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Umbilical cord blood acid-base analysis at delivery

Umbilical cord blood acid-base analysis at delivery
Literature review current through: Sep 2023.
This topic last updated: Aug 04, 2023.

INTRODUCTION — Fetal acid-base balance is assessed using the following techniques:

Antepartum, by percutaneous umbilical cord blood sampling.

Intrapartum, by fetal scalp blood sampling.

Immediately after birth, by umbilical cord blood sampling. This is by far the most common time to assess acid-base balance. The information can be useful from medical and medicolegal perspectives since it provides insight into intrapartum fetal physiology.

This topic will review basic concepts of fetal acid-base physiology and discuss the clinical use of umbilical cord acid-base analysis at delivery. Percutaneous umbilical cord blood sampling and intrapartum fetal scalp blood sampling are reviewed separately. (See "Fetal blood sampling" and "Intrapartum fetal heart rate monitoring: Overview", section on 'Fetal scalp blood sampling'.)

FETAL ACID-BASE PHYSIOLOGY

Acids and buffers — Normal fetal metabolism results in the production of acids that are buffered to maintain extracellular pH within a critical range. Both volatile acids (carbonic acid) and nonvolatile acids (noncarbonic or organic acids) are produced. The major buffers the fetus utilizes for neutralizing hydrogen ion production are plasma bicarbonate and hemoglobin.

Carbonic acid – The fetus produces carbonic acid (H2CO3) during oxidative metabolism (aerobic glycolysis). Since H2CO3 is formed primarily from carbon dioxide (CO2) via hydration in the presence of erythrocyte carbonic anhydrase, the formation of H2CO3 is equivalent to CO2 generation [1]. The rate of CO2 production, in turn, is equivalent to the rate of fetal oxygen consumption [2].

For the most part, the fetus can handle the amount of H2CO3 produced daily from aerobic metabolism since H2CO3 dissociates to water and CO2, and CO2 readily diffuses across the placenta, facilitated by lower maternal alveolar and arterial CO2 (PCO2 and PaCO2) during pregnancy secondary to increased minute ventilation. CO2 retention (hypercarbia) leads to respiratory acidemia (low pH with high PCO2 and normal bicarbonate concentration).

Organic acids – Fetal hypoxia can occur when maternal oxygenation is compromised (eg, respiratory disease), maternal perfusion of the placenta is reduced (eg, preeclampsia, chronic hypertension, hypotension/hypovolemia, cyanotic heart disease), or delivery of oxygenated blood from the placenta to the fetus is impeded (eg, placental abruption, cord compression). When fetal oxygenation is inadequate, complete oxidative metabolism of carbohydrates to CO2 and water is impaired and metabolism proceeds along an anaerobic pathway with production of organic acids, such as lactic acid and ketoacids. In contrast to carbonic acid, organic acids are not readily excreted or metabolized and are cleared very slowly across the placenta; therefore, they accumulate in the fetus. Mixed acidemia (low pH with low bicarbonate concentration and high PCO2) or metabolic acidemia (low pH with normal PCO2 and low bicarbonate concentration) develops when accumulation of organic acids depletes the buffer system to critically low levels of buffers.

Buffers – The fetus utilizes many different buffers to maintain pH in a very narrow range as very small changes in pH may significantly affect function of major fetal organ systems, such as the central nervous system and the cardiovascular system [1]. The two major buffers are bicarbonate and hemoglobin [3]. Inorganic phosphates, erythrocyte bicarbonate, and albumin play lesser roles.

The placenta also has a significant role in helping to maintain the bicarbonate pool and buffering the fetus against changes in maternal pH and blood gases. In a study using a perfused human placental model, acidification of the maternal side of the circulation did not significantly alter fetal acid-base status, likely due to an efflux of bicarbonate from placental tissue into the maternal circulation [4].

A base deficit (or negative base excess) exists when the fetal serum bicarbonate concentration is below normal. A base excess exists when the fetal bicarbonate concentration is above normal; however, alkalemia at birth is rare and always secondary to maternal abnormalities.

