le ph eucapnique néonatale à la naissance: à la recherche ... · le ph eucapnique néonatale à...

Le pH eucapnique néonatale

à la naissance: à la recherche d’un marqueur de l’acidose métabolique

Paul OUELLET, PhD RRT FCCM Claude RACINET, MD (Grenoble) François CHARLES, MD (Toulon) Thierry DABOVAL, MD (Ottawa)

Conflit d’intérêt

•  Propriété intellectuelle de l’application informatique

pH Eucapnique néonatale à la naissance

Neonatal Eucapnic pH at Birth

L'EQUILIBRE ACIDE-BASE

Pr Ph. BAELEUCL St Luc

Service d'Anesthésiologie

Révisé en octobre 1996

"LIFE is a struggle, not against sin, not against the

Money Power, not against malicious animal

magnetism, but against hydrogen ions."

H. L. Mencken

Présentation

•  L’asphyxie périnatale et la paralysie cérébrale •  L’acidose métabolique néonatale (AMN) •  Critères spécifiques et non spécifiques •  Critères de l’ACOG et l’APP pour l’AMN •  Seuils de l’acidose métabolique

•  Les déficits de base (DB) •  Les problèmes avec le pH et les DB •  Le pH eucapnique néonatal à la naissance •  Diagramme CHARLES-RACINET •  L’application informatique

•  1 à 2 cas sur 1 000 naissances vivantes

•  Toujours associée à une importante acidose métabolique néonatale

•  L’absence de l’acidose métabolique: - élimine la responsabilité d’une asphyxie fœtale - argument à décharge en cas de litige médico-légal

•  L’acidémie sévère est décrite par: - pH artériel de l’artère ombilicale ≤ 7,00 - survient dans une naissance sur 100 – 200

COMMUNICATION

Asphyxie périnatale et paralysie cérébrale :implications médico-légalesMOTS-CLÉS : ASPHYXIE NÉONATALE/COMPLICATIONS. HYPOXIE FŒTALE. ACIDOSE/EMBRYOLOGIE. CÉSARIENNE/EFFETS INDÉSIRABLES. PARALYSIE OBSTÉTRICALE. PARALYSIE/CONGÉNITAL. OBSTÉTRIQUE/LÉGISLATION ET JURISPRUDENCE. RESPONSABILITE LÉGALE.

Perinatal asphyxia and cerebral palsy :medicolegal implicationsKEY-WORDS (Index medicus) : ASPHYXIA NEONATORUM/COMPLICATIONS. FETAL HYPOXIA.ACIDOSIS/EMBRYOLOGY. CESAREAN SECTION/ADVERSE EFFECTS. PARALYSIS, OBSTETRIC.PARALYSIS/CONGENITAL. OBSTETRICS/LEGISLATION AND JURISPRUDENCE. LIABILITY, LEGAL

Claude RACINET *, Pascale HOFFMANN.

RÉSUMÉ

Au cours des trente dernières années, la pratique obstétricale s’est notablement modifiée(monitorage fœtal systématique perpartum, augmentation importante du taux de césa-rienne,) dans le but de prévenir l’asphyxie périnatale et tout particulièrement sa fractionperpartum. Mais l’amélioration des paramètres néo-natals ne s’est pas accompagnée d’uneévolution parallèle du taux de paralysie cérébrale qui est resté stable autour de 2 ‰ au coursdes trente dernières années. De fait, les causes de la paralysie cérébrale sont très majoritai-rement anténatales, ce qui explique l’échec de la technologie perpartum censée prévenir cerisque, de même que celui de la césarienne préventive. A partir de l’analyse exhaustive de lalittérature des trente dernières années, des critères ont été proposés pour pouvoir établir uneéventuelle relation causale entre une asphyxie aiguë perpartum et une paralysie cérébrale :des études en population ont démontré que cette relation était très minoritaire. Maisl’obstétrique est une discipline qui est tout particulièrement soumise à une inflation desprimes d’assurance pour faire face à une sinistralité néonatale, très souvent attribuée à unemauvaise gestion de l’accouchement, en particulier pour le cas de la paralysie cérébrale, à undéfaut ou une réalisation trop tardive d’une césarienne. L’expertise périnatale judiciaire estencore trop souvent basée sur des notions devenues obsolètes. Une réforme de l’expertises’impose mais sera probablement inefficiente tant qu’elle se contentera d’améliorer les

* Registre du Handicap de l’Enfant, 23 Boulevard Albert 1er de Belgique, 38000 Grenoble

Tirés à part : Professeur Claude RACINET, 189, Chemin de l’Enclos, 38320 Brié et Angonnes,email : [email protected] reçu le 27 avril 2010, accepté le 31 mai 2010

Bull. Acad. Natle Méd., 2010, 194, no 6, 891-901, séance du 1er juin 2010

891

COMMUNICATION




RÉSUMÉ





891

Bull. Acad. Natle Méd., 2010;194:6:891 – 901

•  Affecte 1 – 6 enfants par 1 000 naissances vivantes •  En dépit des avancés, constitue une cause majeure

de mortalité/morbidité à la naissance •  Conduit à la mort en bas âge •  L’hypothermie thérapeutique constitue le soin de

base pour l’encéphalopathie hypoxo-ischémqiue

Brain Temperature in Neonates with Hypoxic-Ischemic Encephalopathyduring Therapeutic Hypothermia

Tai-Wei Wu, MD1, Claire McLean, MD1, Philippe Friedlich, MD, MS Epi, MBA1, Jessica Wisnowski, PhD2, John Grimm, MD2,Ashok Panigrahy, MD2, Stefan Bluml, PhD2, and Istvan Seri, MD, PhD1

