Neonatal Assessment and Resuscitation




Abstract


The transition from intrauterine to extrauterine life represents the most important adjustment that a neonate will make. This transition occurs uneventfully after most deliveries and is dependent on the anatomic and physiologic condition of the infant, the ease or difficulty of the delivery, and the extrauterine environmental conditions. When the transition is unsuccessful, prompt assessment and supportive care must be initiated immediately.




Keywords

Neonatal transition, Neonatal assessment, Neonatal resuscitation, Prematurity, Congenital anomalies

 






  • Chapter Outline



  • Transition from Intrauterine to Extrauterine Life, 171





  • Antenatal Assessment, 174



  • Neonatal Assessment, 175




    • Apgar Score, 175



    • Umbilical Cord Blood Gas and pH Analysis, 176



    • Respiration and Circulation, 178



    • Neurologic Status, 179



    • Gestational Age, 179




  • Neonatal Resuscitation, 179



  • Special Resuscitation Circumstances, 184




    • Meconium-Stained Amniotic Fluid, 184



    • Preterm Infant, 185



    • Congenital Anomalies, 186




  • Ethical Considerations, 188



  • Neurobehavioral Testing, 189


The transition from intrauterine to extrauterine life represents the most important adjustment that a neonate will make. This transition occurs uneventfully after most deliveries and is dependent on the anatomic and physiologic condition of the infant, the ease or difficulty of the delivery, and the extrauterine environmental conditions. When the transition is unsuccessful, prompt assessment and supportive care must be initiated immediately.


At least one person skilled in neonatal resuscitation should be present at every delivery. The resuscitation team may include personnel from the pediatric, anesthesiology, obstetric, respiratory therapy, and nursing services. The composition of the team varies among institutions, but there should be some form of 24-hour coverage in all hospitals that provide labor and delivery services. A multidisciplinary team should participate in the process of ensuring that appropriate personnel and equipment are available for neonatal resuscitation.


All personnel working in the delivery area should receive basic training in neonatal resuscitation to ensure prompt initiation of care before the arrival of the designated resuscitation team. The 2015 American Heart Association (AHA) Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care led to the publication of updated guidelines for neonatal resuscitation. Changes in these guidelines reflected a review of scientific evidence by members of the American Academy of Pediatrics (AAP), the AHA, and the International Liaison Committee on Resuscitation. These guidelines have been incorporated into the Neonatal Resuscitation Program (NRP), which is the standardized training and certification program administered by the AAP. The NRP, which was originally sponsored by the AAP and the AHA in 1987, is designed to be appropriate for all personnel who attend deliveries. To ensure the implementation of current guidelines for neonatal resuscitation, the AAP recommends that at least one NRP-certified practitioner attend every delivery.


Both the American Society of Anesthesiologists (ASA) and the American College of Obstetricians and Gynecologists (ACOG) have published specific goals and guidelines for neonatal resuscitation ( Box 9.1 ). The ASA has emphasized that a single anesthesiologist should not be expected to assume responsibility for the concurrent care of both the mother and her child. Rather, a second anesthesia provider or a qualified individual from another service should assume responsibility for the care of the neonate, except in an unforeseen emergency.



Box 9.1

Optimal Goals for Anesthesia Care in Obstetrics: Neonatal Resuscitation


Personnel other than the surgical team should be immediately available to assume responsibility for resuscitation of the depressed neonate. The surgeon and anesthesiologist are responsible for the mother and may not be able to leave her to care for the neonate, even when a neuraxial anesthetic is functioning adequately. Individuals qualified to perform neonatal resuscitation should demonstrate:




  • Proficiency in rapid and accurate evaluation of the neonate’s condition, including Apgar scoring



  • Knowledge of the pathogenesis of a depressed neonate (acidosis, drugs, hypovolemia, trauma, anomalies, and infection) as well as specific indications for resuscitation



  • Proficiency in neonatal airway management, laryngoscopy, endotracheal intubation, airway suctioning, artificial ventilation, cardiac massage, and maintenance of thermal stability



In larger maternity units and those functioning as high-risk centers, 24-hour in-house anesthesia, obstetric, and neonatal specialists are usually necessary.


Modified from a joint statement from the American College of Obstetricians and Gynecologists and the American Society of Anesthesiologists. Optimal goals for anesthesia case in obstetrics. Approved by the American Society of Anesthesiologists in October 2008. (See Appendix C for full document.)


Although the anesthesia provider is not usually the primary provider of neonatal resuscitation, he or she may be asked to provide assistance in cases of difficult airway management or when the neonatal resuscitation team has not yet arrived. The anesthesia provider should be prepared to provide assistance, provided that doing so does not compromise the care of the mother. Written hospital policies should identify the personnel responsible for neonatal resuscitation, and obstetric anesthesia providers should also maintain a high level of skill in neonatal resuscitation.




Transition From Intrauterine to Extrauterine Life


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) ( 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 the 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.