Differences from postnatal acid-base physiology — Fetal acid-base physiology is similar to that of the newborn, with some notable differences because fetal physiology is characterized by inability to compensate for acidemia by compensatory respiratory and renal responses in the same way and to the same degree as in the newborn. The lungs and kidneys play significant roles in maintaining acid-base balance in postnatal life, and respiratory and metabolic acidosis are the result of distinct clinical conditions. As an example, postnatally, pulmonary disorders such as asthma, interstitial lung disease, or hypoventilation can lead to respiratory acidemia [1]. Likewise, diabetic ketoacidosis, renal tubular acidosis, or diarrhea can lead to metabolic acidemia. By comparison, the fetus depends primarily upon the placenta to act as lungs (with respect to provision of oxygen and clearance of carbon dioxide) and, to a lesser degree, kidneys to help compensate for acidemia [1,5].

Uteroplacental hypoperfusion is the major cause of both fetal respiratory and metabolic acidemia, with progression from the former to the latter over time if decreased uteroplacental blood flow is not corrected (figure 1). Although the fetus can manifest a blood gas profile in a respiratory or metabolic pattern, acidosis most likely represents a continuum (mixed acidosis) rather than a distinct clinical entity. As an example, if uteroplacental perfusion is corrected during the respiratory phase, respiratory acidosis resolves as CO2 is rapidly cleared across the placenta. However, if the pathologic process is protracted, then in addition to impairment of CO2 excretion, organic acids are produced and cleared very slowly across the placenta so that metabolic acidosis develops [1,3,5].

INDICATIONS FOR FETAL ACID-BASE ANALYSIS — There is no consensus about when to perform umbilical cord blood acid-base analysis and no evidence that routinely measuring pH and blood gases at birth is cost-effective. Based on available evidence, it is reasonable for clinicians and obstetric units to establish their own sampling policies.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics recommend performing umbilical artery blood acid-base analysis after any delivery in which a fetal metabolic abnormality is suspected [6]. Some clinical scenarios where such testing is indicated include, but are not limited to, any delivery with one or more of the following:

Low Apgar score (0 to 3 at ≥5 minutes)

Category III fetal heart rate pattern (table 1)

Operative delivery (cesarean, vacuum, forceps) performed for nonreassuring fetal status

However, using selective rather than routine umbilical cord blood gas analysis can miss collecting appropriate blood samples from some high-risk deliveries and some newborns with birth asphyxia [7]. Acid-base assessment can be valuable in these cases because these neonates are at increased risk of an adverse outcome, but only a minority is acidotic at birth [1,5,6,8-10]. Cord blood analysis will show whether the newborn is acidotic at birth and can help distinguish between respiratory and metabolic acidosis. Severe cord blood acidemia (pH <7.00) is an essential criterion for the diagnosis of intrapartum asphyxia. Absence of metabolic acidemia provides evidence that an observed adverse outcome is likely related to factors other than prolonged intrapartum hypoxia [6,11].

Setting aside a segment of cord preemptively — A section of the umbilical cord can be clamped and set aside at delivery in cases of possible neonatal depression, such as meconium-stained amniotic fluid, fetal growth restriction, breech birth, multiple gestation, category II fetal heart rate pattern, preterm or low birth weight newborn, abruption, assisted vaginal delivery, shoulder dystocia, uterine rupture, maternal substance use, prolonged labor, or intrapartum maternal fever. Subsequent measurement of pH and gases is performed only if clinically indicated because of poor neonatal status in the delivery room. (See 'Technique' below.)

TECHNIQUE

Umbilical artery — Sampling umbilical artery blood is preferable to sampling umbilical vein blood as the arterial pH and base deficit provide the most accurate information on fetal acid-base status and correlate best with newborn morbidity [3,12,13]. This is because umbilical arterial blood primarily reflects fetal metabolism while venous blood primarily reflects placental function [14].