Objective To noninvasively determine brain temperature of neonates with hypoxic-ischemic encephalopathy(HIE) during and after therapeutic hypothermia.Study design Using a phantom, we derived a calibration curve to calculate brain temperature based on chemicalshift differences in magnetic resonance spectroscopy. We enrolled infants admitted for therapeutic hypothermiaand assigned them to a moderate HIE (M-HIE) or severe HIE (S-HIE) group based on Sarnat staging. Rectal(core) temperature and magnetic resonance spectroscopy data used to derive regional brain temperatures (basalganglia, thalamus, and cortical graymatter) were acquired concomitantly during and after therapeutic hypothermia.We compared brain and rectal temperature in the M-HIE and S-HIE groups during and after therapeutic hypother-mia using 2-tailed t-tests.Results Eighteen patients (14 with M-HIE and 4 with S-HIE) were enrolled. As expected, both brain and rectaltemperatures were lower during therapeutic hypothermia than after therapeutic hypothermia. Brain temperaturein patients with S-HIE was higher than in those with M-HIE both during (35.1 ! 1.3"C vs 33.7 ! 1.2"C; P < .01)and after therapeutic hypothermia (38.1 ! 1.5"C vs 36.8 ! 1.3"C; P < .01). The brain–rectal temperature gradientwas also greater in the S-HIE group both during and after therapeutic hypothermia.Conclusion For this analysis of a small number of patients, brain temperature and brain–rectal temperaturegradient were higher in neonates with S-HIE than in those with M-HIE during and after therapeutic hypothermia.Further studies are needed to determine whether further decreasing brain temperature in neonates with S-HIE issafe and effective in improving outcome. (J Pediatr 2014;165:1129-34).

See editorial, p 1081

Hypoxic-ischemic encephalopathy (HIE) affects 1-6 per 1000 live term births and continues to be a major cause ofnewborn morbidity and mortality despite advances in obstetric management.1,2 Adverse outcomes include death, ce-rebral palsy, intellectual disability, developmental delay, and intractable seizures. Indeed, more than 60% of infants

with severe HIE (S-HIE) die, and almost 100% of the survivors suffer from long-term neurologic disabilities.2-4

In animal models of HIE, small increases in brain temperature are associated with increased severity of brain injury, bothclinically and histopathologically,5,6 and prevention of hyperthermia or reducing brain temperature decreases neuronal celldamage.7,8 In humans, brain and/or body temperature elevation often accompanies brain injury, as seen in traumatic braininjury, adult stroke, and HIE.9-12 The magnitude of temperature elevation correlates with infarct size and severity and is arisk factor for poor clinical outcome.12-14 In adult patients with acute ischemic stroke, regional brain temperature measurementby magnetic resonance spectroscopy (MRS) thermometry has revealed that regional brain temperature is correlated with thesize and location of the lesion, as well as with clinical stroke severity as measured by the National Institutes of Health StrokeScale score.15

Therapeutic hypothermia has become the standard of care for neonates with HIE, because it reduces overall neurodevelop-mental disability and mortality.16-19 Owing to the invasive nature of direct brain temperature measurement, esophageal orrectal temperatures are used to guide therapeutic hypothermia; however, given that brain temperature frequently exceeds

systemic temperature in patients with

From the 1Division of Neonatal Medicine, Department ofPediatrics, Center for Fetal and Neonatal Medicine and2Department of Radiology, Children’s Hospital LosAngeles, Keck School of Medicine, University ofSouthern California, Los Angeles, CA

Supported by the Gerber Foundation, United States(507-3217). The authors declare no conflicts of interest.

0022-3476/$ - see front matter. Copyright ª 2014 Elsevier Inc.

All rights reserved.

http://dx.doi.org/10.1016/j.jpeds.2014.07.022

BG Basal ganglia

GM Gray matter

HIE Hypoxic-ischemic encephalopathy

M-HIE Moderate hypoxic-ischemic encephalopathy

MR Magnetic resonance

MRI Magnetic resonance imaging

MRS Magnetic resonance spectroscopy

NAA N-acetyl-asparate

S-HIE Severe hypoxic-ischemic encephalopathy

Thal Thalamus

1129

Brain Temperature in Neonates with Hypoxic-Ischemic Encephalopathyduring Therapeutic Hypothermia

Tai-Wei Wu, MD1, Claire McLean, MD1, Philippe Friedlich, MD, MS Epi, MBA1, Jessica Wisnowski, PhD2, John Grimm, MD2,Ashok Panigrahy, MD2, Stefan Bluml, PhD2, and Istvan Seri, MD, PhD1

Objective To noninvasively determine brain temperature of neonates with hypoxic-ischemic encephalopathy(HIE) during and after therapeutic hypothermia.Study design Using a phantom, we derived a calibration curve to calculate brain temperature based on chemicalshift differences in magnetic resonance spectroscopy. We enrolled infants admitted for therapeutic hypothermiaand assigned them to a moderate HIE (M-HIE) or severe HIE (S-HIE) group based on Sarnat staging. Rectal(core) temperature and magnetic resonance spectroscopy data used to derive regional brain temperatures (basalganglia, thalamus, and cortical graymatter) were acquired concomitantly during and after therapeutic hypothermia.We compared brain and rectal temperature in the M-HIE and S-HIE groups during and after therapeutic hypother-mia using 2-tailed t-tests.Results Eighteen patients (14 with M-HIE and 4 with S-HIE) were enrolled. As expected, both brain and rectaltemperatures were lower during therapeutic hypothermia than after therapeutic hypothermia. Brain temperaturein patients with S-HIE was higher than in those with M-HIE both during (35.1 ! 1.3"C vs 33.7 ! 1.2"C; P < .01)and after therapeutic hypothermia (38.1 ! 1.5"C vs 36.8 ! 1.3"C; P < .01). The brain–rectal temperature gradientwas also greater in the S-HIE group both during and after therapeutic hypothermia.Conclusion For this analysis of a small number of patients, brain temperature and brain–rectal temperaturegradient were higher in neonates with S-HIE than in those with M-HIE during and after therapeutic hypothermia.Further studies are needed to determine whether further decreasing brain temperature in neonates with S-HIE issafe and effective in improving outcome. (J Pediatr 2014;165:1129-34).

