Circulation

At birth, the circulatory system changes from a fetal circulation pattern (which is in parallel), through a transitional circulation, to an adult circulation pattern (which is in series) (Figure 9-1).¹⁰ In the fetus, blood from the placenta travels through the umbilical vein and the ductus venosus to the inferior vena cava and the right side of the heart. The anatomic orientation of the inferior vena caval–right atrial junction favors the shunting (i.e., streaming) of this well-oxygenated blood through the foramen ovale to the left side of the heart. This well-oxygenated blood is pumped through the ascending aorta, where branches that perfuse the upper part of the body (e.g., heart, brain) exit proximal to the entrance of the ductus arteriosus.¹¹ Desaturated blood returns to the heart from the upper part of the body by means of the superior vena cava. The anatomic orientation of the superior vena caval–right atrial junction favors the streaming of blood into the right ventricle. Because fetal pulmonary vascular resistance is higher than systemic vascular resistance (SVR), approximately 90% of the right ventricular output passes through the ductus arteriosus and enters the aorta distal to the branches of the ascending aorta and aortic arch; therefore, less well-oxygenated blood perfuses the lower body, which consumes less oxygen than the heart and brain.

At the time of birth and during the resulting circulatory transition, the amount of blood that shunts through the foramen ovale and ductus arteriosus diminishes and the flow becomes bidirectional. Clamping the umbilical cord (or exposing the umbilical cord to room air) results in increased SVR. Meanwhile, expansion of the lungs and increased alveolar oxygen tension and pH result in decreased pulmonary vascular resistance and subsequently greater flow of pulmonary artery blood through the lungs.^12,13 Increased pulmonary artery blood flow results in improved oxygenation and higher left atrial pressure; the latter leads to a diminished shunt across the foramen ovale. Increased PaO₂ and SVR and decreased pulmonary vascular resistance result in a constriction of the ductus arteriosus.^14,15 Together, these changes in vascular resistance result in functional closure of the foramen ovale and the ductus arteriosus. This process does not occur instantaneously, and arterial oxygen saturation (SaO₂) remains higher in the right upper extremity (which is preductal) than in the left upper extremity and the lower extremities until blood flow through the ductus arteriosus is minimal.¹⁶ Differences in SaO₂ are usually minimal by 10 minutes and absent by 24 hours after birth. Provided that there is no interference with the normal drop in pulmonary vascular resistance, both the foramen ovale and the ductus arteriosus close functionally, and the infant develops an adult circulation (which is in series).

Persistent fetal circulation—more correctly called persistent pulmonary hypertension of the newborn—can occur when the pulmonary vascular resistance remains elevated at the time of birth. Factors that may contribute to this problem include hypoxia, acidosis, hypovolemia, and hypothermia.^13,17 Maternal use of nonsteroidal anti-inflammatory drugs may also cause premature constriction of the ductus arteriosus in the fetus and thus predispose to persistent pulmonary hypertension of the newborn.¹⁸

Respiration

Fetal breathing movements have been observed in utero as early as 11 weeks’ gestation. These movements increase with advancing gestational age but undergo a marked reduction within days of the onset of labor. They are stimulated by hypercapnia and maternal smoking and are inhibited by hypoxia and central nervous system (CNS) depressants (e.g., barbiturates). Under normal conditions, this fetal breathing activity results only in the movement of pulmonary dead space.¹⁹

The fetal lung contains a liquid composed of an ultrafiltrate of plasma, which is secreted by the lungs in utero²⁰; the volume of this lung liquid is approximately 30 mL/kg. Partial reabsorption of this liquid occurs during labor and delivery, and approximately two thirds is expelled from the lungs of the term neonate by the time of delivery.²¹ Small preterm infants and those requiring cesarean delivery may have a greater amount of residual lung liquid after delivery. These infants experience less chest compression at delivery than infants who are larger or delivered vaginally; this difference can lead to difficulty in the initiation and maintenance of a normal breathing pattern. Retained fetal lung liquid is the presumed cause of transient tachypnea of the newborn (TTN).²²

The first breath occurs approximately 9 seconds after delivery. Air enters the lungs as soon as the intrathoracic pressure begins to fall. This air movement during the first breath is important, because it establishes the neonate’s functional residual capacity (Figure 9-2).

