This scoring system is a useful clinical tool to identify those neonates who require resuscitation as well as to assess the effectiveness of any resuscitative measures (Apgar, 1953). As shown in Table 28-2, each of the five easily identifiable characteristics—heart rate, respiratory effort, muscle tone, reflex irritability, and color—is assessed and assigned a value of 0 to 2. The total score, based on the sum of the five components, is determined 1 and 5 minutes after delivery.
Table 28-2. Apgar Scoring System |Favorite Table|Download (.pdf)
Table 28-2. Apgar Scoring System
Some flexion of extremities
Body pink, extremities blue
The 1-minute Apgar score reflects the need for immediate resuscitation. The 5-minute score, and particularly the change in score between 1 and 5 minutes, is a useful index of the effectiveness of resuscitative efforts. The 5-minute Apgar score also has prognostic significance for neonatal survival, because survival is related closely to the condition of the neonate in the delivery room (Apgar and associates, 1958). In an analysis of more than 150,000 infants delivered at Parkland Hospital, Casey and associates (2001b) assessed the contemporaneous significance of the 5-minute score for predicting survival during the first 28 days of life. They found that in term neonates, the risk of neonatal death was approximately 1 in 5000 for those with Apgar scores of 7 to 10. This risk compares with a mortality rate of 1 in 4 for term infants with scores of 3 or less. Low 5-minute scores were comparably predictive of neonatal death in preterm infants. These investigators concluded that the Apgar scoring system is as relevant for the prediction of neonatal survival today as it was almost 50 years ago.
There have been attempts to use Apgar scores to define asphyxial injury and to predict subsequent neurological outcome—uses for which the Apgar score was never intended. Such associations are difficult to measure with reliability given that both asphyxial injury and low Apgar scores are infrequent outcomes. For example, according to United States birth certificate records for 2006, only 1.6 percent of newborns had a 5-minute score below 7 (Martin and co-workers, 2009). Similarly, in a population-based study of more than 1 million term infants born in Sweden between 1988 and 1997, the incidence of 5-minute Apgar scores of 3 or less was approximately 2 per 1000 (Thorngren-Jerneck and Herbst, 2001).
Despite the methodological challenges, erroneous definitions of asphyxia by many groups were established solely based upon low Apgar scores. These prompted the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics to issue a joint statement in 1986 concerning “Use and Abuse of the Apgar Score.” The statement was updated in 1996 and has been reaffirmed several times, the most recent in 2006. Important caveats regarding Apgar score interpretation addressed in this statement include the following:
Because certain elements of the Apgar score are partially dependent on the physiological maturity of the newborn, a healthy preterm infant may receive a low score only because of immaturity (Amon and associates, 1987; Catlin and co-workers, 1986).
Given that Apgar scores may be influenced by a variety of factors including, but not limited to, fetal malformations, maternal medications, and infection, to equate the presence of a low Apgar score solely with asphyxia or hypoxia represents a misuse of the score.
Correlation of the Apgar score with adverse future neurological outcome increases when the score remains 3 or less at 10, 15, and 20 minutes, but still does not indicate the cause of future disability (Freeman and Nelson, 1988; Nelson and Ellenberg, 1981).
The Apgar score alone cannot establish hypoxia as the cause of cerebral palsy (Chap. 29, Apgar Scores). A neonate who has had an asphyxial insult proximate to delivery that is severe enough to result in acute neurological injury should demonstrate all of the following: (1) profound acidemia with cord artery blood pH < 7 and acid-base deficit ≥ 12mmol/L; (2) Apgar score of 0–3 persisting for 10 minutes or longer; (3) neurological manifestations such as seizures, coma, or hypotonia; and (4) multisystem organ dysfunction—cardiovascular, gastrointestinal, hematological, pulmonary, or renal.
Umbilical Cord Blood Acid–Base Studies
Blood taken from umbilical vessels may be used for acid-base studies to assess the metabolic status of the neonate. Blood collection is performed following delivery by immediately isolating a 10- to 20-cm segment of cord with two clamps near the neonate and two clamps nearer the placenta. The importance of clamping the cord is underscored by the fact that delays of 20 to 30 seconds can alter both the Pco2 and pH (Lievaart and deJong, 1984). The cord is then cut between the two proximal and two distal clamps.
Arterial blood is drawn from the isolated segment of cord into a 1- to 2-ml commercially prepared plastic syringe containing lyophilized heparin or a similar syringe that has been flushed with a heparin solution containing 1000 U/mL. The needle is capped and the syringe transported, on ice, to the laboratory. Although efforts should be made for prompt transport, neither the pH nor Pco2 change significantly in blood kept at room temperature for up to 60 minutes (Duerbeck and associates, 1992). In fact, Chauhan and colleagues (1994) developed mathematical models allowing reasonable prediction of birth acid–base status in properly collected cord blood samples analyzed as late as 60 hours after delivery.