See editorial, p 1081

Hypoxic-ischemic encephalopathy (HIE) affects 1-6 per 1000 live term births and continues to be a major cause ofnewborn morbidity and mortality despite advances in obstetric management.1,2 Adverse outcomes include death, ce-rebral palsy, intellectual disability, developmental delay, and intractable seizures. Indeed, more than 60% of infants

with severe HIE (S-HIE) die, and almost 100% of the survivors suffer from long-term neurologic disabilities.2-4

In animal models of HIE, small increases in brain temperature are associated with increased severity of brain injury, bothclinically and histopathologically,5,6 and prevention of hyperthermia or reducing brain temperature decreases neuronal celldamage.7,8 In humans, brain and/or body temperature elevation often accompanies brain injury, as seen in traumatic braininjury, adult stroke, and HIE.9-12 The magnitude of temperature elevation correlates with infarct size and severity and is arisk factor for poor clinical outcome.12-14 In adult patients with acute ischemic stroke, regional brain temperature measurementby magnetic resonance spectroscopy (MRS) thermometry has revealed that regional brain temperature is correlated with thesize and location of the lesion, as well as with clinical stroke severity as measured by the National Institutes of Health StrokeScale score.15

Therapeutic hypothermia has become the standard of care for neonates with HIE, because it reduces overall neurodevelop-mental disability and mortality.16-19 Owing to the invasive nature of direct brain temperature measurement, esophageal orrectal temperatures are used to guide therapeutic hypothermia; however, given that brain temperature frequently exceeds

systemic temperature in patients with

From the 1Division of Neonatal Medicine, Department ofPediatrics, Center for Fetal and Neonatal Medicine and2Department of Radiology, Children’s Hospital LosAngeles, Keck School of Medicine, University ofSouthern California, Los Angeles, CA

Supported by the Gerber Foundation, United States(507-3217). The authors declare no conflicts of interest.

0022-3476/$ - see front matter. Copyright ª 2014 Elsevier Inc.

All rights reserved.

http://dx.doi.org/10.1016/j.jpeds.2014.07.022

BG Basal ganglia

GM Gray matter

HIE Hypoxic-ischemic encephalopathy

M-HIE Moderate hypoxic-ischemic encephalopathy

MR Magnetic resonance

MRI Magnetic resonance imaging

MRS Magnetic resonance spectroscopy

NAA N-acetyl-asparate

S-HIE Severe hypoxic-ischemic encephalopathy

Thal Thalamus

1129

Cerebral palsy: causes, pathways, and the roleof genetic variantsAlastair H. MacLennan, MD, FRANZCOG; Suzanna C. Thompson, MBBS, FRACP; Jozef Gecz, PhD

T wo international expert task forcesaddressed cerebral palsy (CP) cau-

sation in 19991 and 2003.2 In 2014, theAmerican Congress of Obstetricians andGynecologists and the American Acad-emy of Pediatrics, with many interna-tional consultants, updated these reportsbut chose to focus on neonatal enceph-alopathy and a variety of neurologicaloutcomes rather than discuss CP causa-tion specifically and did not directlyaddress the ramifications of litigationfollowing a diagnosis of CP.3 Recentfindings published after the 2014 reporthave identified likely causative geneticvariants associated with CP cases andthis review contributes to updatingclinicians.

CP is a heterogeneous conditionwith multiple causes; multiple clinicaltypes; multiple patterns of neuropa-thology on brain imaging; multipleassociated developmental pathologies,such as intellectual disability, autism,epilepsy, and visual impairment; andmore recently multiple rare pathogenicgenetic variations (mutations). CPwould be better named “the cerebralpalsies” given that within the CP clinicalspectrum there are many causal path-ways and many types and degrees ofdisability. These various pathways andetiologies have each resulted in anonspecific nonprogressive disorder of

posture and movement control. Thus,CP should be considered as a descriptiveterm for affected individuals, with eachcase receiving adequate consideration ofan underlying etiology. There has beenlittle change in the prevalence of thisdiagnosis throughout the world, where

population data are available.1 It remainsaround 2-2.5/1000 births. Althoughthere have been small statistical fluctua-tions in the CP rates among childrenborn preterm, the rates of CP at termremain stable.4 New interventions suchas head or body cooling in selected

From the Australian Collaborative Cerebral Palsy Research Group at the Robinson Research Institute, the University of Adelaide, Adelaide, Australia(Dr MacLennan); and Department of Paediatric Neurology, Adelaide Women’s and Children’s Hospital (Dr Thompson) and Neurogenetics ResearchProgram (Dr Gecz), School of Pediatrics and Reproductive Health, the University of Adelaide, Adelaide, Australia.

Received Jan. 28, 2015; revised May 11, 2015; accepted May 15, 2015.

These studies have been supported by grants from the Australian National Health andMedical ResearchCouncil (1041920 and 1019928), Cerebral PalsyFoundation, Tenix Foundation, Women’s and Children’s Research Foundation, and Robinson Research Institute Foundation.

The authors report no conflict of interest.

Corresponding author: Alastair H. MacLennan, MD, FRANZCOG. [email protected]

0002-9378 ! Crown Copyright ª 2015 Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). ! http://dx.doi.org/10.1016/j.ajog.2015.05.034

Click Supplemental Materials under the article title in the online Table of Contents

Cerebral palsy (CP) is heterogeneous with different clinical types, comorbidities, brainimaging patterns, causes, and now also heterogeneous underlying genetic variants. Feware solely due to severe hypoxia or ischemia at birth. This common myth has held backresearch in causation. The cost of litigation has devastating effects on maternity serviceswith unnecessarily high cesarean delivery rates and subsequent maternal morbidity andmortality. CP rates have remained the same for 50 years despite a 6-fold increase incesarean birth. Epidemiological studies have shown that the origins of most CP are priorto labor. Increased risk is associated with preterm delivery, congenital malformations,intrauterine infection, fetal growth restriction, multiple pregnancy, and placental ab-normalities. Hypoxia at birth may be primary or secondary to preexisting pathology andinternational criteria help to separate the few cases of CP due to acute intrapartumhypoxia. Until recently, 1-2% of CP (mostly familial) had been linked to causative mu-tations. Recent genetic studies of sporadic CP cases using new-generation exomesequencing show that 14% of cases have likely causative single-gene mutations and upto 31% have clinically relevant copy number variations. The genetic variants are het-erogeneous and require function investigations to prove causation. Whole genomesequencing, fine scale copy number variant investigations, and gene expression studiesmay extend the percentage of cases with a genetic pathway. Clinical risk factors couldact as triggers for CP where there is genetic susceptibility. These new findings shouldrefocus research about the causes of these complex and varied neurodevelopmentaldisorders.