To obtain fetal blood for acid-base analysis from the in vivo placenta and cord:

A 10 to 20 cm segment of umbilical cord is doubly clamped as soon as possible after delivery [1,5,12,15], because delay in both clamping and sampling may affect pH and gas values due to gaseous diffusion and continuing metabolism [15-17]. However, it is possible to delay clamping but not sampling. (See 'Can cord blood analysis be performed after delayed cord clamping?' below.)

Blood is drawn from the umbilical artery into a 1 to 2 mL syringe (preferably glass), which has been flushed with heparin, and the syringe is immediately transported on ice to the laboratory. The two umbilical arteries are smaller than the umbilical vein; either of the arteries can be sampled.

Ideally, the test is performed as soon as possible after delivery; however, a sample may be obtained immediately but held on ice until a decision is made for or against these tests. Most studies have found that a cord blood sample prepared in this way is reasonably stable for assessment of both pH and base deficit for 60 minutes [18-21], similar to maternal arterial blood [22].

Alternatively, acid-base analysis of umbilical artery blood can be performed on a sample drawn from a clamped umbilical cord segment kept at room temperature for no more than 20 minutes [15]. If more than 20 minutes have elapsed, the values can be estimated by testing a blood sample obtained from a clamped umbilical cord up to 90 minutes after birth [23]. The estimate is based on studies reporting the rate of fall of pH over time (eg, cord pH falls 0.05 at 30 minutes, 0.087 at 60 minutes, and 0.112 at 90 minutes after birth).

If obtaining umbilical artery blood samples is difficult, the vessels on the fetal surface of the placenta can be utilized ("arteries cross over veins" (picture 1)) and will provide similar, but not necessarily equivalent, results [15,24,25].

Can cord blood analysis be performed after delayed cord clamping? — Delayed cord clamping is generally restricted to vigorous infants who are not candidates for acid-base analysis. Cord clamping should not be delayed when prompt newborn resuscitation is needed. (See "Labor and delivery: Management of the normal third stage after vaginal birth", section on 'Early versus delayed cord clamping'.)

When cord clamping is delayed, samples of umbilical arterial and venous blood can be obtained for gas analysis by drawing the samples from the pulsating, unclamped cord immediately after birth [26]. The procedure appears to be safe and has no effect on either the accuracy of the gas analysis or the volume of transfusion that the newborn receives.

If a blood specimen for acid-base testing is desired after delayed cord clamping has been completed, a delay of up to two minutes appears to have no or only a small effect on the results [27].

Can umbilical venous blood be used? — The normal umbilical vein pH is higher than umbilical artery pH (7.25 to 7.45 versus 7.18-7.38 [28]). A sample from the umbilical vein should be sent if an umbilical artery sample cannot be obtained. In one study, over 50 percent of newborns with cord venous pH ≥7.07 had cord arterial pH >7.0 and over 90 percent with cord venous pH ≥7.14 had cord arterial pH >7.0 [29]. Base deficit values are typically 1 mmol/L lower in the umbilical vein than the umbilical artery, unless placental blood flow is obstructed.

Sampling both the umbilical artery and vein — Some clinicians prefer to obtain two samples, one from the artery and the other from the vein, although the cost-effectiveness for this practice has not been established [6,30]. If both vessels are sampled, the median arteriovenous pH difference is 0.09 (range 0.02 to 0.49).

One advantage to sampling both the vein and artery is that it will be clear which set of values reflect the vein versus the artery. If only one sample from one vessel is collected, it is not necessarily readily apparent from the values whether the sample reflects the artery or the vein.

In cases of sudden catastrophic events, such as acute abruption or cord occlusion, the arterial value best represents the neonate's blood gas at birth whereas the venous sample reflects the status just before the event. Therefore, in such cases, clinicians are encouraged to obtain both umbilical artery and venous blood gas samples to provide a better index of the fetal acid-base status before an often unpredictable event.