Fetal Acid-Base Physiology
The fetus produces both carbonic and organic acids. Carbonic acid (H2CO3) is formed by oxidative metabolism of CO2. The fetus usually rapidly clears CO2 through the placental circulation, which limits the buildup of carbonic acid. When H2CO3 accumulates in fetal blood and there is no concurrent increase in organic acids—as occurs in impaired placental exchange—the result is termed respiratory acidemia.
Organic acids primarily include lactic and β-hydroxybutyric acids. Increased levels of these acids follow persistent placental exchange impairment and result from anaerobic glycolysis. These organic acids are cleared slowly from fetal blood, and when they accumulate without a concurrent increase in H2CO3, the result is termed metabolic acidemia. With the development of metabolic acidemia, bicarbonate (HCO3−) decreases because it is used to buffer the organic acid. An increase in H2CO3 accompanied by an increase in organic acid reflected by decreased HCO3− causes mixed respiratory-metabolic acidemia.
In the fetus, respiratory and metabolic acidemia, and ultimately tissue acidosis, are most likely part of a progressively worsening continuum. This is different from the adult pathophysiology, in which distinct conditions result in either respiratory (pulmonary disease) or metabolic (diabetes) acidemia. In the fetus, the placenta serves as both the lungs and to a certain degree, the kidneys. One principal cause of developing fetal acidemia is a decrease in uteroplacental perfusion. This results in the retention of CO2 (respiratory acidemia), and if protracted and severe enough, a mixed or metabolic acidemia.
Assuming that maternal pH and blood gases are normal, the actual pH of fetal blood is dependent on the proportion of carbonic and organic acids as well as the amount of bicarbonate, which is the major buffer in blood. This can best be illustrated by the Henderson–Hasselbalch equation:
For clinical purposes, HCO3− represents the metabolic component and is reported in mEq/L. The H2CO3 concentration represents the respiratory component and is reported as the Pco2 in mm Hg. Thus:
The result of this equation is a pH value. However, pH is a logarithmic term and does not give a linear measure of acid accumulation. For example, a change in hydrogen ion concentration associated with a fall in pH from 7.0 to 6.9 is almost twice that which is associated with a fall in pH from 7.3 to 7.2. For this reason, the delta base offers a more linear measure of the degree of accumulation of metabolic acid (Armstrong and Stenson, 2007). The change in base, or delta base, is a calculated number used as a measure of the change in buffering capacity of bicarbonate (HCO3−). For example, HCO3− concentration will be decreased with a metabolic acidemia as it is consumed to maintain a normal pH. A base deficit occurs when HCO3− concentration decreases to below normal levels, and a base excess occurs when HCO3− values are above normal. Importantly, a mixed respiratory–metabolic acidemia with a large base deficit and a low HCO3−—less than 12 mmol/L—is more often associated with a depressed neonate than is a mixed acidemia with a minimal base deficit and a more nearly normal HCO3−. A nomogram for calculating the delta base has been published by Siggaard-Anderson (1963).
Clinical Significance of Acidemia
Fetal oxygenation and pH generally decline during the course of normal labor (Dildy and co-workers, 1994). Normal umbilical cord blood pH and blood gas values at delivery in term newborns are summarized in Table 28-3. Similar values have been measured in preterm infants (Dickinson and co-workers, 1992; Ramin and associates, 1989; Riley and Johnson, 1993). Using data from more than 19,000 deliveries, the lower limits of normal pH in the newborn have been found to range from 7.04 to 7.10 (Boylan and Parisi, 1994). Thus, these values should be considered to define neonatal acidemia. Most fetuses will tolerate intrapartum acidemia with a pH as low as 7.00 without incurring neurological impairment (Freeman and Nelson, 1988; Gilstrap and associates, 1989). Supportive of this threshold, Goldaber and associates (1991) found that there were significantly more neonatal deaths and infants with neurological dysfunction below a pH of 7.00 (Table 28-4).
Table 28-3. Umbilical Cord Blood pH and Blood Gas Values in Normal Term Newborns |Favorite Table|Download (.pdf)
Table 28-3. Umbilical Cord Blood pH and Blood Gas Values in Normal Term Newborns
Ramin et al, 1989a (n = 1292)c
Riley and Johnson, 1993b (n = 3522)c
Arikan et al, 2000a (n = 1281)d
Pco2 (mm Hg)
Base excess (mEq/L)
Pco2 (mm Hg)
Base excess (mEq/L)
Table 28-4. Umbilical Arterial Blood pH Related to Neonatal Morbidity, Mortality, and Apgar Scores in Term Infants |Favorite Table|Download (.pdf)
Table 28-4. Umbilical Arterial Blood pH Related to Neonatal Morbidity, Mortality, and Apgar Scores in Term Infants
Umbilical Artery pH
<7.00 (n = 87) No. (%)
7.00–7.04 (n = 95) No. (%)
7.05–7.09 (n = 290) No. (%)
7.10–7.14 (n = 798) No. (%)
Intensive care nursery
Apgar scores ≤ 3
Another important prognostic consideration is the direction of pH change from birth to the immediate neonatal period. Casey and co-workers (2001a) found that the risk of seizures during the first 24 hours of life was reduced fivefold if an umbilical artery cord pH below 7.2 normalized within 2 hours after delivery.