Lung inflation is a major physiologic stimulus for the release of lung surfactant into the alveoli.²³ Surfactant, which is necessary for normal breathing, is present within the alveolar lining cells by 20 weeks’ gestation²⁴ and within the lumen of the airways by 28 to 32 weeks’ gestation. However, significant amounts of surfactant do not appear in terminal airways until 34 to 38 weeks’ gestation unless surfactant production has been stimulated by chronic stress or maternal corticosteroid administration.²⁵

Stress during labor and delivery can lead to gasping efforts by the fetus, which may result in the inhalation of amniotic fluid into the lungs.²⁶ This event can produce problems if the stress causes the fetus to pass meconium into the amniotic fluid before gasping.

Catecholamines

Transition to extrauterine life is associated with a catecholamine surge, which may be necessary for the process to be successful. In chronically catheterized sheep, catecholamine levels begin to rise a few hours before delivery and may be higher at the time of delivery than at any other time during life.²⁷ Catecholamines have an important role in the following areas: (1) the production and release of surfactant, (2) the mediation of preferential blood flow to vital organs during the period of stress that occurs during every delivery, and (3) thermoregulation of the neonate.

Thermal Regulation

Thermal stress challenges the neonate in the extrauterine environment. Neonates raise their metabolic rates and release norepinephrine in response to cold; this response facilitates the oxidation of brown fat, which contains numerous mitochondria. The oxidation results in nonshivering thermogenesis, the major mechanism for neonatal heat regulation.²⁸ This process may lead to significant oxygen consumption, especially if the neonate has not been dried off and kept in an appropriate thermoneutral environment, such as a radiant warmer. Thermal stress is an even greater problem in infants with low fat stores, such as preterm infants or infants who are small for gestational age. An alternative method to eliminate heat loss from evaporation is to provide an occlusive wrap rather than drying the infant. For infants born at less than 28 weeks’ gestation, the use of polythene wraps or bags is recommended to minimize heat loss.^29,30 The maintenance of a neutral thermal environment (i.e., 34° to 35° C) is recommended. However, in the neonate with a perinatal brain injury, mild hypothermia therapy through selective head or whole body cooling is initiated in the first 6 hours of life and may be neuroprotective in the setting of hypoxia-ischemia.^31,32 Hyperthermia may worsen neurologic outcomes and should be avoided.^2,33 Hypothermia therapy, via selective head cooling or whole body hypothermia, is continued for 72 hours after initiation. Consequently, if an infant is delivered at a center where hypothermia therapy is unavailable, passive cooling can be initiated by turning the radiant warmer off while awaiting infant transfer.

Administration of epidural analgesia during labor is associated with an increase in maternal and fetal temperature.³⁴ Concern has been expressed that the temperature elevation associated with intrapartum epidural analgesia might result in an increase in the frequency of neonatal sepsis evaluations.^34,35 However, a number of variables (e.g., preeclampsia/hypertension, gestational age, birth weight, meconium aspiration, respiratory distress at birth, hypothermia at birth, and group B beta-hemolytic streptococcal colonization of the maternal birth canal) have been observed to be strong predictors of the performance of neonatal sepsis evaluations, whereas maternal fever and epidural analgesia have not.³⁶ Confounding variables may influence the findings of these types of association studies; patients who choose either to receive or not receive epidural analgesia may be inherently different. The incidence of actual neonatal sepsis is not different in term infants whose mothers either did or did not receive epidural analgesia.

Apgar Score

Resuscitative efforts typically precede the performance of a thorough physical examination of the neonate. Because NRP instructions require simultaneous assessment and treatment, it is important that the neonatal assessment be both simple and sensitive. In 1953, Dr. Virginia Apgar, an anesthesiologist, described a simple method for neonatal assessment that could be performed while care was being delivered.⁴³ She suggested that this standardized and relatively objective scoring system would differentiate between infants who require resuscitation and those who need only routine care.⁴⁴