Key words: causes, cerebral palsy, DNA variants, epidemiological risk factors, geneticvariants, genomics, heterogeneity, whole exome sequencing

DECEMBER 2015 American Journal of Obstetrics & Gynecology 779

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American Journal of Obstetrics & Gynecology 2015;December:779 - 88 causative intrapartum neuropatholog-ical event.3

Intrapartum cardiotocographyIt is important to understand the greatlimitations of intrapartum electronicfetal heart rate monitoring, and inparticular its inability to reduce or pre-vent CP. Cochrane systematic reviews ofrelevant randomized controlled trialsof electronic fetal heart rate monitoringshow no reduction in CP rates with itsuse compared to intermittent ausculta-tion of the fetal heart.16 Continuouselectronic fetal heart rate monitoringwas introduced in the 1960s, withoutprior testing in randomized controlledtrials, partly in the belief that it wouldallow early recognition of acute fetalcompromise and in particular hypoxia.It was hoped that this would reduceintrapartum brain injury, because ofthe long-standing assumption and beliefthat many cases of CP were due topreventable acute hypoxia beginningin labor. However, fetal heart rate is avery indirect and poor measure of pastand present fetal brain function anddamage.

Intrapartum cardiotocography has avery high false-positive rate and with thepressures of obstetric litigation in manycountries, birth attendants and espe-cially individuals giving private care,who cannot be in continuous atten-dance, often opt for cesarean delivery.Defensive obstetrics, often in responseto uncertain cardiotocographic inter-pretation, has contributed to a large in-crease in cesarean delivery rates withouta change in CP rates (Figure 1). Thequantum of claims following CP is veryhigh in countries such as the UnitedStates, Australia, and the United King-dom. English health trusts paid £482million for “maternity negligence” co-verage in 2012 through 2013 equatingto a fifth of all spending on maternityservices.17 A small group of expert wit-nesses for the plaintiff regularly opinethat the cause of the CP was birth as-phyxia that was recognizable in laborand preventable by earlier delivery. Tochallenge such nonevidence-based opi-nion, it is time for obstetric colleges andacademic scientific societies in this field

to spell out that cardiotocography: (1)cannot detect the timing of the onset ofneuropathology; (2) cannot determinea time when it would be reversibleand then irreversible; and (3) cannot beused to determine that earlier deliveryby cesarean delivery “on the balance ofprobabilities” would have prevented theCP outcome.18 Courts should find thatjunk science is inadmissible in deter-mining CP causation and prevention.19

Clinical risk factors for CPduring pregnancyThere is increasing scientific evidencethat CP is usually associated with long-standing intrauterine pathology likegenetic mutations and probable envi-ronmental triggers such as bacterialand viral intrauterine infection, intra-uterine growth restriction (IUGR),antepartum hemorrhage, tight nuchalcord, and threatened miscarriage.20 Itcan be difficult to pinpoint adversepregnancy factors in retrospect, manyyears after birth, that individually ortogether might have triggered the path-ways to the neuropathology.

Preterm deliveryPreterm delivery is a major risk factorfor CP and is seen in approximately35% of all cases, and the risk increasesthe lower the viable gestational age.20,21

The risk of subsequent CP <33 weeks’gestation is 30 times higher than among

those born at term and is approximately70/1000 deliveries.7 The prevalence ofCP is highest in children born <28weeks’ gestational age (111.8/1000neonatal survivors; 82.25/1000 livebirths) and declines with increasinggestational age, being 43.15/1000 livebirths between 28-31 weeks, 6.75/1000between 32-36 weeks, and 1.35/1000 forthose born >36 weeks.22 The mecha-nisms and pathways to the neuropa-thology of CP may differ from termbabies, although associated risk factorssuch as infection, genetic variations,and growth restriction are likely tocontribute.

Coexisting congenital anomaliesThe prevalence of congenital anomaliesin children with CP is much higherthan in the general population and mostare cerebral, such as schizencephalyand hydrocephaly.23 Noncerebral mal-formations are also increased, such ascardiac, musculoskeletal, and urinary.24

In a case-control study of 494 singletoninfants with CP born >35 weeks’ gesta-tion included on the Western AustralianRegister of Developmental Anomaliesand 508 matched controls, birth defects(42.3%) and fetal growth restriction(16.5%) were more strongly associatedwith CP than potentially asphyxialbirth events (8.5%) and inflammation(4.8%).25 Birth defects had the largestassociation with CP in that study in both

FIGURE 1Six-fold increase in cesarean delivery without change in CP prevalence

Prevalence of CP/1000 births compared with cesarean rates over the past 50 years.68

CP, cerebral palsy.

MacLennan. Cerebral palsies: new insights and causes. Am J Obstet Gynecol 2015.

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cases with acute hypoxia have yet tosignificantly lower overall rates. Onlya small percentage of cases are associ-ated solely with acute intrapartumhypoxia.5-8 Despite this, many cases aremislabeled as due to birth asphyxia.

Birth asphyxia“Birth asphyxia” is an outdated term thatmay wrongly convey that a baby bornwith signs of fetal and neonatalcompromise must have undergone anacute hypoxic event in late labor and/orbirth. These clinical signs may also bepresent when there has been muchlonger-standing fetal compromise withpossible secondary hypoxia near de-livery.1 Similarly, the term “hypoxicischemic encephalopathy” has beenreplaced by the term “neonatal enceph-alopathy” as the large majority ofnewborn infants showing signs of en-cephalopathy does not have objectiveproof of acute hypoxia or ischemia atbirth, but have other causes of perinatalcompromise such as infectious or ge-netic.9 Of note, only 13% of term babieswho exhibit neonatal encephalopathyare later diagnosed with CP.10

At birth, nonspecific signs of fetalcompromise such as meconium-stainedamniotic fluid, nonreassuring fetal

heart rate patterns, low Apgar scores,and neonatal encephalopathy could allbe associated with either acute intra-partum timing or chronic long-standingtiming of the pathologies (ie, beginningbefore labor and during pregnancy).The same signs can be caused by notonly hypoxia and/or ischemia, but alsoby other factors such as infection,placental and umbilical vessel throm-bosis, or an altered fetal inflammatoryresponse.1 Very recent studies suggestthat many cases of CP are associatedwith genetic alterations (mutations) thatmay either directly cause CP orcontribute to susceptibility to CP.11,12 Asyet, they are not detectable antenatally orpreventable.