Fig. 9.1


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, Northwestern University Feinberg School of Medicine, Chicago, 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 a 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) 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. 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.


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.


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 that promotes sodium channel transport; 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 ).




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.


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. 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 Regulation


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 with 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. 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. Hyperthermia may worsen neurologic outcomes and should be avoided. 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, which might result in an increase in the frequency of neonatal sepsis evaluations. 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. 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.


In infants not requiring immediate resuscitation, providing skin-to-skin contact with the mother can allow for appropriate thermal regulation, enhance breast-feeding, 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, and requires adequate personnel to provide observation, monitoring, and treatment.




Antenatal Assessment


Approximately 10% of neonates require some level of resuscitation. The need for resuscitation can be predicted before labor and delivery with approximately 80% accuracy on the basis of a number of antepartum factors ( Box 9.2 ).



Box 9.2

Risk Factors Suggesting a Greater Need for Neonatal Resuscitation


Antepartum Risk Factors





  • Maternal diabetes



  • Hypertensive disorder of pregnancy



  • Chronic hypertension



  • Fetal anemia or isoimmunization



  • Previous fetal or neonatal death



  • Bleeding in second or third trimester



  • Maternal infection



  • Maternal cardiac, pulmonary, renal, thyroid, or neurologic disease



  • Polyhydramnios



  • Oligohydramnios



  • Premature rupture of membranes



  • Fetal hydrops



  • Postterm gestation



  • Multiple gestation



  • Discrepancy between fetal size and dates (i.e., last menstrual period)



  • Drug therapy (e.g., lithium carbonate, magnesium, adrenergic-blocking drugs)



  • Maternal substance abuse



  • Fetal malformation



  • Diminished fetal activity



  • No prenatal care



  • Maternal age > 35 years



Intrapartum Risk Factors





  • Emergency cesarean delivery



  • Forceps or vacuum-assisted delivery



  • Breech or other abnormal presentation



  • Preterm labor



  • Precipitous labor



  • Chorioamnionitis



  • Prolonged rupture of membranes (> 18 hours before delivery)



  • Prolonged labor (> 24 hours)



  • Macrosomia



  • Category II or III fetal heart rate patterns



  • Use of general anesthesia



  • Uterine tachysystole with fetal heart rate changes



  • Maternal administration of opioids within 4 hours of delivery



  • Meconium-stained amniotic fluid



  • Prolapsed umbilical cord



  • Placental abruption



  • Placenta previa



  • Significant intrapartum bleeding



Modified from Textbook of Neonatal Resuscitation , 6th ed. Elk Grove Village, IL: American Academy of Pediatrics and American Heart Association; 2011:216.


Preterm delivery increases the likelihood that the neonate will require resuscitation. When a mother is admitted with either preterm labor or premature rupture of membranes, plans should be made for neonatal care in the event of delivery. The antenatal assessment of gestational age is based on the presumed date of the last menstrual period, the fundal height, and ultrasonographic measurements of the fetus. Unfortunately, it may be difficult to assess gestational age accurately, because menstrual dates may be unknown or incorrect, the fundal height may be affected by abnormalities of fetal growth or amniotic fluid volume, and ultrasonographic assessment of fetal age is less precise after mid-pregnancy. The assessment of gestational age is most accurate in patients who receive prenatal care in early pregnancy and enables the health care team to plan for the neonatal needs and to appropriately counsel the parents regarding neonatal morbidity and mortality. These plans and expectations must be formulated with caution and flexibility, because the antenatal assessment may not accurately predict neonatal size, maturity, and/or condition at delivery.


A variety of intrauterine insults can impair the fetal transition to extrauterine life. For example, neonatal depression at birth can result from acute or chronic uteroplacental insufficiency or acute umbilical cord compression. Chronic uteroplacental insufficiency, regardless of its etiology, may result in fetal growth restriction. Fetal hemorrhage, viral or bacterial infection, meconium aspiration, and exposure to opioids or other CNS depressants also can result in neonatal depression. Although randomized trials have not confirmed that fetal heart rate (FHR) monitoring improves neonatal outcome, a nonreassuring FHR tracing is considered a predictor of the need for neonatal resuscitation.


Studies have evaluated the use of fetal pulse oximetry for the evaluation of fetal well-being during labor. This technique involves the transcervical insertion of a flexible fetal oxygen sensor until it rests against the fetal cheek. A randomized trial found that use of fetal pulse oximetry in conjunction with FHR monitoring led to a reduction in the number of cesarean deliveries performed for a nonreassuring FHR tracing. However, this decrease was offset by an increased number of cesarean deliveries performed for dystocia, raising the concern that the presence of the probe might predispose to dystocia. As a consequence, the ACOG has recommended further study before fetal pulse oximetry is used routinely in clinical practice. A meta-analysis of five trials concluded that there was some benefit to fetal pulse oximetry in the presence of a nonreassuring FHR tracing, but the use of fetal pulse oximetry did not lead to an overall reduction in the cesarean delivery rate.


