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 ( Fig. 9.1 ). 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 shunting (i.e., streaming) of this well-oxygenated blood through the foramen ovale to the left side of the heart. The blood is then 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. Desaturated blood returns to the heart from the upper part of the body via 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, blood that is less well-oxygenated perfuses the lower body, which has a lower oxygen consumption than the heart and brain. Deoxygenated blood from the fetus returns to the placental circulation via the umbilical arteries.

Modification of Blood Flow Patterns From the Fetal (Left) , via the Transitional (Center) , to the Neonatal (Right) Circulation. In the fetal circulation, oxygenated blood (white) from the placenta travels through the umbilical vein (1) into the ductus venosus and the inferior vena cava (2) . The majority of oxygenated blood passes through the patent foramen ovale (PFO) from the right atrium to the left atrium (3) and ventricle (4) , and distributes this blood to the brain (5) . The deoxygenated blood (blue) from the brain and upper extremities enters the superior vena cava, mixing with a small portion of the oxygenated blood in the right atrium, before entering the right ventricle (RV, 7 ). The mostly deoxygenated blood is transported into the pulmonary artery, where the majority is diverted through the patent ductus arteriosus (PDA, 8 ) into the descending aorta (9) , thereby bypassing the lungs. Some blood enters the lower body (10) , but the majority returns to the placenta via the umbilical arteries (11) . A small amount of blood from the pulmonary artery enters the lungs (12) . During the transitional circulation, which occurs over a few days, the PFO closes, diverting blood from the right atrium to the right ventricle. Closure of the PDA diverts deoxygenated blood through the pulmonary arteries to the lungs. The neonatal circulation separates the oxygenated and deoxygenated blood flow pathways.

Illustration by Naveen Nathan, MD, NorthShore University HealthSystem, University of Chicago Pritzker School of Medicine, Evanston, IL.

At the time of birth and during the subsequent period of circulatory transition, the amount of blood that shunts through the foramen ovale and ductus arteriosus diminishes, and flow becomes bidirectional. Clamping the umbilical cord (or exposing the umbilical cord to room air) results in increased SVR. Concurrently, expansion of the lungs and increased alveolar oxygen tension and pH result in decreased pulmonary vascular resistance and greater flow of pulmonary artery blood through the lungs. 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 P o ₂ and SVR and decreased pulmonary vascular resistance result in constriction of the ductus arteriosus. 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 (Sa o ₂ ) 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. Differences in Sa o ₂ are usually minimal by 10 minutes and absent by 24 hours after birth. Provided there is no interference with the normal drop in pulmonary vascular resistance, both the foramen ovale and the ductus arteriosus close functionally as the infant transitions to an adult circulation.

Persistent pulmonary hypertension of the newborn (previously referred to as persistent fetal circulation) occurs when the pulmonary vascular resistance remains elevated after the time of birth. Factors that may exacerbate this problem include hypoxia, acidosis, hypovolemia, and hypothermia. Maternal use of nonsteroidal antiinflammatory drugs may cause premature constriction of the ductus arteriosus in the fetus and thus predispose to persistent pulmonary hypertension of the newborn.

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.

The fetal lung contains a liquid composed of an ultrafiltrate of plasma, which is secreted by the lungs in utero ; 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. Preterm infants and infants requiring cesarean delivery without labor may have a greater amount of residual lung liquid after delivery owing to a reduced catecholamine surge at delivery. This residual lung liquid leads to difficulty in the initiation and maintenance of normal breathing patterns and is the presumed cause of transient tachypnea of the newborn (TTN) .

The first breath occurs approximately 9 seconds after delivery. Air enters the lungs as soon as the intrathoracic pressure begins to decrease. This air movement during the first breath is important because it establishes the neonate’s functional residual capacity ( Fig. 9.2 ).

Typical Pressure-Volume Loop of the Neonate’s First Breath. The intrathoracic pressure decreases to −30 to −40 cm H ₂ O, drawing air into the lungs. The expiratory pressure is much greater than the inspiratory pressure.

Modified from Milner AD, Vyas H. Lung expansion at birth. J Pediatr . 1982;101:879–886.