International consensus criteria toidentify severe acute intrapartumhypoxiaThere is now increasing evidence thatbabies given a “birth asphyxia” label dueto clinical signs such as low Apgar scoresoften do not have primary asphyxia.13,14

Many such babies are in ill health dueto longer-standing problems. Acute orchronic hypoxia can cause a metabolicacidosis in the blood of the newborn andthis has to be objectively measured inumbilical arterial blood gases at birth to

ascertain if clinically severe hypoxia iscontributing to the poor condition ofthe newborn.Whenmetabolic acidosis isproven to be present, this is evidence ofeither acute hypoxia beginning in laboror chronic hypoxia (ie, long-standingcompromise in pregnancy beginningbefore labor). Secondary asphyxia in la-bor is not necessarily the initial cause ofthe brain injury but may be a subsequentresult of the established neuropatholog-ical process. International consensuscriteria have been published and refinedto help define cases where neuropa-thology may have become establishedonly in labor and birth.1,2 These 9 cri-teria have helped recognize the few casesof severe de novo acute intrapartumhypoxia (Table 1). These criteria, as agroup, have been well verified.15 Thefirst 4 essential criteria have a highbut not individually perfect correlation(94-100%) in acutely asphyxiated neo-nates. The 5 nonspecific timing criteriawere individually less predictive, butwere to be assessed together, andtheir consensus helps understand thelikely timing of the neuropathology. In2014, a third consensus statementsimilarly examined neonatal encepha-lopathy, rather than CP, and largelysupported the criteria that define a

TABLE 1International consensus criteria to determine a severe acute hypoxic event as a potential cause of cerebral palsyEssential criteria to show presence of hypoxia at birth are:1. A metabolic acidosis at birth (pH <7.00 and Base Excess <e12).2. Early moderate to severe neonatal encephalopathy.3. Cerebral palsy of spastic quadriplegic or dyskinetic type.4. Exclusion of other identifiable causes of cerebral palsy, eg, coagulation or genetic disorders, infectious conditions, intrapartum pyrexia,

antepartum hemorrhage, prematurity, intrauterine growth restriction, tight nuchal cord, complications of multiple pregnancy.

Five nonspecific criteria collectively point toward acute or chronic causes of hypoxia.If most are met they suggest timing of neuropathology near delivery. If most are not met they suggest longer-standing pathological process. Thesecriteria are:5. Sentinel (signal) hypoxic event sufficient to cause sudden severe hypoxia in healthy fetus, eg, cord prolapse, antepartum hemorrhage, ruptured

uterus.6. Sudden sustained fetal heart rate bradycardia from that event.7. Apgar score <4 after 5 min.8. Signs of multisystem failure in neonate.9. Early (within 5 d) neuroimaging signs of edema and intracranial hemorrhage.

In 2003, American College of Obstetricians and Gynecologists/American Academy of Pediatrics Cerebral Palsy Expert Task Force2 updated 1999 criteria1 on basis of published evidence to that date.Task force agreed with 1999 task force criteria and added fourth essential criterion was necessary, ie, that no major chronic cause of neuropathology should be present if intrapartum acute asphyxialcause was to be presumed. Also acute de novo intrapartum event severe enough to be associated with cerebral palsy would cause Apgar scores to remain at!3 after 5 min of birth. Lastly, it onlyaccepted evidence of severe metabolic acidosis from arterial umbilical samples taken at birth, as blood gases can improve or worsen in first hour depending on successful or problematic neonatalresuscitation.

MacLennan. Cerebral palsies: new insights and causes. Am J Obstet Gynecol 2015.

Expert Reviews Obstetrics ajog.org

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896 VOL. 123, NO. 4, APRIL 2014 OBSTETRICS & GYNECOLOGY

Neonatal Encephalopathy and Neurologic Outcome, Second EditionReport of the American College of Obstetricians and Gynecologists’ Task Force on Neonatal Encephalopathy

Executive Summary

In the first edition of this report, the Task Force on Neona-tal Encephalopathy and Cerebral Palsy outlined criteria deemed essential to establish a causal link between intra-partum hypoxic events and cerebral palsy. It is now known

that there are multiple potential causal pathways that lead to cerebral palsy in term infants (see Fig. 1), and the signs and symptoms of neonatal encephalopathy may range from mild to severe, depending on the nature and timing of the brain injury. Thus, for the current edition, the Task Force on Neonatal Encephalopathy determined that a broader per-spective may be more fruitful. This conclusion reflects the sober recognition that knowledge gaps still preclude a defin-itive test or set of markers that accurately identifies, with high sensitivity and specificity, an infant in whom neonatal encephalopathy is attributable to an acute intrapartum event. The information necessary for assessment of likeli-hood can be derived from a comprehensive evaluation of all potential contributing factors in cases of neonatal enceph-alopathy. This is the broader perspective championed in the current report. If a comprehensive etiologic evaluation is not possible, the term hypoxic–ischemic encephalopathy should best be replaced by neonatal encephalopathy because neither hypoxia nor ischemia can be assumed to have been the unique initiating causal mechanism. The title of this report has been changed from Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiol-ogy to Neonatal Encephalopathy and Neurologic Outcome to indicate that an array of developmental outcomes may arise after neonatal encephalopathy in addition to cerebral palsy.

In order to determine the likelihood that an acute hypoxic–ischemia event that occurred within close temporal proximity to labor and delivery contributed to neonatal encephalopathy, it is recommended that a comprehensive multidimensional assessment be performed of neonatal sta-tus and all potential contributing factors, including maternal medical history, obstetric antecedents, intrapartum factors (including fetal heart rate monitoring results and issues relating to the delivery itself), and placental pathology. A description of the items to be included in the assessment follows.

I. Case DefinitionNeonatal encephalopathy is a clinically defined syn-drome of disturbed neurologic function in the earliest days of life in an infant born at or beyond 35 weeks of gestation, manifested by a subnormal level of conscious-ness or seizures, and often accompanied by difficulty with initiating and maintaining respiration and depres-sion of tone and reflexes. This expanded clinical defini-tion must be put into use based on measures that can be reliably and accurately implemented by trained staff. The first mandatory step in an assessment of neonatal encephalopathy is to confirm whether a specific infant meets the case definition.