The Apgar score is based on five parameters that are assessed at 1 and 5 minutes after birth. Further scoring at 5- or 10-minute intervals may be done if initial scores are low. The parameters are heart rate, respiratory effort, muscle tone, reflex irritability, and color. A score of 0, 1, or 2 is assigned for each of these five entities (Table 9-1). A total score of 8 to 10 is normal; a score of 4 to 7 indicates moderate impairment; and a score of 0 to 3 signals the need for immediate resuscitation. Dr. Apgar emphasized that this system does not replace a complete physical examination and serial observations of the neonate for several hours after birth.⁴⁵

The Apgar score is widely used to assess neonates, although its value has been questioned. The scoring system may help predict mortality and neurologic morbidity in populations of infants, but Dr. Apgar cautioned against the use of the Apgar score to make these predictions in an individual infant. She noted that the risk for neonatal mortality was inversely proportional to the 1-minute score.⁴⁵ In addition, the 1-minute Apgar score was a better predictor of mortality within the first 2 days of life than within 2 to 28 days of life.

Several studies have challenged the notion that a low Apgar score signals perinatal asphyxia. In a prospective study of 1210 deliveries, Sykes et al.⁴⁶ noted a poor correlation between the Apgar score and the umbilical cord blood pH. Other studies, including those of low-birth-weight infants, have found that a low Apgar score is a poor predictor of neonatal acidosis, although a high score is reasonably specific for excluding the presence of severe acidosis.^47–53 By contrast, the fetal biophysical profile has a good correlation with the acid-base status of the fetus and the neonate (see Chapter 6).⁵⁴ The biophysical profile includes performance of a nonstress test and ultrasonographic assessment of fetal tone, fetal movement, fetal breathing movements, and amniotic fluid volume.⁵⁴

Additional studies have suggested that Apgar scores are poor predictors of long-term neurologic impairment.^55,56 The Apgar score is more likely to predict a poor neurologic outcome when the score remains 3 or less at 10, 15, and 20 minutes. However, when a child has cerebral palsy, low Apgar scores alone are not adequate evidence that perinatal hypoxia was responsible for the neurologic injury.

The ACOG Task Force on Neonatal Encephalopathy and Cerebral Palsy published criteria for defining an intrapartum event sufficient to cause cerebral palsy.⁵⁷ An Apgar score of 0 to 3 beyond 5 minutes of age is not included in the list of “essential criteria”; rather, it is one of five criteria that “collectively suggest an intrapartum timing (within close proximity to labor and delivery…) but are nonspecific to asphyxial insults.”^57–62

In a retrospective analysis of 151,891 singleton infants born at 26 weeks’ gestation or later between 1988 and 1998, Casey et al.⁶³ examined the relationship between Apgar scores and neonatal death rates during the first 28 days of life. The highest relative risk for neonatal death was observed in infants with an Apgar score of 3 or less at 5 minutes of age. The 5-minute Apgar score was a better predictor of neonatal death than the umbilical arterial blood pH. In term infants, the relative risk for neonatal death was eight times higher in infants with a 5-minute Apgar score of 3 or less than in those with an umbilical arterial blood pH of 7.0 or less.^63,64 In preterm infants, lower 5-minute Apgar scores were associated with younger gestational ages (i.e., mean score 6.6 ± 2.1 for infants born at 26 to 27 weeks’ and 8.7 ± 0.8 for infants born at 34 to 36 weeks’ gestation).^63,64 Similarly, earlier studies found that preterm infants were more likely than term infants to have low 1- and 5-minute Apgar scores, independent of neonatal oxygenation and acid-base status. Respiratory effort, muscle tone, and reflex irritability are the components of the score that are most influenced by gestational age.⁶⁵

The earlier the gestational age, the greater the likelihood of a low Apgar score, even in the presence of a normal umbilical cord blood pH. Preterm infants often require active resuscitation efforts immediately after delivery, and these manipulations may affect the components of the Apgar score. For example, pharyngeal and tracheal stimulation may cause a reflex bradycardia, which affects the heart rate score.⁴⁹ In addition, it is difficult to judge respiratory effort during suctioning or endotracheal intubation.

During cases of active neonatal resuscitation, the Apgar scores often are not assigned at the appropriate times; rather, these scores may be assigned retrospectively. In these situations, the individual must rely on recall of the infant’s condition at earlier times, introducing inaccuracy. Even if the scores are assigned at the appropriate times, there may be disagreement among the several individuals who are providing care for the infant. To avoid bias, Dr. Apgar recommended that someone not involved in the care of the mother assign the score.

