Severe acidosis and subsequent neurologic status

doi:10.1016/0002-9378(90)91014-4

American Journal of Obstetrics and Gynecology

Volume 162, Issue 3, March 1990, Pages 802-806

https://doi.org/10.1016/0002-9378(90)91014-4 Get rights and content

Abstract

To examine the relationship between severe acidosis at birth and evidence of subsequent neurologic dysfunction, a 4-year review was performed encompassing 15,528 neonates. One hundred forty-two (0.91%) of these neonates had an umbilical cord arterial pH ≤7.05 with a base deficit ≥10 mEq/L. Neurologic assessments found 101 of 110 term neonates (91.8%) and 17 of 32 preterm neonates (53.1 %) with severe acidosis to be free of neurologic deficits at the time of hospital discharge. Follow-up developmental evaluation data were available for 7 of 9 term neonates and 8 of 15 preterm neonates with abnormal examinations. Although 5 term and 6 preterm infants demonstrated mild developmental delays or mild tone abnormalities in the first year of life, none exhibited a major motor or cognitive abnormality at 12 to 24 months of age. Consequently, acidosis in umbilical cord blood, even when severe, is a poor predictor of subsequent neurologic dysfunction.

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Cited by (116)

Umbilical cord pH, blood gases, and lactate at birth: normal values, interpretation, and clinical utility
2023, American Journal of Obstetrics and Gynecology
Normal birth is a eustress reaction, a beneficial hedonic stress with extremely high catecholamines that protects us from intrauterine hypoxia and assists in the rapid shift to extrauterine life. Occasionally the cellular O₂ requirement becomes critical and an O₂ deficit in blood (hypoxemia) may evolve to a tissue deficit (hypoxia) and finally a risk of organ damage (asphyxia). An increase in H⁺ concentration is reflected in a decrease in pH, which together with increased base deficit is a proxy for the level of fetal O₂ deficit. Base deficit (or its negative value, base excess) was introduced to reflect the metabolic component of a low pH and to distinguish from the respiratory cause of a low pH, which is a high CO₂ concentration. Base deficit is a theoretical estimate and not a measured parameter, calculated by the blood gas analyzer from values of pH, the partial pressure of CO₂, and hemoglobin. Different brands of analyzers use different calculation equations, and base deficit values can thus differ by multiples. This could influence the diagnosis of metabolic acidosis, which is commonly defined as a pH <7.00 combined with a base deficit ≥12.0 mmol/L in umbilical cord arterial blood. Base deficit can be calculated as base deficit in blood (or actual base deficit) or base deficit in extracellular fluid (or standard base deficit). The extracellular fluid compartment represents the blood volume diluted with the interstitial fluid. Base deficit in extracellular fluid is advocated for fetal blood because a high partial pressure of CO₂ (hypercapnia) is common in newborns without concomitant hypoxia, and hypercapnia has a strong influence on the pH value, then termed respiratory acidosis. An increase in partial pressure of CO₂ causes less increase in base deficit in extracellular fluid than in base deficit in blood, thus base deficit in extracellular fluid better represents the metabolic component of acidosis. The different types of base deficit for defining metabolic acidosis in cord blood have unfortunately not been noticed by many obstetrical experts and organizations. In addition to an increase in H⁺ concentration, the lactate production is accelerated during hypoxia and anaerobic metabolism. There is no global consensus on definitions of normal cord blood gases and lactate, and different cutoff values for abnormality are used. At a pH <7.20, 7% to 9% of newborns are deemed academic; at <7.10, 1% to 3%; and at <7.00, 0.26% to 1.3%. From numerous studies of different eras and sizes, it can firmly be concluded that in the cord artery, the statistically defined lower pH limit (mean -2 standard deviations) is 7.10. Given that the pH for optimal enzyme activity differs between different cell types and organs, it seems difficult to establish a general biologically critical pH limit. The blood gases and lactate in cord blood change with the progression of pregnancy toward a mixed metabolic and respiratory acidemia because of increased metabolism and CO₂ production in the growing fetus. Gestational age-adjusted normal reference values have accordingly been published for pH and lactate, and they associate with Apgar score slightly better than stationary cutoffs, but they are not widely used in clinical practice. On the basis of good-quality data, it is reasonable to set a cord artery lactate cutoff (mean +2 standard deviations) at 10 mmol/L at 39 to 40 weeks’ gestation. For base deficit, it is not possible to establish statistically defined reference values because base deficit is calculated with different equations, and there is no consensus on which to use. Arterial cord blood represents the fetus better than venous blood, and samples from both vessels are needed to validate the arterial origin. A venoarterial pH gradient of <0.02 is commonly used to