Lung inflation is a major physiologic stimulus for the release of lung surfactant into the alveoli. Surfactant, which is necessary for normal breathing, is present within the alveolar lining cells by 20 weeks’ gestation 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 its production has been stimulated by chronic stress or maternal corticosteroid administration. Stress during labor and delivery can lead to the passage of meconium into the amniotic fluid and gasping efforts by the fetus, which may result in the aspiration of amniotic fluid into the lungs.

Transition to extrauterine life is associated with a catecholamine surge. 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. Catecholamines have an important role in the following areas: (1) the production and release of surfactant, (2) the transition to active sodium transport for absorption of lung fluid, (3) the mediation of preferential blood flow to vital organs during the period of stress that occurs during every delivery, and (4) thermoregulation of the neonate.

Thermal stress challenges the neonate in the extrauterine environment. Neonates raise their metabolic rate 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. This process may lead to significant oxygen consumption, especially if the neonate has not been dried and placed in an appropriate thermoneutral environment, for example, under 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. For extreme preterm infants, increasing the ambient room temperature from 20°C to 23°C may minimize the risk for hypothermia. The maintenance of a neutral thermal environment (i.e., 34°C to 35°C) is recommended.

In the neonate with a perinatal brain injury, however, 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. Hyperthermia may worsen neurologic outcomes and should be avoided. Hypothermia therapy, via selective head cooling or whole-body hypothermia, is usually continued for several days 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 neuraxial analgesia during labor is associated with an increase in maternal and fetal temperature, which might result in an increase in the frequency of neonatal sepsis evaluations (see Chapter 24 ). 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 neonatal sepsis evaluations, whereas maternal fever and epidural analgesia have not. Confounding variables may influence the findings of these types of association studies; patients who choose either to receive or not receive neuraxial analgesia are inherently different. The incidence of actual neonatal sepsis is not different in term infants whose mothers either do or do not receive neuraxial analgesia.

In infants not requiring immediate resuscitation, providing skin-to-skin contact with the mother can allow for appropriate thermal regulation, enhance breastfeeding, and reduce maternal stress. This practice must be associated with close monitoring to prevent the infant from slipping off the mother and to detect sudden unexpected postnatal collapse (SUPC). Although rare, SUPC can be a fatal event in an otherwise healthy-appearing infant; prevention requires adequate personnel for observation, monitoring, and treatment.

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, Virginia Apgar, an anesthesiologist, described a simple method for neonatal assessment that could be performed while care was being delivered. She suggested that this standardized and relatively objective scoring system would differentiate between infants who require resuscitation and those who need only routine care.

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.

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. 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. 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. By contrast, the fetal biophysical profile has a good correlation with the acid-base status of the fetus and the neonate (see Chapter 6 ). The biophysical profile includes the performance of a nonstress test and ultrasonographic assessment of fetal tone, fetal movement, fetal breathing movements, and amniotic fluid volume.

Additional studies have suggested that Apgar scores are poor predictors of long-term neurologic impairment. 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 American College of Obstetricians and Gynecologists (ACOG) and AAP Task Force on Neonatal Encephalopathy recommend a comprehensive multidimensional assessment be performed of neonatal status and all potential contributing factors (maternal history, obstetric antecedents, intrapartum factors, placental pathology) to assess the likelihood that an acute peripartum or intrapartum event was sufficient to cause neonatal encephalopathy. An Apgar score of less than 5 at 5 minutes and 10 minutes of age confers an increased risk of cerebral palsy, but most infants with low Apgar scores will not develop cerebral palsy. If the 5-minute Apgar score is greater than or equal to 7, it is unlikely that peripartum hypoxia-ischemia caused the neonatal encephalopathy.

In summary, the Apgar scoring system is used throughout the world; it is a convenient method for assessing the status of the neonate immediately after birth as well as the infant’s response to resuscitation. Low Apgar scores alone do not predict individual neonatal mortality or neurologic outcome; 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 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, because of the delay between obtaining the samples and reporting the results, decisions must be made based on clinical assessment until the results are available. The ACOG and AAP have recommended that cord blood gas measurements be obtained in cases for which fetal metabolic status is in question.

