

Certain newborn characteristics predispose them to heat loss. The skin is thin, blood vessels are close to the surface, and there is little subcutaneous (white) fat to provide a barrier to loss of heat. Heat is readily transferred from the warmer internal areas of the body to the cooler skin surfaces and then to the surrounding air. Newborns have three times more surface area to body mass than the adult and the rate of heat loss is four times greater than in adults (Carlo, 2011a).

The flexed position of the healthy full-term infant reduces the amount of skin surface exposed to the surrounding temperatures and decreases heat loss. Because of decreased muscle tone, the sick or preterm infant does not maintain a flexed position and is more susceptible to loss of heat.

The four methods of heat loss in the neonate are (Figure 21-2):

When newborns become cold they become restless and cry, increasing flexion and activity to help maintain heat. Vasoconstriction occurs to decrease heat loss and acrocyanosis (bluish discoloration of the hands and feet) may result. Body metabolism rises increasing the need for oxygen and glucose (Blackburn, 2013). Adults shiver when they are cold, but shivering is rare in newborns. It is seen only after prolonged exposure to cold and is not an important method of heat production. The primary method of heat production is nonshivering thermogenesis (NST), the metabolism of brown fat to produce heat. Newborns can increase heat production by 100% using NST (Blackburn, 2013).

Brown fat, also called brown adipose tissue, or BAT, is the vascular specialized fat that provides heat when metabolized. It is located primarily around the back of the neck, in the axillae, between the scapulae, along the abdominal aorta, and around the kidneys, adrenals, and sternum (Figure 21-3). As brown fat is metabolized, it generates more heat than white subcutaneous fat. Blood passing through brown fat is warmed and carries heat to the rest of the body.

Cold stress causes many body changes (Figure 21-4, Box 21-1). An increase in metabolic rate and metabolism of brown fat can lead to a significant rise in the need for oxygen. If an infant is having even mild respiratory distress, the problem may be increased as oxygen is used for heat production. Cold stress also causes diminished production of surfactant, impeding lung expansion and leading to more respiratory distress.

A neutral thermal environment is one in which the infant can maintain a stable body temperature with minimal oxygen need and without an increase in metabolic rate. The range of environmental temperature that allows this maintenance is called the thermoneutral zone. In healthy unclothed full-term newborns, an environmental temperature of 32° C to 33.5° C (89.6° F to 92.3° F) provides a thermoneutral zone. When the infant is dressed, the thermoneutral range is 24° C to 27° C (75.2° F to 80.6° F) (Blackburn, 2013). The thermoneutral zone varies according to an infant’s gestational age, size, and postnatal age.

The blood volume of the term newborn is 80 to 100 mL/kg, but this varies according to the time of cord clamping, the position of the infant when the cord is clamped, and the gestational age of the infant (Diehl-Jones & Askin, 2010). Preterm infants have a greater blood volume per kilogram than term infants.

Blood samples drawn from the heel, where the circulation is sluggish, show higher hemoglobin and hematocrit levels than samples taken from central areas. Venous blood samples are more accurate and are taken when precise measurement is essential. (Newborn values for common laboratory tests are listed in Table 21-1.)

Newborns have low levels of vitamin K, which is necessary to activate several of the clotting factors (factors II [prothrombin], VII, IX, and X). Vitamin K is synthesized in the intestines, but food and normal intestinal flora are necessary for this process (Luchtman-Jones & Wilson, 2011). To decrease the risk of hemorrhagic disease of the newborn, vitamin K is administered intramuscularly to most newborns. Drugs such as phenytoin (Dilantin), phenobarbital, and antituberculosis drugs taken by the mother during pregnancy interfere with clotting ability in the infant after birth.

Although the platelet counts in term newborns are near adult levels, platelet response to stimuli is decreased during the first few days of life.

The newborn’s stomach capacity is approximately 6 mL/kg at birth. Gastric emptying may be delayed at first. It is more rapid after ingestion of human milk than after formula and slower if the infant has swallowed mucus (Blackburn, 2013). The gastrocolic reflex is stimulated when the stomach fills, causing increased intestinal peristalsis. Infants frequently pass a stool during or after a feeding. The cardiac sphincter between the esophagus and the stomach is relaxed, which explains the tendency to regurgitate feedings easily.

Maturation of the ability to digest and absorb occurs at different rates for various nutrients. Pancreatic amylase, needed to digest complex carbohydrates is deficient for the first 4 to 6 months after birth (Blackburn, 2013). As a result, newborn digestion of complex carbohydrates such as those in cereals is limited. Amylase is also produced by the salivary glands, but in low amounts until about the third month of life. Amylase is present in breast milk.

The newborn is also deficient in pancreatic lipase, limiting fat absorption significantly. Lipase present in the mouth and stomach helps with some digestion of fat. Lipase is present in breast milk, which may make it more digestible for the newborn than formula. Protein and lactose, the major carbohydrate in the infant’s milk diet, are both well digested.

Meconium is the first stool excreted by the newborn. It consists of particles from amniotic fluid such as vernix, skin cells, and hair, along with cells shed from the intestinal tract, bile, and other intestinal secretions. Meconium is greenish black with a thick, sticky, tarlike consistency. The first meconium stool is usually passed within 12 hours of birth, and 99% of newborns have the first stool within 48 hours (Carlo, 2011b). If meconium is not passed within that time, obstruction is suspected.

Meconium stools are followed by transitional stools, a combination of meconium and milk stools. Transitional stools are greenish brown and of a looser consistency than meconium. They are followed by milk stools characteristic of the type of feeding the infant receives.