Although there is some appeal to the use of objective measurements (i.e., SaO_2, heart rate) rather than subjective observations, it should not be inferred that the subjective components of the Apgar score (e.g., muscle tone) are less important. There are some practical limitations that may make objective measurements difficult to obtain (e.g., movement artifact with pulse oximetry).¹⁶ However, newer-generation pulse oximeters provide more accurate estimations of SaO₂ (see later discussion).⁶⁶

In summary, the usefulness of the Apgar score is still being debated more than 50 years after its inception.^63,64 The Apgar scoring system is used throughout the world, but its limitations must be kept in mind. Low Apgar scores alone do not provide sufficient evidence of perinatal asphyxia; rather, Apgar scores can be low for a variety of reasons. Preterm delivery, congenital anomalies, neuromuscular diseases, antenatal drug exposure, manipulation at delivery, and subjectivity and error may influence the Apgar score.

Umbilical Cord Blood Gas and pH Analysis

Umbilical cord blood gas and pH measurements reflect the fetal condition immediately before delivery and can be obtained routinely after delivery or measured only in cases of neonatal depression. These measurements may be a more objective indication of a neonate’s condition than the Apgar score. However, there is a delay between obtaining the samples and completing the analysis; during this interval, decisions must be made on the basis of clinical assessment. The ACOG⁶⁷ has recommended that cord blood gas measurements be obtained in circumstances of cesarean delivery for fetal compromise, low 5-minute Apgar score, severe growth restriction, abnormal FHR tracing, maternal thyroid disease, intrapartum fever, and/or multiple gestations.

The fetus produces carbonic acid (from oxidative metabolism) and lactic and beta-hydroxybutyric acids (primarily from anaerobic metabolism). Carbonic acid, which is often called respiratory acid, is cleared rapidly by the placenta as carbon dioxide when placental blood flow is normal. However, metabolic clearance of lactic and beta-hydroxybutyric acids requires hours; thus, these acids are called metabolic or fixed acids. In the fetus, metabolic acidemia is more ominous than respiratory acidemia because the former reflects a significant amount of anaerobic metabolism.

The measured components of umbilical cord blood gas analysis are pH, PCO₂, PO₂, and HCO₃⁻. Bicarbonate (HCO₃⁻) is a major buffer in fetal blood. The measure of change in the buffering capacity of umbilical cord blood is reflected in the delta base, which is also known as the base excess or deficit; this value can be calculated from the pH, PCO₂, and HCO₃⁻. Ideally, blood samples from both the umbilical artery and vein are collected. Umbilical artery blood gas measurements represent the fetal condition, whereas umbilical vein measurements reflect the maternal condition and uteroplacental gas exchange. Unfortunately, it may be difficult to obtain blood from the umbilical artery, especially when it is small, as it is in very low-birth-weight (VLBW) infants. Caution should be used in the interpretation of an isolated umbilical venous blood pH measurement, which can be normal despite the presence of arterial acidemia.

Proper blood sampling and handling are necessary. The measurements should be accurate, provided that (1) the umbilical cord is double clamped immediately after delivery^68–70; (2) the samples are drawn, within 15 minutes of delivery,⁷¹ into a syringe containing the proper amount of heparin⁷²; and (3) the samples are analyzed within 30 to 60 minutes.^71,73 The PO₂ measurement is more accurate if residual air bubbles are removed from the syringe.

Historically, a normal umbilical cord blood pH measurement was believed to be 7.2 or higher.⁷⁴ However, investigators have challenged the validity of this number, given its lack of distinction between umbilical arterial and venous blood despite clear differences in their normal measurements.⁷⁵ One study noted that the median umbilical arterial blood pH in vigorous infants (those with 5-minute Apgar scores of 7 or higher) was 7.26, with a measurement of 7.10 representing the 2.5^th percentile.⁷⁶ Published studies suggest that the lower limit of normal umbilical arterial blood pH measurements may range from 7.02 to 7.18 (Table 9-2).^46,77–86 A number of factors may also influence the umbilical arterial blood pH measurement. A fetus subjected to the stress of labor has lower pH measurements than one born by cesarean delivery without labor.⁸³ Offspring of nulliparous women tend to have a lower pH than offspring of parous women, a difference that is likely related to a difference in the duration of labor.⁸⁷

Some studies have suggested that preterm infants have a higher incidence of acidemia; however, later studies have observed that term and preterm infants have similar umbilical cord blood gas and pH measurements.^78,79,87 Preterm infants often receive low Apgar scores despite the presence of normal umbilical cord blood gas and pH measurements; therefore, the assessment of umbilical cord blood may be especially helpful in the evaluation of preterm neonates.