In the fetus, metabolic acidemia develops when oxygen deprivation is of sufficient duration and magnitude to require anaerobic metabolism for fetal cellular energy needs. Low and associates (1997) defined fetal acidosis as a base deficit of greater than 12 mmol/L and severe fetal acidosis as a base deficit greater than 16 mmol/L. In the study of more than 150,000 newborns cited earlier, Casey and associates (2001b) defined metabolic acidemia using umbilical cord blood gas cutoffs that were 2 standard deviations below the mean, that is, an umbilical artery blood pH less than 7.00 accompanied by a Pco2 of no more than 76.3 mm Hg (higher values indicate a respiratory component), HCO3− concentration of no more than 17.7 mmol/L, and base deficit of at least 10.3 mEq/L. From the standpoint of possible cerebral palsy causation, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2003), in their widely endorsed monograph, defined metabolic acidosis as umbilical arterial pH <7.0 and a base deficit of at least 12 mmol/L.
Metabolic acidemia is associated with a high rate of multiorgan dysfunction. In rare cases, such hypoxia-induced metabolic acidemia may be so severe as to cause subsequent neurological impairment. In fact, a fetus without such acidemia cannot by definition have suffered recent hypoxic-induced injury. Even severe metabolic acidosis, however, is poorly predictive of subsequent neurological impairment in the term neonate. Although metabolic acidosis was associated with an increase in immediate neonatal complications in a group of infants with depressed 5-minute Apgar scores, Socol and colleagues (1994) found no difference in umbilical artery blood gas measurements among infants who subsequently developed cerebral palsy and those with normal long-term neurological outcome. In very-low-birthweight infants—those less than 1000 g—newborn acid-base status may be more closely linked to long-term neurological outcome (Gaudier and co-workers, 1994; Low and associates, 1995). In the study cited above, Casey and associates (2001b) measured the association between metabolic acidemia, low Apgar scores, and neonatal death in term and preterm infants. As shown in Figure 28-5, relative to newborns with a 5-minute Apgar score of at least 7, the risk of neonatal death was more than 3200-fold greater in term infants with metabolic acidemia and 5-minute scores of 3 or less.
Relative risk for neonatal death in term infants with low Apgar score or umbilical artery acidemia—or both. Actual number of infants are cited above each bar.
Respiratory acidemia generally develops as a result of an acute interruption in placental gas exchange with subsequent CO2 retention. Transient umbilical cord compression is the most common antecedent factor. In general, respiratory acidemia is not harmful to the fetus. Low and co-workers (1994) found no increase in newborn complications after respiratory acidosis. The degree to which pH is affected by Pco2, the respiratory component of the acidosis, can be calculated. First, the upper normal neonatal Pco2 (49 mm Hg) is subtracted from the cord blood gas Pco2 value. Each 10 additional mm Hg Pco2 will lower the pH by 0.08 units (Eisenberg and colleagues, 1987). Thus, in a mixed respiratory–metabolic acidemia, the benign respiratory component can be calculated as in the following example: During labor, an acute cord prolapse occurred and the fetus was delivered by cesarean 20 minutes later. The umbilical artery blood gas pH was 6.95, with a Pco2 of 89 mm Hg. To calculate the degree to which the cord compression and subsequent impairment of CO2 exchange affected the pH, the relationship given earlier is applied: 89 mm Hg minus 49 mm Hg = 40 mm Hg (excess CO2). To correct pH: (40 ÷ 10) × 0.08 = 0.32; 6.95 + 0.32 = 7.27. Therefore, the pH prior to cord prolapse was approximately 7.27, well within normal limits. Thus, the entire pH resulted from respiratory acidosis.
Recommendations for Cord Blood Gas Determinations
A cost-effectiveness analysis for universal cord blood gas measurements has not been conducted. In some centers, cord gas analysis is performed in all neonates at birth. The American College of Obstetricians and Gynecologists (2006) recommends that cord blood gas and pH analyses be obtained in the following circumstances:
Cesarean delivery for fetal compromise
Low 5-minute Apgar score
Severe growth restriction
Abnormal fetal heart rate tracing
Maternal thyroid disease
Although umbilical cord acid-base blood determinations are poorly predictive of either immediate or long-term adverse neurological outcome, they provide the most objective evidence of the fetal metabolic status at birth.