Infants with congenital anomalies (e.g., tracheoesophageal fistula, diaphragmatic hernia, CNS and cardiac malformations) may need resuscitation and cardiorespiratory support. Improved ultrasonography allows for the antenatal diagnosis of many congenital anomalies and other fetal abnormalities (e.g., nonimmune hydrops). Obstetricians should communicate knowledge or suspicions regarding these entities to those who will provide care for the neonate in the delivery room to allow the resuscitation team to make specific resuscitation plans.


In the past, infants born by either elective or emergency cesarean delivery were considered more likely to require resuscitation than infants delivered vaginally. Evidence suggests that repeat cesarean deliveries and those performed for dystocia—in patients without FHR abnormalities—result in the delivery of infants at low risk for neonatal resuscitation, especially when the cesarean deliveries are performed with neuraxial anesthesia. Of interest, infants born by elective repeat cesarean delivery are at higher risk for subsequent respiratory problems (e.g., TTN) than infants born vaginally. In addition, infants born by cesarean delivery after a failed trial of labor are at a higher risk for neonatal sepsis than similar infants born vaginally. Emergency cesarean delivery is considered a risk factor for the need for neonatal resuscitation.




Neonatal Assessment


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, Virginia Apgar, an anesthesiologist, described a simple method for neonatal assessment that could be performed while care is 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.



TABLE 9.1

Apgar Scoring System




































Parameter SCORE
0 1 2
Heart rate (bpm) Absent < 100 > 100
Respiratory effort Absent Irregular, slow, shallow, or gasping respirations Robust, crying
Muscle tone Absent, limp Some flexion of extremities Active movement
Reflex irritability (nasal catheter, oropharyngeal suctioning) No response Grimace Active coughing and sneezing
Color Cyanotic Acrocyanotic (trunk pink, extremities blue) Pink

Modified from Tabata BK. Neonatal resuscitation. In: Rogers MC, ed. Current Practice in Anesthesiology , 2nd ed. St. Louis, MO: Mosby; 1990:368.


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 one-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 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 ACOG Task Force on Neonatal Encephalopathy and Cerebral Palsy published criteria for defining an intrapartum event sufficient to cause cerebral palsy. 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.”


In summary, the usefulness of the Apgar score is still being debated more than 50 years after its inception. 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 ACOG 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 gestation.


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 15 minutes of delivery, into a syringe containing the proper amount of heparin ; and (3) the samples are analyzed within 30 to 60 minutes. 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. 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 2.5th percentile. 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 ). A number of factors may also influence the umbilical arterial blood pH measurement. A fetus subjected to the stress of labor has 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.



TABLE 9.2

Studies Reporting Umbilical Cord Arterial Blood Gas Measurements a






























































































Study Sample Size pH Pco 2 (mm Hg) Bicarbonate (mmol/L) Base Deficit (mmol/L) P o 2 (mm Hg)
Huisjes and Aarnoudse (1979) 852 7.20 ± 0.09
(7.02–7.38)
Sykes et al. (1982) 899 7.20 ± 0.08
(7.04–7.36)
8.3 ± 4.0
(0.3–16.3)
Eskes et al. (1983) 4667 7.23 ± 0.07
(7.09–7.37)
Yeomans et al. (1985) 146 7.28 ± 0.05
(7.18–7.38)
49.2 ± 8.4
(32.4–66.0)
22.3 ± 2.5
(17.3–27.3)
Low (1988) 4500 7.26 ± 0.07
(7.12–7.40)
54.9 ± 9.9
(35.1–74.7)
15.1 ± 4.9
(5.3–24.9)
Ruth and Raivio (1988) 106 7.29 ± 0.07
(7.15–7.43)
4.7 ± 4.0
(−3.3–12.7)
Thorp et al. (1989) 1694 7.24 ± 0.07
(7.10–7.38)
56.3 ± 8.6
(39.1–73.5)
24.1 ± 2.2
(19.7–28.5)
3.6 ± 2.7
(−1.8–9.0)
17.9 ± 6.9
(4.1–31.7)
Ramin et al. (1989) 1292 7.28 ± 0.07
(7.14–7.42)
49.9 ± 14.2
(21.5–78.3)
23.1 ± 2.8
(17.5–28.7)
3.6 ± 2.8
(−2.0–9.4)
23.7 ± 10.0
(3.7–43.7)
Riley and Johnson (1993) 3522 7.27 ± 0.07
(7.13–7.41)
50.3 ± 11.1
(28.1–72.5)
22.0 ± 3.6
(14.8–29.2)
2.7 ± 2.8
(−2.9–8.3)
18.4 ± 8.2
(2.0–34.8)
Nagel et al. (1995) 1614 7.21 ± 0.09
(7.03–7.39)

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