differentiate arterial from venous samples. Reference values for pH in cord venous blood have been determined, but venous blood comes from the placenta after clearance of a surplus of arterial CO₂, and base deficit in venous blood then overestimates the metabolic component of fetal acidosis. The ambition to increase neonatal hemoglobin and iron depots by delaying cord clamping after birth results in falsely acidic blood gas and lactate values if the blood sampling is also delayed. Within seconds after birth, sour metabolites accumulated in peripheral tissues and organs will flood into the central circulation and further to the cord arteries when the newborn starts to breathe, move, and cry. This influence of “hidden acidosis” can be avoided by needle puncture of unclamped cord vessels and blood collection immediately after birth. Because of a continuing anaerobic glycolysis in the collected blood, it should be analyzed within 5 minutes to not result in a falsely high lactate value. If the syringe is placed in ice slurry, the time limit is 20 minutes. For pH, it is reasonable to wait no longer than 15 minutes if not in ice. Routine analyses of cord blood gases enable perinatal audits to gain the wisdom of hindsight, to maintain quality assurance at a maternity unit over years by following the rate of neonatal acidosis, to compare results between hospitals on regional or national bases, and to obtain an objective outcome measure in clinical research. Given that the intrapartum cardiotocogram is an uncertain proxy for fetal hypoxia, and there is no strong correlation between pathologic cardiotocograms and fetal acidosis, a cord artery pH may help rather than hurt a staff person subjected to a malpractice suit based on undesirable cardiotocogram patterns. Contrary to common beliefs and assumptions, up to 90% of cases of cerebral palsy do not originate from intrapartum events. Future research will elucidate whether cell injury markers with point-of-care analysis will become valuable in improving the dating of perinatal injuries and differentiating hypoxic from nonhypoxic injuries.
Threshold of metabolic acidosis associated with newborn cerebral palsy: medical legal implications
2019, American Journal of Obstetrics and Gynecology
Citation Excerpt :
Studies that have reported scoring systems for the prediction of neonatal morbidity after acute perinatal asphyxia have not demonstrated a predictive value of increasing umbilical artery BD but rather use only the threshold BD.57–60 In fact, several studies emphasize that the degree of fetal acidemia does not correlate with long-term neurodevelopmental sequela.61–63 A recent metaanalysis of the strength of the association between umbilical cord acidosis and both perinatal and long-term outcomes64 demonstrated that a low arterial cord pH (defined as <7.0–7.2) was associated with the development of cerebral palsy but failed to demonstrate any dose-response association of the degree of acidosis with the rate of occurrence or severity of cerebral palsy.
Obstetricians and gynecologists belong to 1 of the medical specialties with the highest rate of litigation claims. Among birth injury cases, those cases with cerebral palsy outcomes account for litigation settlements or judgments often in the millions of dollars. In cases of potential perinatal asphyxia, a threshold level of metabolic acidosis (base deficit ≥12 mmol/L) is necessary to attribute neonatal encephalopathy to an intrapartum hypoxic event. With increasing duration or severity of a hypoxic stress resulting in metabolic acidosis, newborn infant umbilical artery base deficit increases. It may be alleged that, as base deficit levels increase beyond 12 mmol/L, there is an increased likelihood and severity of cerebral palsy. As a corollary, it may be claimed that an earlier delivery (by minutes) would reduce the base deficit and prevent or reduce the severity of cerebral palsy. This issue is of relevance to obstetricians as defendants, because retrospective “expert” analysis of cases may suggest that optimal management decisions would have resulted in an earlier delivery. In addressing the association of metabolic acidosis and cerebral palsy, base deficit should be measured as the extracellular component (base deficit_{extracellular fluid}) rather than the commonly used base deficit_blood. Studies suggest that, beyond the base deficit threshold of 12 mmol/L, the incidence and severity of cerebral palsy does not significantly increase (until ≥20 mmol/L), although the risk of neonatal death rises markedly. Thus, among most infants with hypoxia-associated neonatal encephalopathy, the occurrence of cerebral palsy is unlikely to be impacted by delivery time variation of few minutes, and this argument should not serve as the basis for medical legal claims.
Intrauterine, Intrapartum Assessments in the Term Infant
2018, Volpe's Neurology of the Newborn