TEST RESULTS — The pH, PCO2, PO2, CO2, hemoglobin, and oxygen content of the blood are measured, whereas bicarbonate concentration, percentage oxygen saturation, and base excess (or deficit) are calculated. The most useful values for interpretation of fetal-newborn condition and prognosis are the pH and base excess (or deficit) [6,13,31].

Normal pH, blood gas, and buffer values — Fetal pH is normally 0.1 unit lower than maternal pH. The mean umbilical arterial blood pH, base deficit, and gas values for preterm infants (table 2) and term infants (table 3) are almost identical, with small differences in values among studies depending on the patient population [24,28,32-35].

Base deficit slowly increases during active labor and the second stage [36], although one review reported that the mean umbilical cord blood gas values obtained at cesarean birth for term pregnancies not in labor were similar to those described in the table for vaginal births: umbilical artery pH 7.27, umbilical artery PCO2 49 mmHg, and umbilical artery base excess -4 mEq/L, with slight variations from these values depending on type of anesthesia [37].

Acidosis — The risk of neonatal morbidity is inversely related to pH, with the highest risks at the lowest pHs [13,38]. A practical pH threshold for defining pathologic fetal acidemia that is used by the author of this topic and others is umbilical artery pH <7.00 [6,39-45], which occurs in 3.7 per 1000 nonanomalous term births [46]. Umbilical artery pH >7.00 and <7.20 [6] or <7.10 [47-50] has been proposed as the threshold for identifying fetuses with abnormal fetal heart rate tracings who might benefit from intervention prior to the development of pathologic fetal acidosis and fetal injury [6].

Support for a pH <7.00 threshold is derived from several lines of evidence:

In a 2010 meta-analysis of 51 cohort and case-control studies including over 480,000 newborns, subgroup analysis indicated that the strongest association between neonatal morbidity and pH was at a pH threshold of 7.0 (odds ratio [OR] 12.5, 95% CI 6.1-25.6); for neonatal mortality the strongest association was at pH 7.1 (OR 7.1, 95% CI 3.3-15.3) [13].

In a 2008 systematic review of studies of nonanomalous term births with pH less <7.0, the overall incidence of neonatal neurologic morbidity or mortality was increased at this threshold (23.1 percent): Survival with neonatal neurologic morbidity occurred in 51 of 297 newborns (17.2 percent), seizures occurred in 45 of 276 newborns (16.3 percent), and neonatal death occurred in 24 of 407 newborns (5.9 percent) [46].

In a cohort study of over 8700 singleton nonanomalous newborns at term (520 with umbilical artery pH <7.1 and 84 with umbilical artery pH <7.0), umbilical artery pH was a strong predictor of all adverse outcomes [51]. Encephalopathy or death occurred in 2.3 percent of all acidemic newborns and 8.5 percent of newborns with severe acidemia. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy" and "Etiology and pathogenesis of neonatal encephalopathy".)

The majority of newborns with umbilical artery pH <7.0 will not be at increased risk for neurologic or behavioral problems when followed to school age [38,50,52-54]. In a study of 93 neonates with umbilical artery pH <7.0, 97.8 percent had no hypoxic-ischemic encephalopathy, 94.6 percent had no seizures, 89.2 percent did not need cardiopulmonary resuscitation, and 60.2 percent did not require intubation [38]. In a study of 248 neonates born after 34 weeks of gestation with umbilical artery pH <7.0 or base deficit ≥12 mmol/L at birth, 222 (89.5 percent) survived intact [55]. Of the remaining 26 newborns, 8 died and 18 were diagnosed with cerebral palsy and/or developmental delay. The risk of adverse outcome was 4.3 percent when the arterial pH was between 6.9 and <7.0 but 30 percent when <6.9.