Physicians should use strict definitions when interpreting umbilical cord blood gas and pH measurements. Terms such as birth asphyxia should be avoided in most cases.⁵⁷ Acidemia refers to an increase in the hydrogen ion concentration in the blood. Acidosis occurs when there is an increased hydrogen ion concentration in tissue. Asphyxia is a clinical situation that involves hypoxia (i.e., a decreased level of oxygen in tissue), damaging acidemia, and metabolic acidosis.

When acidemia is present, the type—respiratory, metabolic, or mixed—must be identified (Table 9-3). Metabolic acidemia is more likely to be associated with acidosis than respiratory acidemia and is clinically more significant. Similarly, mixed acidemia with a high PCO₂, an extremely low HCO₃⁻, and a high base deficit is more ominous than a mixed acidemia with a high PCO₂ but only a slightly reduced HCO₃⁻ and a low base deficit. Mixed or metabolic acidemia (but not respiratory acidemia) is associated with an increased incidence of neonatal complications and death.⁸⁷ In their study of 3506 term neonates, Goldaber et al.⁸⁸ noted that an umbilical arterial blood pH measurement less than 7.00 was associated with a significantly higher incidence of neonatal death. All neonatal seizures in their study occurred in infants with an umbilical arterial blood pH less than 7.05. By contrast, a short-term outcome study failed to show a good correlation between arterial blood pH and the subsequent health of an infant.⁵³ In the previously discussed large study reported by Casey et al.,⁶³ an umbilical arterial blood pH of 7.0 or less was a poorer predictor of the relative risk for neonatal death during the first 28 days of life than a 5-minute Apgar score of 3 or less. However, 6264 infants were excluded from their study because umbilical arterial blood gas measurements could not be obtained, and these infants had a higher incidence of neonatal death than those for whom blood gas measurements were available (4.5 per 1000 versus 1.2 per 1000, respectively). In a separate review of 51,519 term deliveries, Yeh et al.⁸⁹ found an increased risk for adverse outcomes in infants with a pH less than 7.10, with the lowest risk in infants with a pH between 7.26 and 7.30; however, 75% of infants with neurologic morbidity had a normal pH. Thus, it is important to remember that neonates may suffer multiorgan system damage, including neurologic injury, even in the absence of low pH and Apgar scores.

According to the ACOG Task Force, an umbilical arterial blood pH less than 7.0 and a base deficit greater than or equal to 12 mmol/L at delivery are considered one part of the definition of an acute intrapartum hypoxic event sufficient to cause cerebral palsy.⁵⁷ The base deficit and bicarbonate (the metabolic component) values are the most significant factors associated with morbidity in neonates with an umbilical arterial blood pH less than 7.0. Ten percent of infants with an umbilical arterial base deficit of 12 to 16 mmol/L have moderate to severe complications, which increases to 40% when the deficit is greater than 16 mmol/L.⁶⁷

Abnormal FHR patterns and umbilical cord blood gas measurements are not consistently correlated with poor neonatal outcomes.³⁷ In a longitudinal study that evaluated outcomes at 6.5 years of age, Hafstrom et al.⁹⁰ found that infants with an umbilical arterial blood pH less than 7.05 but a normal examination at birth had outcomes that did not differ from those for matched infants with a normal umbilical arterial blood pH.

As Dr. Apgar emphasized in 1962, the most important components of neonatal assessment are a careful physical examination and continued observation for several hours.⁴⁵ Additional information can be gained from the antenatal history, Apgar scores, and umbilical cord blood gas and pH measurements, provided that clinicians are aware of the proper methods of interpretation as well as the limitations of these methods of assessment.