The assessment of fetal well-being is a critical tool in ensuring optimal neonatal outcomes from both pregnancy and labor. This is particularly relevant for the recognition of the infant that may be at risk of hypoxic-ischemic cerebral injury. The identification of an intrauterine disturbance in gas exchange between the human fetus and mother (i.e., asphyxia) or the likelihood that such a disturbance will occur during labor or delivery is critical to improving the neurological outcomes for all infants, particularly those at greatest risk such as the growth-restricted infant. Moreover, attempts at prevention of the brain injury caused by intrauterine asphyxia, antepartum and intrapartum, demand precise awareness of when such injury is imminent. Although the most definitive information concerning the detection of hypoxic-ischemic insult to the fetus still applies primarily to the intrapartum period, major advances in antepartum assessment have been made. Thus, this chapter reviews the major current means of antepartum assessment of the fetus and then the approach to intrapartum assessment. In addition, we briefly summarize novel fetal and placental imaging techniques using magnetic resonance imaging.
Pathophysiology of Birth Asphyxia
2016, Clinics in Perinatology
Citation Excerpt :
The majority of these infants (>60%) have an uneventful delivery, remain in the well nursery, and are discharged home without complication.36 Even when infants with severe fetal acidemia are admitted to intensive care (usually because of respiratory difficulties) about 80% to 90% exhibit a benign neurologic course and it is only a small percentage present with encephalopathy.37–39 In 1 study, 8 of 47 infants (12%) with severe fetal acidemia admitted to the intensive care unit developed HIE, including seizures.37
Cerebral palsy and perinatal asphyxia (II - Medicolegal implications and prevention)
2011, Gynecologie Obstetrique et Fertilite
La constante augmentation de la pression médicolégale en obstétrique constitue un problème préoccupant dans les pays développés, du fait des indemnisations croissantes des paralysies cérébrales, avec comme conséquence une flambée des primes d’assurance professionnelle conduisant de nombreux obstétriciens à abandonner la pratique des accouchements. Cinquante-quatre à 74 % des plaintes en responsabilité concernent des anomalies des tracés cardiotocographiques (CTG), mal interprétées ou suivies de réactions inadéquates ou trop tardives. Une revue critique des neuf critères retenus par le Collège des obstétriciens et gynécologues américains et par l’Académie américaine de pédiatrie pour caractériser l’encéphalopathie néonatale et la paralysie cérébrale, est effectuée à propos des quatre paramètres essentiels définissant l’asphyxie chez le nouveau-né à terme et des cinq critères mineurs évoquant une atteinte intrapartum. La nécessité d’un examen anatomopathologique du placenta est soulignée afin de pouvoir rattacher une paralysie cérébrale à une asphyxie fœtale, grâce à la confirmation d’événements « sentinelles » survenus avant ou pendant le travail ou bien grâce à la découverte de lésions thrombotiques affectant la circulation fœtale, d’aspects évoquant une insuffisance placentaire ou de réponses circulatoires d’adaptation à une hypoxie chronique dans les villosités. L’histologie placentaire doit aussi permettre d’exclure l’origine asphyxique d’une paralysie cérébrale en révélant des réactions inflammatoires aiguës de chorioamniotite avec dissémination au fœtus ou des aspects compatibles avec une maladie métabolique. L’imagerie cérébrale par résonance magnétique (IRM) nucléaire est fondamentale pour élucider le mécanisme et la chronologie des atteintes tissulaires hypoxiques, en localisant préférentiellement les lésions sur la substance blanche ou sur la substance grise du cerveau. Certaines asphyxies intrapartum peuvent être prévenues en effectuant une césarienne programmée pour un fœtus fragile, en évitant la survenue de certains événements « sentinelles » et surtout en répondant de façon appropriée aux anomalies CTG et en procédant avec compétence à la réanimation néonatale. Au cours de la réunion d’expertise contradictoire, il est indispensable de disposer d’un CTG lisible, d’un partogramme bien documenté, d’une analyse des gaz du sang au cordon ombilical, d’un examen anatomopathologique du placenta et d’une évaluation complète du nouveau-né incluant une IRM cérébrale. Le risque médicolégal peut être réduit par une formation continue en CTG, en respectant les recommandations nationales concernant le rythme cardiaque fœtal (RCF), en utilisant des méthodes complémentaires comme le pH ou les lactates au scalp, en réalisant de régulières revues de mortalité et morbidité (RMM) des dossiers litigieux et en instaurant la pratique périodique d’audits ou d’évaluations de la pratique professionnelle (EPP) à propos des acidoses néonatales sévères, des transferts en réanimation néonatale, des ventilations assistées et des délais observés entre la décision et la réalisation des accouchements opératoires. Compte tenu de la rapidité d’installation des lésions cérébrales fœtales en cas d’asphyxie aiguë, il reste de nombreux dossiers où aucune faute ne peut être retenue contre l’accoucheur. Inversement, un épisode hypoxique anténatal bien documenté au niveau cérébral n’exclut pas automatiquement une aggravation par une prise en charge défaillante pendant l’accouchement.