Although the umbilical artery pH can be used alone to classify the presence or absence of acidosis, the base deficit is helpful in distinguishing whether umbilical artery acidemia is respiratory or metabolic (see 'Base deficit (negative base excess)' below). Umbilical artery acidosis with a metabolic component, especially if persistent after birth, is a strong predictor of an increased risk of neonatal morbidity or mortality, whereas respiratory acidosis is not usually associated with complications in the newborn [6,38,56,57]. Nevertheless, most newborns with metabolic acidosis still have a good prognosis. In a study of 1265 neonates with metabolic acidosis (umbilical artery pH <7.0 and base deficit ≥12 mmol/L), 98 percent had no intracranial hemorrhage, 94 percent had no seizures within 24 hours of birth, and 86 percent had no respiratory distress [58]. (See 'Limitations' below.)

Newborns with metabolic acidosis who exhibit features of encephalopathy may be candidates for therapeutic hypothermia, an intervention that is customarily provided in a neonatal intensive care unit. Clinical features, diagnosis, and treatment of neonatal encephalopathy are described in detail separately. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy", section on 'Therapeutic hypothermia'.)

Base deficit (negative base excess) — The decreased concentration of buffers (primarily bicarbonate) associated with metabolic acidosis is reported as the base deficit or negative base excess. As discussed above, consideration of the base deficit is useful for interpretation of umbilical artery pH because an increase in base deficit distinguishes acidosis with a metabolic component (low pH, low bicarbonate concentration) from respiratory acidosis (low pH, normal bicarbonate concentration).

The base deficit has a linear relationship with lactic acid accumulation and correlates with the risk of neonatal neurologic morbidity [6]. An umbilical artery base deficit ≥12 mmol/L, which is >2 standard deviations above the mean [34], is commonly accepted as a reasonable threshold for predicting an increased risk of moderate or severe newborn complications [6,36,59-61]. A base deficit of 12 to 16 mmol/L is associated with an increase in newborn mortality, moderate to severe neonatal encephalopathy, multiorgan failure, and long-term neurologic dysfunction [13,59,62,63]. In one study, moderate or severe complications occurred in 10 percent of newborns with umbilical artery base deficit 12 to 16 mmol/L and in 40 percent of those >16 mmol/L [59].

Whether base deficit in acidemic newborn at term is an independent marker for neonatal morbidity and mortality has been questioned. In one study, for example, base deficit did not provide any additional prognostic information over pH alone, suggesting that the poor neonatal outcomes associated with a greater base deficit may just mirror the lower pH [51]. A limitation of this study was the lack of a cohort of nonacidemic newborns with an elevated base deficit.

It has been estimated that fetal stress characterized by repetitive moderate or severe variable decelerations may increase the base deficit by 1 mmol/L per 30 minutes; repetitive late or severe atypical variable decelerations (subacute fetal compromise) may increase the base deficit by 1 mmol/L per 6 to 15 minutes; and terminal bradycardia (eg, from ruptured uterus, major abruption, or complete cord occlusion) may increase the base deficit by as much as 1 mmol/L per two to three minutes [36]. By comparison, an uncomplicated labor results in a 3 mmol/L change in base deficit over many hours (the average umbilical artery base deficit at vaginal birth is 5 mmol/L). However, many factors affect the fetal response to hypoxia; these include an acute versus chronic process, presence of hypotension/hypoperfusion, preterm versus term fetus, and presence of anemia or functional cardiovascular anomalies.

It is important to note that base deficit is calculated from pH and PCO2 using an algorithm and that blood gas analyzers do not use a universal standard algorithm for this calculation. Studies have shown that the base deficit value reported by a laboratory is impacted by the fetal fluid compartment sampled (blood, extracellular fluid), choice of algorithm, and brand of blood gas analyzer [60,64].