Respiration and Circulation

There are some similarities between the initial assessment of the neonate and the initial assessment of an adult who requires resuscitation. In both situations, the physician should give immediate attention to the ABCs of resuscitation (i.e., airway, breathing, circulation).

The normal neonatal respiratory rate is between 30 and 60 breaths per minute. Breathing should begin by 30 seconds and be regular by 90 seconds of age. Failure of the neonate to breathe by 90 seconds of age represents either primary or secondary apnea, based on the neonatal rhesus monkey asphyxia model.⁹¹ In this model, gasping motions were observed for approximately 1 minute immediately after delivery; this was followed by a 1-minute period of apnea (primary apnea), then 5 minutes of gasping motions, and a final period of apnea (secondary or “terminal” apnea). During primary apnea, but not secondary apnea, tactile stimulation of the newborn monkey initiated breathing efforts. In addition, although heart rate was low with both periods of apnea, a reduction in blood pressure was observed only during secondary apnea. With the onset of secondary apnea (approximately 8 minutes after birth), the pH was 6.8 and the PaO₂ and PaCO₂ measurements were less than 2 and 150 mm Hg, respectively.

This experimental model illustrates two important points. First, distinguishing primary from secondary apnea is not possible unless blood pressure and/or blood gases and pH are measured. Second, by the time secondary apnea has begun, blood gas measurements have deteriorated significantly. Therefore, during evaluation of the apneic neonate, aggressive resuscitation must be initiated promptly if tactile stimulation does not result in the initiation of spontaneous breathing.

Assessment of the adequacy of respiratory function requires comprehensive observation for signs of neonatal respiratory distress. These signs include cyanosis, grunting, flaring of the nares, retracting chest motions, and unequal breath sounds. The adequacy of respiratory function can also be assessed by the estimation of SaO₂. The reliability of pulse oximetry for the assessment of neonatal SaO₂ was questioned initially because of concerns about the accuracy of spectrophotometric assessments of fetal hemoglobin and the difficult signal detection caused by the rapidity of the neonate’s heart rate.^92,93 The newer generation of pulse oximetry monitors, which employ signal extraction and averaging techniques, are able to provide more reliable measurements, especially in the presence of poor perfusion, patient movement, and ambient light artifacts.^66,94

Pulse oximetry provides accurate estimates of SaO₂ during periods of stability but may overestimate values during rapid desaturation.⁹⁵ In addition, the SaO₂ (SpO₂) measurements may fluctuate in the delivery room as a result of the ongoing transition from the fetal to the neonatal circulation, and it may take more than 10 minutes to achieve a preductal SaO₂ greater than 95% in a healthy term infant. Overall, the newer-generation pulse oximeters reliably provide continuous noninvasive SaO₂ measurements and are useful for neonatal monitoring.^96–98

The pulse oximeter sensor should be applied to the neonate’s right upper extremity, which receives preductal blood flow (see earlier discussion); because CNS blood flow is also preductal, right upper extremity SaO₂ measurements provide a more accurate assessment of CNS oxygenation.¹⁶ Sensor placement can be difficult on skin that is wet and covered with vernix caseosa; therefore, it may be easier to place the sensor over the right radial artery, especially in preterm infants.⁹⁴

Neonatal arterial blood sampling is technically difficult and thus rarely obtained in the delivery room. Cannulation of the umbilical artery is useful in infants who will require frequent blood sampling. This procedure often requires the use of microinstruments (especially in preterm and VLBW infants) and the ability to monitor the infant when obscured from view by surgical drapes; therefore, this procedure is usually performed in the neonatal intensive care unit (NICU).

The normal neonatal heart rate may be greater than 160 beats per minute (bpm) in the very early preterm neonate, but it should be within the range of 120 to 160 bpm by 28 weeks’ gestational age. The heart rate can be determined in several ways. The clinician can lightly grasp the base of the umbilical cord and feel the arterial pulsations. (This method cannot be used in situations in which the pulsations become difficult to feel, such as in an infant with a low cardiac output.) Alternatively, the clinician can listen to the apical heartbeat. When either of these two methods is used, the evaluator should tap a hand with each heartbeat so that other members of the resuscitation team are aware of the rate. By contrast, the use of a pulse oximeter provides an audible heart rate, the additional benefit of SaO₂ monitoring, and the ability to eliminate the need for an additional team member.