In confirmed cases of neonatal encephalopathy, the following assessment will determine the likelihood that an acute peripartum or intrapartum event was a contrib-utor. This list is based on the premise that neonatal

Neonatal Encephalopathy and Neurologic Outcome, Second Edition, was developed by the Task Force on Neonatal Encephalopathy: Mary E. D’Alton, MD, Chair; Gary D.V. Hankins, MD, Vice Chair; Richard L. Berkowitz, MD; Jessica Bienstock, MD, MPH; Alessandro Ghidini, MD; Jay Goldsmith, MD; Rosemary Higgins, MD; Thomas R. Moore, MD; Renato Natale, MD; Karin B. Nelson, MD; Lu-Ann Papile, MD; Donald Peebles, MD; Roberto Jose Romero, MD; Diana Schendel, PhD; Catherine Yvonne Spong, MD; Richard N. Waldman, MD; Yvonne Wu, MD, MPH; and the American College of Obstetricians and Gynecologists’ staff: Gerald F. Joseph Jr, MD; Debra Hawks, MPH; Alyssa Politzer, MA; Chuck Emig, MA; and Kelly Thomas.

STATEMENT OF ENDORSEMENT

Neonatal Encephalopathy and Neurologic Outcome,Second Edition

The American Academy of Pediatrics has endorsed the following publication: American College of Obstetricians andGynecologists. Executive summary: neonatal encephalopathy and neurologic outcome. Obstet Gynecol. 2014;123:896–901(executive summary follows on next page).

All statements of endorsement from the American Academy of Pediatrics automatically expire 5 years after publication unless reaffirmed, revised, or retired at orbefore that time.

www.pediatrics.org/cgi/doi/10.1542/peds.2014-0724

doi:10.1542/peds.2014-0724

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2014 by the American Academy of Pediatrics

e1482 FROM THE AMERICAN ACADEMY OF PEDIATRICS

Organizational Principles to Guide and Define the ChildHealth Care System and/or Improve the Health of all Children

by guest on November 15, 2016Downloaded from

pH < 7,0 et/ou DB ≥ 12 mmol/L

Pour l’hypothermie thérapeutique (DB> 16 mmol/L)

Obstetrics & Gynecology 2014;123:896 - 901

GENERAI, OBSTETRICS AND GYNECOLOGY

Fetus-Placenta-Newborn

Threshold of metabolic newborn complications

acidosis associated with

James A. Low, MD, Brian G. Lindsay, BSc, and E. Jane Derrick, BA Kingston, Ontario, Canada

OBJECTIVE: Our purpose was to determine the threshold of metabolic acidosis at delivery associated with newborn complications. STUDY DESI6N: This study was a matched case-control study of 174 term newborn infants. Three groups defined by umbilical artery base deficit at birth were 4 to 8 mmol/L, 8 to 12 mmot/L, and 12 to 16 mmol/L. Newborn complications during the 5 days after birth were documented. A composite complication score defined the magnitude of all complications in each neonate. RESULTS = Moderate and severe newborn encephalopathy and respiratory complications and composite complication scores.>3 were increased in the group with an umbilical artery base deficit of 12 to 16 mmol/L. Moderate or severe newborn complications occurred in 10% of newborns in the same group, whereas such complications occur in 40% of neonates with an umbilical artery base deficit >16 mmol/L at birth. CONCLUSION: The threshold of fetal metabolic acidosis at delivery when moderate or severe newborn complications may occur is in an umbilical artery base deficit of 12 mmol/L. Thereafter, increasing metabolic acidosis is associated with a progression of severity of newborn complications. (Am J Obstet Gynecol 1997;177:1391-4.)

Key words: Fetal metabolic acidosis, newborn complications

The importance of fetal asphyxia has been confirmed in the research laboratory. These studies have demonstrated that fetal asphyxia of a particular degree and duration may cause brain damage. The findings have been consistent in studies of anoxia, ~' z hypoxia,3_6 and ischemia. 7 In each model brain damage did not occur until the asphyxia was severe.

A task force set up by the World Federation of Neu- rology Group defined asph~xia as a condition of impaired blood gas exchange leading, if it persists, to progressive hypoxemia and hypercapnia, s This is a good definition of asphyxia as it may affect the fetus and neonate. However, this may occur in a transient fashion that, although of physiologic interest, has no pathologic significance. Significant fetal exposure to asphyxia leads to tissue oxygen debt, accumulation of fixed acidosis, and a metabolic acidosis. Thus for intrapartum fetal asphyxia the following addition is proposed for this definition:

From the Department of Obstetrics and Gynaecology, Queen's University. ~eceived for publication February 21, 1997; revised May 22, 1997; accepted June 5, 199Z Reprint requests: J.A. Low, Nil), Department of Obstetrics and Gynae- cology, Queen's University, Kingston, Ontario, Canada K7L 3N6. Copyright © 1997 by Mosby-Year Book, Inc. 0002-9378/97 $5.00 + 0 6/1/83732

Fetal asphyxia is a condition of impaired blood gas exchange leading to progressive hypoxemia and hypercapnia with a significant metabolic acidosis.

The diagnosis of intrapartum fetal asphyxia requires a blood gas and acid-base assessment. The important question for the clinician is the threshold of metabolic acidosis beyond which fetal morbidity or mortality may O c c u r .

Severe metabolic acidosis at delivery is associated with newborn morbidity. This question was examined in a matched case-control study of 59 term fetuses with a metabolic acidosis, an umbilical artery base deficit >16 mmol /L and 59 fetuses with normal blood gas measures at delivery. Forty percent of the neonates in the asphyxia group had moderate or severe complications in one or more of the central nervous system, respiratory system, cardiovascular system, or kidney. 9 A similar association was demonstrated in a matched case-control study of preterm newborns between 32 and 36 weeks of gestation. 1°

In view of these findings, the objective of this study was to determine in term neonates the threshold of metabolic acidosis at delivery associated with newborn complications in the central nervous system, respiratory system, cardiovascular system, and kidney.