The stools of infants fed with breast milk are seedy, and the color and consistency of mustard with a sweet-sour smell. The breastfed infant generally has more frequent stools than the infant who is formula fed. A stool may be passed with each feeding. Some older infants pass only one stool every 2 to 3 days. The normal breastfed newborn should have at least four or more stools daily (Lawrence & Lawrence, 2011).

The formula-fed infant excretes pale yellow to light brown stools. They are firmer in consistency than those of the breastfed infant. The infant may excrete several stools daily, or only one or two. The stools have the characteristic odor of feces.

Until newborn feedings are adequate to meet energy requirements, glucose present in the body is used, and stored glycogen is converted by the liver to glucose for use. In the term infant, glucose levels should be 40 to 60 mg/dL at day 1 and 50 to 90 mg/dL thereafter (Lo, 2011). There is no general consensus about glucose level that defines hypoglycemia, but a level less than 40 to 45 mg/dL in the term infant is often used as the lower limit of normal plasma glucose (Kubicka & Little, 2009; McGowan, Rozance, Price-Douglas, et al, 2011).

Many newborns are at increased risk for hypoglycemia. In the preterm, late preterm (born between 34 weeks and 366⁄7 weeks of gestation), and small-for-gestational-age infant, adequate stores of glycogen may not have accumulated. Stores may be used up before birth in the postterm infant because of poor intrauterine nourishment from a deteriorating placenta. Large-for-gestational-age infants and those with diabetic mothers may produce excessive insulin that consumes available glucose quickly (see Chapters 29 and 30). Infants exposed to such stressors as asphyxia or infection may exhaust their stores of glycogen. Cold-stressed infants may deplete glycogen to increase metabolism and raise body temperature.

A major function of the liver is the conjugation of bilirubin (Figure 21-5). The newborn’s liver may not be mature enough to prevent jaundice during the first week of life. Jaundice results from hyperbilirubinemia, excessive bilirubin in the blood. Jaundice (or icterus) occurs in 60% of term newborns and 80% of preterm infants (Ambalavanan & Carlo, 2011).

Iron is stored in the fetal liver and spleen during the last months of pregnancy. Full-term infants who are breastfeeding usually do not need added iron until 4 to 6 months of age. At that time, they should begin iron-containing foods or iron supplements. All infants who are not breastfeeding should be given iron-fortified formula (American Academy of Pediatrics [AAP] & American College of Obstetricians and Gynecologists [ACOG], 2007; Holt, Wooldridge, Story, et al., 2011).

The kidney’s nephrons are formed by 34 to 36 weeks of gestation (Frost, Fashaw, Hernandez, et al., 2011). Full kidney function, however, does not occur until after birth. Blood flow to the kidneys increases after birth because of decreased resistance in the renal vessels. The improved perfusion results in a steady improvement in kidney function during the first few days of life.

The newborn’s kidney function is immature compared with that of the adult. The ability of the glomeruli to filter and the renal tubules to reabsorb is considerably less than in adults. The glomerular filtration rate doubles or triples during the first weeks after full term birth, but does not reach adult levels until 1 to 2 years of age (Frost et al., 2011). Therefore infants have a decreased ability to remove waste products from the blood.

Small amounts of substances such as glucose and amino acids may escape into the urine of the neonate (Blackburn, 2013; Frost et al., 2011). Uric acid crystals may give a reddish color to the urine that is sometimes mistaken for blood.

Voiding occurs within 12 hours for 50% of newborns, 92% void within 24 hours, and 99% void within 48 hours of life (Frost et al., 2011). Absence of kidneys or abnormalities that interfere with excretion of urine are usually discovered before birth because they cause low amniotic fluid volume. Only one or two voidings may occur during the first 2 days of life. The infant voids at least six times a day by the fourth day.

Newborns have a lower tolerance for changes in total volume of body fluid than do older infants. In addition, the fluid turnover rate is greater than that in adults (Box 21-2). To maintain fluid balance, full-term infants need 60 to 100 mL/kg (27 to 45 mL/lb) daily during the first 3 to 5 days of life and 150 to 175 mL/kg (68 to 80 mL/lb) a day by 7 days of age (Halbardier, 2010).

IgG, the only immunoglobulin that crosses the placenta, provides the fetus with passive temporary immunity to bacteria, bacterial toxins, and viruses to which the mother has immunity. Preterm infants have less IgG because transfer is greatest during the third trimester. Although the fetus makes some IgG, production at significant levels is delayed until after 6 months of age (Blackburn, 2013). The passive immunity from the mother gradually disappears over the first 6 to 8 months of life (Buckley, 2011).

IgM helps protect against gram-negative bacteria. Production increases rapidly a few days after birth as the infant is exposed to environmental antigens. IgM reaches adult levels at about 1 year of age (Buckley, 2011). If IgM is found in larger-than-normal amounts in the neonate, exposure to infection in utero is probable because IgM does not cross the placenta.

IgA also does not cross the placenta and must be produced by the infant. Because IgA is important in protection of the gastrointestinal and respiratory systems, newborns are particularly susceptible to infections of those systems. The immunoglobulin is produced beginning about 2 weeks of age. Secretory IgA is included in colostrum and breast milk (Kapur, Yoder, & Polin, 2011). Therefore breastfed infants may receive protection that formula-fed infants do not.

In the early hours after birth, the infant goes through changes called periods of reactivity. The two periods of reactivity are separated by a period of sleep or decreased activity (Gardner & Hernandez, 2011).