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, P co ₂ , P o ₂ , and bicarbonate (HCO ₃ ^– ). HCO ₃ ⁻ 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, P co ₂ , and HCO ₃ ⁻ . 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; (2) the samples are drawn within 20 minutes of delivery into a syringe containing the proper amount of heparin; and (3) the samples are analyzed within 20 minutes. If the delay is longer than 20 minutes, the sample should be placed on ice. The base deficit and lactate values increase with longer delays and, thus, should be interpreted with caution. The P o ₂ 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. However, investigators have challenged the validity of this number, given the lack of distinction between umbilical arterial and venous blood despite clear differences in their normal measurements. There is no global consensus on the definition of acidemia. One study noted that the median umbilical arterial blood pH in vigorous infants (those with 5-minute Apgar scores of ≥ 7) was 7.26, with a measurement of 7.10 representing the 2.5th percentile. The statistical lower limit of umbilical artery pH is approximately 7.10 (mean minus two standard deviations). A number of factors may also influence the umbilical arterial blood pH measurement. A fetus subjected to the stress of labor has a lower pH than one born by cesarean delivery without labor. 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. Other factors influencing fetal acid-base status include the maternal condition, temperature, gestational age, fetal body mass, and infection. Delayed umbilical cord clamping is associated with lower pH and higher P co ₂ , base deficit, and lactate because acidic metabolites, which have accumulated in peripheral tissue during labor, are washed into the central circulation as the infant begins to cry and move after delivery.

Fetal arterial pH and P o ₂ decrease and P co ₂ increases with gestational age, but base deficit values do not change. Preterm infants often have 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 whose low tone or poor respiratory effort may be related to gestational age alone.

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. 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 9.2 ). Metabolic acidemia is more likely to be associated with acidosis than respiratory acidemia and is clinically more significant. Similarly, mixed acidemia with a high P co ₂ , an extremely low HCO ₃ ⁻ , and a high base deficit is more ominous than a mixed acidemia with a high P co ₂ but only a slightly reduced HCO ₃ ⁻ and a low base deficit. Mixed or metabolic acidemia (but not respiratory acidemia) is associated with an increased incidence of neonatal complications and death.

In their study of 3506 term neonates, Goldaber et al. noted that an umbilical arterial blood pH measurement < 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 < 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. In the large study reported by Casey et al., umbilical arterial blood pH of ≤ 7.0 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. 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 obtained. In a separate review of 51,519 term deliveries, Yeh et al. found an increased risk for adverse outcomes in infants with a pH < 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/APP Task Force, an umbilical arterial blood pH < 7.0 and a base deficit ≥ 12 mmol/L at delivery are considered one part of the definition of an acute intrapartum hypoxic event sufficient to cause cerebral palsy. 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 < 7.0. Twenty-three percent of infants with an umbilical arterial base deficit of 12 to 16 mmol/L have moderate to severe complications, which increases to 37% when the deficit is greater than 16 mmol/L.

Abnormal FHR patterns and umbilical cord blood gas measurements are not consistently correlated with poor neonatal outcomes. In a longitudinal study that evaluated outcomes at 6.5 years of age, Hafstrom et al. found that infants with an umbilical arterial blood pH < 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 Virginia Apgar emphasized in 1962, the most important components of neonatal assessment are a careful physical examination and continued observation for several hours. 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.

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. During primary apnea , but not secondary apnea, tactile stimulation can initiate breathing efforts. In addition, although heart rate may be low with both periods of apnea, a reduction in blood pressure occurs only during secondary apnea. 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 Sa o ₂ . Pulse oximetry provides accurate estimates of Sa o ₂ during periods of stability but may overestimate values during rapid desaturation. In addition, the Sa o ₂ (Sp o ₂ ) 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 Sa o ₂ > 95% in a healthy term infant. Targeted preductal Sp o ₂ values are shown in Table 9.3 . Supplemental oxygen may be administered, titrated to achieve the normal range for healthy term infants after vaginal delivery.