1391

GENERAI, OBSTETRICS AND GYNECOLOGY

Fetus-Placenta-Newborn

Threshold of metabolic newborn complications

acidosis associated with

James A. Low, MD, Brian G. Lindsay, BSc, and E. Jane Derrick, BA Kingston, Ontario, Canada

OBJECTIVE: Our purpose was to determine the threshold of metabolic acidosis at delivery associated with newborn complications. STUDY DESI6N: This study was a matched case-control study of 174 term newborn infants. Three groups defined by umbilical artery base deficit at birth were 4 to 8 mmol/L, 8 to 12 mmot/L, and 12 to 16 mmol/L. Newborn complications during the 5 days after birth were documented. A composite complication score defined the magnitude of all complications in each neonate. RESULTS = Moderate and severe newborn encephalopathy and respiratory complications and composite complication scores.>3 were increased in the group with an umbilical artery base deficit of 12 to 16 mmol/L. Moderate or severe newborn complications occurred in 10% of newborns in the same group, whereas such complications occur in 40% of neonates with an umbilical artery base deficit >16 mmol/L at birth. CONCLUSION: The threshold of fetal metabolic acidosis at delivery when moderate or severe newborn complications may occur is in an umbilical artery base deficit of 12 mmol/L. Thereafter, increasing metabolic acidosis is associated with a progression of severity of newborn complications. (Am J Obstet Gynecol 1997;177:1391-4.)

Key words: Fetal metabolic acidosis, newborn complications

The importance of fetal asphyxia has been confirmed in the research laboratory. These studies have demonstrated that fetal asphyxia of a particular degree and duration may cause brain damage. The findings have been consistent in studies of anoxia, ~' z hypoxia,3_6 and ischemia. 7 In each model brain damage did not occur until the asphyxia was severe.

A task force set up by the World Federation of Neu- rology Group defined asph~xia as a condition of impaired blood gas exchange leading, if it persists, to progressive hypoxemia and hypercapnia, s This is a good definition of asphyxia as it may affect the fetus and neonate. However, this may occur in a transient fashion that, although of physiologic interest, has no pathologic significance. Significant fetal exposure to asphyxia leads to tissue oxygen debt, accumulation of fixed acidosis, and a metabolic acidosis. Thus for intrapartum fetal asphyxia the following addition is proposed for this definition:

From the Department of Obstetrics and Gynaecology, Queen's University. ~eceived for publication February 21, 1997; revised May 22, 1997; accepted June 5, 199Z Reprint requests: J.A. Low, Nil), Department of Obstetrics and Gynae- cology, Queen's University, Kingston, Ontario, Canada K7L 3N6. Copyright © 1997 by Mosby-Year Book, Inc. 0002-9378/97 $5.00 + 0 6/1/83732

Fetal asphyxia is a condition of impaired blood gas exchange leading to progressive hypoxemia and hypercapnia with a significant metabolic acidosis.

The diagnosis of intrapartum fetal asphyxia requires a blood gas and acid-base assessment. The important question for the clinician is the threshold of metabolic acidosis beyond which fetal morbidity or mortality may O c c u r .

Severe metabolic acidosis at delivery is associated with newborn morbidity. This question was examined in a matched case-control study of 59 term fetuses with a metabolic acidosis, an umbilical artery base deficit >16 mmol /L and 59 fetuses with normal blood gas measures at delivery. Forty percent of the neonates in the asphyxia group had moderate or severe complications in one or more of the central nervous system, respiratory system, cardiovascular system, or kidney. 9 A similar association was demonstrated in a matched case-control study of preterm newborns between 32 and 36 weeks of gestation. 1°

In view of these findings, the objective of this study was to determine in term neonates the threshold of metabolic acidosis at delivery associated with newborn complications in the central nervous system, respiratory system, cardiovascular system, and kidney.

1391

Am J Obstet Gynecol 1997;177:1391 – 4

•  Cohorte de 174 n-n et trois catégories de DB: (8 – 12) (12 – 16) et (>16 mmol/L)

•  Aucune mention du type de DB, ni manufacturier •  Pas de mention du pH •  Prévalence du pH ≤ 7,00 et BD ≥ 12 mmol/L est

4 –15 fois moins fréquent que seul le BD ≥12 seul •  Aucune données sur la PCO2 •  Aucun algorithme de calcul du BD

Seuil de pathogénicité cérébrale fixé à DB > 12 mmol/L

Les déficits de base

•  Quantité de base requise pour rétablir un pH de 7,40 sous une PCO2 de 40 mm Hg à 37°C (1977)

•  Pour épurer la composante respiratoire de l’acidose •  Deux types de DB: in vitro (std) et in vivo (ecf) •  Rarement spécifié quel type de DB est calculé •  En condition de pH près de 7,40, les valeurs des

deux types de DB se rapprochent •  Pas d’uniformité d’algorithme de calcul par les

manufacturiers BE in vitro = (1– 0,014 Hb) (HCO3 – 24,8 + 7,7) (pH – 7,40) BE in vivo = HCO3 – 24,8 + 16,2(pH – 7,40)

C46-A2

Vol. 29 No. 8 Replaces C46-A

Vol. 21 No. 14

Blood Gas and pH Analysis and Related Measurements; Approved Guideline—Second Edition

This document provides clear definitions of the quantities in current use, and provides a single source of information on appropriate specimen collection, preanalytical variables, calibration, and quality control for blood pH and gas analysis and related measurements. A guideline for global application developed through the Clinical and Laboratory Standards Institute consensus process.

Product Name: Infobase 2010 - Release Date: February 2010

This document is protected by international copyright laws.

Blood Gas pH Analysis and Related Measurements Février 2016;29:8

AOGS MAIN RESEARCH ARTICLE

An overlooked aspect on metabolic acidosis at birth: bloodgas analyzers calculate base deficit differentlyPARISA MOKARAMI, NANA WIBERG & PER OLOFSSON

Institution of Clinical Sciences, Department of Obstetrics and Gynecology, Skane University Hospital, Lund University,Malmo, Sweden

Key wordsBase deficit, blood gases, metabolic acidosis,pH, pregnancy, umbilical cord

CorrespondencePer Olofsson, MD, Department of Obstetricsand Gynecology, Skane University Hospital,S-205 02 Malmo, Sweden.E-mail: [email protected]

Conflict of interestThe authors have stated explicitly that thereare no conflicts of interest in connection withthis article.

Please cite this article as: Mokarami P, WibergN, Olofsson P. An overlooked aspect onmetabolic acidosis at birth: blood gas analyzerscalculate base deficit differently. Acta ObstetGynecol Scand 2012; 91:574–579.