Laboratories will often report base excess using an equation in which the result is contingent on the bicarbonate concentration, which may be directly measured as total dissolved carbon dioxide rather than calculated from the measured pH and PaCO2 using the Henderson-Hasselbalch equation. By comparison, the Henderson-Hasselbalch equation to calculate base excess uses only PaCO2 and pH and is not contingent upon the bicarbonate concentration. This difference can be important in clinical interpretation. As an example, a laboratory reported the following umbilical artery results for a mildly depressed newborn: pH 6.90, PaCO2 >109 mmHg, bicarbonate 20.3 mEq/L, base excess -16.1. Using the Henderson-Hasselbalch equation, the base excess is -10.4, which is more consistent with what appears to be primarily a respiratory acidosis.

Lactate levels — The umbilical artery lactate concentration has also been used as a marker of fetal metabolic acidosis. Lactate can be measured using a handheld meter at the point-of-care or by a blood gas machine in the laboratory. The mean umbilical artery lactate level after a normal birth has been reported to range from 2.55 to 4.63 mmol/L, but data are limited [65,66]. Differences in calibration of blood gas meters may explain the variation in mean lactate values.

Routine assessment of umbilical artery lactate levels is not recommended given the poor predictive value of newborn outcome. The threshold lactate concentration predictive of adverse short-term neonatal outcome is controversial and depends on the specimen (hemolyzed or whole blood) and the lactate meter used. The significant variability introduced by measurement and assay parameters limits the clinical utility of lactate measures in cord samples. An appropriate threshold is difficult to identify because of the low frequency of neonatal encephalopathy. In one of the largest series (28 validated cases >23 weeks), umbilical artery lactate 5.70 mmol/L had sensitivity and specificity of 69 and 88 percent for the outcome of moderate or severe neonatal encephalopathy [67]. Using a broad composite endpoint (neonatal intubation, mechanical ventilation, meconium aspiration syndrome, encephalopathy, hypothermic therapy, or death), a prospective study including 56 term neonates with this composite endpoint concluded the optimal umbilical artery threshold for predicting serious neonatal morbidity was 3.90 mmol/L, with sensitivity and specificity of 84 and 74 percent, respectively [65]. At this threshold, umbilical artery lactate level performed better than pH 7.25 for predicting the composite outcome. In both studies, however, lactate levels were poor predictors of neonatal encephalopathy. A systematic review that evaluated the diagnostic test accuracy of umbilical artery lactate reported sensitivity and specificity for prediction of poor neurological outcome was 70 and 93 percent, respectively, but the analysis was limited by the broad differences in study methodologies (eg, variation in thresholds for defining acidosis, variation in definitions of neonatal outcome) [68].

Umbilical venous lactate levels have also been evaluated as a marker for fetal metabolic acidosis as umbilical venous blood is more readily available than umbilical artery blood. In a prospective study of almost 8000 consecutive singleton births at term with no anomalies, the umbilical venous lactate concentration was predictive of umbilical artery lactic acidemia defined as >3.9 mmol/L [69]. An umbilical venous lactate level of 3.4 mmol/L was the optimal value in predicting both arterial lactic acidemia and a composite neonatal outcome defined as neonatal demise and any neonatal morbidities including intubation, mechanical ventilation, meconium aspiration syndrome, neonatal encephalopathy, and therapeutic hypothermia. Although predictive of arterial lactic acidemia, umbilical venous lactate is no better for predicting neonatal morbidity.

Hypoxemia — Measurement of umbilical artery PO2 appears to have no clinical utility as a low PO2 is not an independent risk factor for neonatal morbidity or mortality [38]. The hypoxic or ischemic threshold at which neuronal necrosis increases in the developing human brain is unclear [6].

LIMITATIONS — Fetal blood gas analysis has some limitations that should be considered when interpreting results.

The cord blood pH value alone does not distinguish between a primary fetal or placental disorder and the contribution of a maternal acid-base disorder. Rarely, alterations in maternal acid-base balance, such as renal tubular acidosis or diabetic ketoacidosis, result in fetal acidosis. Since fetal pH is normally 0.1 unit lower than that of the mother, maternal pH should be determined if fetal acidosis is suspected to be a result of maternal acidosis. The primary pathologic process can usually be determined by consideration of the maternal health status and maternal metabolic state together with the umbilical cord acid-base results.