Pulse oximetry is recommended when resuscitation is anticipated, when positive pressure ventilation or supplemental oxygen is administered, or when central cyanosis persists beyond 5 to 10 minutes of life. 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 Sa o ₂ measurements provide a more accurate assessment of CNS oxygenation. 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.

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. Clinical determination of the heart rate can be done by lightly grasping the base of the umbilical cord to feel the arterial pulsations or by listening to the apical heartbeat. These methods have been found to be less reliable than electrocardiography (ECG). Additionally, several studies have found the ECG to be more accurate than pulse oximetry and is now recommended by the NRP for infants requiring resuscitation.

Measurement of arterial blood pressure is not a priority during the initial assessment and resuscitation of the neonate. 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 signs of abnormal circulatory function as well as tachycardia and tachypnea (neonatal hypovolemia usually does not accompany placental abruption, which may cause maternal bleeding, or other conditions associated with fetal asphyxia).

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. The modified Sarnat tool distinguishes three stages of encephalopathy based on physical signs and symptoms. The stages of hypoxic-ischemic encephalopathy are associated with different outcomes: stage I, good; stage II, moderate; and stage III, poor. Although detailed neurologic assessment, including head imaging, 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.

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 most accurate method of estimating gestational age combines consideration of the last menstrual period and early fetal ultrasound as well as physical and neurologic characteristics of the newborn. The neonatal gestational age is often assessed with the use of the scoring systems described initially by Dubowitz et al. and subsequently modified by Ballard et al., using physical and neurologic criteria.

The Ballard score is most accurate when used to estimate gestational age at 30 to 42 hours, rather than during the first several minutes after birth, and is less accurate in very small preterm infants.

Another commonly used criterion for the estimation of gestational age is birth weight. Normal values for birth weight are published and readily available. 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 fetal 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 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.

Meconium is present in the intestinal tract of the fetus after approximately 31 weeks’ gestation. Meconium-stained amniotic fluid is present in 10% to 15% of all pregnancies; the incidence is higher in postterm pregnancies. Intrapartum passage of meconium may be associated with fetal stress and hypoxia.

Meconium aspiration syndrome (MAS) is defined as respiratory distress in a neonate whose airway was exposed to meconium and whose chest radiograph exhibits characteristic findings, including pulmonary consolidation and atelectasis. Treatment of MAS often involves the use of positive-pressure ventilation and is associated with a 5% to 20% incidence of pneumothorax from pulmonary air leaks. It can be associated with persistent pulmonary hypertension of the newborn. The use of extracorporeal membrane oxygenation (ECMO) and inhaled nitric oxide for the treatment of pulmonary hypertension associated with MAS has been shown to reduce mortality rates. In a US study published in 2009, the mortality in neonates admitted to the intensive care unit with MAS was 1.2%.

In an attempt to reduce inhalation of meconium from the pharynx and thus prevent or reduce the severity of MAS, the practice of suctioning the mouth and pharynx after delivery of the head, and subsequent intubation to remove meconium from the trachea was a common practice. However, studies have documented that airway suctioning at birth does not prevent MAS and its associated mortality ; these studies indicated that MAS was primarily a result of intrauterine events such as asphyxia or sepsis. Hypoxia induces pathologic changes in the pulmonary vasculature, which results in pulmonary hypertension and respiratory distress after birth. The pulmonary damage is independent of meconium aspiration; therefore, it is not prevented by the suctioning of meconium. A prospective study designed to assess the efficacy of routine tracheal suctioning of meconium to prevent MAS indicated little or no benefit to this practice. Current guidelines do not recommend routine intrapartum oropharyngeal and nasopharyngeal suctioning after delivery of the infant’s head, given that a large multicenter randomized trial showed no benefit to this practice in term-gestation infants.

Amnioinfusion —the instillation of saline into the amniotic cavity—has been used successfully for reduction of cord compression in the presence of oligohydramnios during labor. It has also been proposed as a potential treatment to reduce the incidence of MAS in infants born to women with thick meconium staining of the amniotic fluid. A large multicenter randomized trial found no difference in rates of MAS or other neonatal disorders with the use of amnioinfusion. Thus, the routine practice of amnioinfusion for meconium-stained fluid alone is not recommended.