Obstetric litigation is a growing problem in developed countries and its escalating cost together with increasing medical insurance premiums is a major concern for maternity service providers, leading to obstetric practice cessation by many practitioners. Fifty-four to 74 % of claims are based on cardiotocographic (CTG) abnormalities and their interpretation followed by inappropriate or delayed reactions. A critical analysis is performed about the nine criteria identified by the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics in their task force on Neonatal Encephalopathy and Cerebral Palsy: four essential criteria defining neonatal asphyxia and five other suggesting an acute intrapartum event sufficient to cause cerebral palsy in term newborns. The importance of placental histologic examination is emphasized in order to confirm sudden catastrophic events occurring before or during labor or to detect occult thrombotic processes affecting the fetal circulation, patterns of decreased placenta reserve and adaptative responses to chronic hypoxia. It may also exclude intrapartum hypoxia by revealing some histologic patterns typical of acute chorioamnionitis and fetal inflammatory response or compatible with metabolic diseases. Magnetic resonance imaging (MRI) of the infant's damaged brain is very contributive to elucidate the mechanism and timing of asphyxia in conjunction with the clinical picture, by locating cerebral injuries predominantly in white or grey matter. Intrapartum asphyxia is sometimes preventable by delivering weak fetuses by cesarean sections before birth, by avoiding some “sentinel” events, and essentially by responding appropriately to CTG anomalies and performing an efficient neonatal resuscitation. During litigation procedures, it is necessary to have access to a readable CTG, a well-documented partogram, a complete analysis of umbilical cord gases, a placental pathology and an extensive clinical work-up of the newborn infant including cerebral MRI. Malpractice litigation in obstetric care can be reduced by permanent CTG education, respect of national CTG guidelines, use of adjuncts such as fetal blood sampling for pH or lactates, regular review of adverse events in Clinical Risk Management (CRM) groups and periodic audits about low arterial cord pH in newborns, admission to neonatal unit, the need for assisted ventilation and the decision-to-delivery interval for emergency operative deliveries. Considering the fast occurrence of fetal cerebral hypoxic injuries, and thus despite an adequate management, many intrapartum asphyxias will not be preventable. Conversely, well-documented hypoxic-ischemic brain insults during the antenatal period do not automatically exclude intrapartum suboptimal obstetric care.
A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathy
2008, American Journal of Obstetrics and Gynecology
Citation Excerpt :
Prior studies that have failed to show a correlation between umbilical arterial pH at birth and neonatal neurologic abnormalities failed to look specifically at those neonates with pH < 7.0.46-48 When 110 term infants with pH < 7.05 and base deficit > 10 mM were examined, it was found that 5 demonstrated mild developmental delays or mild tone abnormalities in the first year of life, but none exhibited a major motor or cognitive abnormality at 12-24 months of age.48 They concluded that even severe acidosis in umbilical cord blood is insufficient evidence of intrapartum hypoxia-ischemia profound enough to cause neurologic damage and that most mild neurologic deficits noted in an infant after severe acidosis can be expected to resolve in the first year of life, but they did not look specifically at neonates with pH < 7.0 or base deficit > 12 mM, the cutoffs that have been linked with an increased risk of neurologic complications.
The object of this review was to determine the incidence, morbidity, and mortality of an umbilical arterial pH < 7.0; the incidence of hypoxic-ischemic encephalopathy; and the proportion of cerebral palsy associated with intrapartum hypoxia-ischemia in nonanomalous term infants. A systematic review of the English language literature on the association between intrapartum hypoxia-ischemia and neonatal encephalopathy was conducted by using Pubmed and Embase. For nonanomalous term infants, the incidence of an umbilical arterial pH < 7.0 at birth is 3.7 of 1000, of which 51 of 297 (17.2%) survived with neonatal neurologic morbidity, 45 of 276 (16.3%) had seizures, and 24 of 407 (5.9%) died during the neonatal period. The incidence of neonatal neurologic morbidity and mortality for term infants born with cord pH < 7.0 was 23.1%. The incidence of hypoxic-ischemic encephalopathy is 2.5 of 1000 live births. The proportion of cerebral palsy associated with intrapartum hypoxia-ischemia is 14.5%. The vast majority of cases of cerebral palsy in nonanomalous term infants are not associated with intrapartum hypoxia-ischemia.

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Severe acidosis and subsequent neurologic status

Abstract

Lancet

Am J Obstet GynecolOt.

Early Human Dev

Ant.

Am J Obstet Gvnecot.

Asphyxia in the fetus and cerebral palsy

Apgar scores as predictors of chronic neurologic disability

Pediatrics

Perinatal brain damage: predictive value of metabolic acidosis and the Apgar score

Br Med J