Fetal pH and blood gases do not necessarily reflect asphyxial events that occurred remote from delivery or localized ischemia and infarction.

Comorbidities (eg, fetal growth restriction, anemia) and duration of the insult are important biological modifiers of neurological and other end-organ risk.

pH, base deficit, and lactate levels are only metabolic surrogate markers for key clinical outcomes, including neonatal morbidity, neonatal mortality, and long-term neurodevelopment.

SUMMARY AND RECOMMENDATIONS

Overview – When adequate fetal oxygenation does not occur, complete oxidative metabolism of carbohydrates to carbon dioxide (CO2) and water is impaired and metabolism proceeds along an anaerobic pathway with production of organic acids, such as lactic acid and ketoacids. In contrast to carbonic acid, organic acids are not readily excreted or metabolized and are cleared very slowly across the placenta; therefore, they accumulate in the fetus. Mixed acidemia (low pH with low bicarbonate concentration and high PCO2) or metabolic acidemia (low pH with normal PCO2 and low bicarbonate concentration) develops when accumulation of organic acids depletes the buffer system to critically low levels of buffers. (See 'Fetal acid-base physiology' above.)

Indications – Umbilical artery blood acid-base analysis should be performed after any delivery in which a fetal metabolic abnormality is suspected, such as any delivery with low Apgar scores (0 to 3 at ≥5 minutes), a category III fetal heart rate pattern, or an operative delivery (cesarean, vacuum, forceps) performed for nonreassuring fetal status. These neonates are at increased risk of an adverse outcome, but only a minority are acidotic at delivery. (See 'Indications for fetal acid-base analysis' above.)

A section of the umbilical cord can be clamped and set aside at delivery in cases of possible neonatal depression, such as meconium-stained amniotic fluid, fetal growth restriction, breech birth, multiple gestation, category II fetal heart rate pattern, preterm or low birth weight newborn, abruption, assisted vaginal delivery, shoulder dystocia, uterine rupture, maternal substance use, prolonged labor, or intrapartum maternal fever. Measurement of pH and gases is subsequently performed only if clinically indicated because of poor neonatal status in the delivery room. (See 'Indications for fetal acid-base analysis' above.)

Performance – If acid-base analysis is planned, the cord should be doubly clamped as soon as possible after birth. The blood specimen is collected in a syringe flushed with heparin and obtained from the umbilical artery of the doubly-clamped segment of umbilical cord. A cord blood sample prepared in this way is reasonably stable for assessment of both pH and base deficit for 60 minutes. (See 'Technique' above.)

Cases with delayed cord clamping – If cord clamping is delayed, samples of umbilical arterial and venous blood can be obtained for gas analysis by drawing the samples from the pulsating, unclamped cord immediately after birth. The procedure appears to be safe and has no effect on either the accuracy of the gas analysis or the volume of transfusion that the infant receives. (See 'Can cord blood analysis be performed after delayed cord clamping?' above.)

Normal values – Fetal pH is normally 0.1 units lower than maternal pH. The mean normal umbilical arterial blood pH and gas values for preterm neonates (table 2) and term neonates (table 3) are almost identical. (See 'Normal pH, blood gas, and buffer values' above.)

Pathologic fetal acidemia – The most useful values for interpretation of fetal-newborn condition and prognosis are the pH and base excess (or deficit). A pH <7.00 is a practical threshold for defining pathologic fetal acidemia. Although respiratory acidosis is not usually associated with complications in the newborn, a base deficit greater ≥12 mmol/L suggests metabolic acidosis and is associated with an increased risk of moderate or severe newborn complications. (See 'Acidosis' above and 'Base deficit (negative base excess)' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Susan M Ramin, MD, and Edward R Yeomans, MD, who contributed to earlier versions of this topic review.

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Topic 5400 Version 46.0

References

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