Measurement of arterial blood pressure is not a priority during the initial assessment and resuscitation of the neonate.² However, observation for signs of abnormal circulatory function is considered essential. These signs include cyanosis, pallor, mottled coloring, prolonged capillary refill time, and weakness or absence of pulses in the extremities. One of the causes of abnormal circulatory function is hypovolemia, which should be anticipated in cases of bleeding from the umbilical cord or the fetal side of the placenta or whenever a neonate does not respond appropriately to resuscitation. The hypovolemic neonate may exhibit not only signs of abnormal circulatory function but also tachycardia and tachypnea. (Neonatal hypovolemia usually does not accompany placental abruption, which may cause maternal bleeding or other conditions associated with fetal asphyxia.)

Neurologic Status

The initial neonatal neurologic assessment requires only simple observation. The neonate should demonstrate evidence of vigorous activity, including crying and active flexion of the extremities. Signs of possible neurologic abnormalities include apnea, seizures, hypotonia, and unresponsiveness. Neonates should be assessed for physical signs of hypoxic-ischemic encephalopathy (Table 9-4). The stages of hypoxic-ischemic encephalopathy are associated with different outcomes: stage I, good; stage II, moderate; and stage III, poor.⁹⁹ Although detailed neurologic assessment is performed after the neonate is transferred to the NICU, assessment of tone, baseline heart rate, respirations, and reflex activity is part of both the Apgar scoring system and the assessment for hypoxic-ischemic encephalopathy and is made initially in the delivery room.

Gestational Age

When assessing a very small neonate whose gestational age appears to be lower than that of viability, the evaluator must consider whether it is appropriate to initiate and maintain resuscitation efforts. The neonatal gestational age is often assessed with the use of the scoring systems described initially by Dubowitz et al.¹⁰⁰ and subsequently modified by Ballard et al.¹⁰¹ The Dubowitz system makes use of an external score based on physical characteristics, described previously by Farr et al.,^102,103 and a neurologic score. The Ballard system uses simplified scoring criteria to assess gestational age. Ballard et al.¹⁰¹ eliminated certain physical criteria such as edema and skin color because of the unreliability of these criteria in some clinical conditions. In addition, they abbreviated the neurologic criteria on the basis of observations by Amiel-Tison.¹⁰⁴

The Dubowitz and Ballard scores are most accurate when used to estimate gestational age at 30 to 42 hours, rather than during the first several minutes, after birth. These scoring systems are also less accurate in very small preterm infants. In one study of 100 preterm infants with birth weights less than 1500 g, agreement among antenatal measures of gestational age (e.g., last menstrual period, ultrasonography determination) and postnatal measures (e.g., Dubowitz and Ballard scores) was poor.¹⁰⁵ Both scoring systems overestimated gestational age in this subset of VLBW infants. Ballard et al.¹⁰⁶ refined their scoring system to provide a more accurate estimate of gestational age in preterm infants (Figure 9-3). The new Ballard score assesses physical criteria, such as eyelid fusion, breast tissue, lanugo hair, and genitalia, and neurologic criteria, such as wrist “square window.” (The square window assessment is performed by flexing the infant’s wrist on the forearm and noting the angle between the hypothenar eminence and the ventral aspect of the forearm.) Although the new Ballard score may be more accurate than the older score for the assessment of preterm infants, inconsistencies occur with all of these methods. Of particular interest is the observation that fetuses of different racial origin appear to mature at different rates (i.e., black fetuses mature faster than white fetuses).¹⁰⁷

Another commonly used criterion for the estimation of gestational age is birth weight. Normal values for birth weight are published and readily available.¹⁰⁸ Although birth weight may help physicians estimate the gestational age of an otherwise healthy preterm infant, physicians cannot rely on birth weight to provide an accurate estimate of gestational age in an infant who suffered from intrauterine growth restriction or who is large for gestational age.

Because of the potential for inaccurate gestational age estimation in the delivery room, it is best not to use these scoring systems to guide decisions regarding the initiation or continuation of neonatal resuscitation immediately after delivery. In most circumstances, the neonate’s response to resuscitative efforts is the best indicator as to whether further intervention is warranted.