Received: 1 December 2010Accepted: 13 January 2012

DOI: 10.1111/j.1600-0412.2011.01364.x

Abstract

Objective. Metabolic acidosis (MA) at birth is commonly defined as umbilical cordarterial pH<7.0 plus base deficit (BD)≥12.0 mmol/L. Base deficit is not a measuredentity but is calculated from pH and Pco2 values, with the hemoglobin (Hb)concentration [Hb] included in the calculation algorithm as a fixed or measuredvalue. Various blood gas analyzers use different algorithms, indicating variationsin the MA diagnosis. The objective was therefore to calculate the prevalence ofMA in blood and extracellular fluid with algorithms from three blood gas analyzerbrands relative to the Clinical and Laboratory Standards Institute (CLSI) algorithm.Design. Comparative study. Setting . University hospital. Sample. Arterial cord bloodfrom 15 354 newborns. Main outcome measure. Prevalence of MA. Methods. Bloodwas analyzed in a Radiometer ABL 735 analyzer. Base deficit was calculated posthoc with algorithms from CLSI and Corning and Roche blood gas analyzers, andwith measured and fixed (9.3 mmol/L) values of [Hb]. Results. The prevalence ofBD ≥12.0 mmol/L in blood was with the CLSI algorithm 1.97%, Radiometer 5.18%,Corning 3.84% and Roche 3.29% (CLSI vs. other; McNemar test, p < 0.000001).Likewise, MA prevalences were 0.58, 0.66, 0.64 and 0.64%, respectively (p ≤ 0.02).Base deficit ≥12.0 mmol/L and MA rates were lower in extracellular fluid than inblood (p ≤ 0.002). Algorithms with measured or fixed Hb concentration made nodifferences to MA rates (p ≥ 0.1). Conclusions. The neonatal metabolic acidosis ratevaried significantly with blood gas analyzer brand and fetal fluid compartment forcalculation of BD.

Abbreviations: BD, base deficit; BDblood, base deficit in blood; BE, base excess; CLSI,Clinical and Laboratory Standards Institute; CTG, cardiotocography; ECF, extra-cellular fluid; Hb, hemoglobin; [Hb], hemoglobin concentration; MA, metabolicacidosis; STAN, ST analysis.

Introduction

During sustained hypoxia, the fetus eventually devel-ops metabolic acidosis due to anaerobic glycogenolysis.Metabolic acidosis in umbilical cord blood at birth is thusan objective measure of the fetus’s exposure and ability toresist hypoxia; therefore, metabolic acidosis is widely used asa reliable fetal outcome parameter.

Metabolic acidosis is usually defined as a low cord artery pHand a high base deficit [BD; the positive value of base excess(BE)]. The fact that BD is not a measured but a calculated en-tity from pH and Pco2 values is a problem, because differentbrands and models of blood gas analyzers use different algo-

rithms to calculate BD. This results in significantly differentBD values, although the pH and Pco2 values are the same (1).Older blood gas analyzers include a fixed hemoglobin (Hb)concentration [Hb] value in the algorithm, whereas somemodern blood gas analyzers measure the Hb concentration.This introduces another methodological problem when com-paring BD from different analyzers.

The aim of the study was to demonstrate how the preva-lence of neonatal metabolic acidosis would vary by calculatingthe rate of BD ≥ 12.0 mmol/L with algorithms from threebrands of commonly used blood gas analyzers and to com-pare this with standards recommended by the Clinical andLaboratory Standards Institute (CLSI) (2). The study also

574C⃝ 2012 The Authors

Acta Obstetricia et Gynecologica Scandinavica C⃝ 2012 Nordic Federation of Societies of Obstetrics and Gynecology 91 (2012) 574–579

A C TA Obstetricia et Gynecologica

Conclusions. The neonatal metabolic acidosis rate varied significantly with blood gas analyzer brand and fetal fluid compartment for calculation of BD.

Acta Obst et Gyn Scand 2012;91:574-579

n = 15 354 accouchements

OBSTETRICS

The significance of base deficit in acidemicterm neonatesLiv Knutzen, MD; Elena Svirko, DPhil; Lawrence Impey, MD

OBJECTIVE:Much emphasis is placed on the metabolic component ofumbilical cord acidemia at birth, with an importance attached to anarterial level of <7.00 accompanied by a base deficit of 12 mmol/L.We hypothesized that in acidemic neonates, the level of arterial basedeficit provides no prognostic information beyond that provided by thelevel of arterial pH.

STUDY DESIGN: This is a cohort study using a database of deliveriesfrom amajor teaching hospital, with additional information from neonatalrecords. A total of 8797 term, singleton, nonanomalous neonates wereidentified who had paired and validated cord blood gas analysis. Ofthese, 520were acidemic (pH<7.1) and 84were severely acidemic (pH<7.0). Outcomes examined were encephalopathy grade 2/3 and/ordeath, Apgar<7 at 5 minutes, neonatal unit admission, and compositeoutcomes of neurological and systemic involvement. Hierarchical logisticregressions were done using IBM SPSS Statistics 20.0 (Armonk, NY) toassess the predictive value of arterial pH and arterial base deficit.

RESULTS: For each outcome the median pH and base deficit ofthose neonates affected by the adverse outcome was significantlylower than for those who were unaffected. Hierarchical logisticregressions showed that pH is a significant predictor of alladverse outcomes studied (P < .001 for all outcomes). Whenbase deficit, and then the cross-product, are added to the model,neither add predictive value.

CONCLUSION: In acidemic neonates, the metabolic component doesnot predict those at risk of adverse outcomes once pH is taken intoaccount. The apparently worse outcomes with greater base deficitsimply reflect a greater degree of acidemia. The prognostic signifi-cance attached to the base deficit among acidemic neonates isquestionable.

Key words: adverse neonatal outcome, base deficit, metabolicacidosis, pH, umbilical cord

Cite this article as: Knutzen L, Svirko E, Impey L. The significance of base deficit in acidemic term neonates. Am J Obstet Gynecol 2015;212:x.ex-x.ex.

I ntrapartum hypoxia is an importantand high-profile precursor of cere-

bral palsy and neonatal death. Assess-ment of its severity at birth is currentlyperformed by analysis of umbilical vesselgas parameters, particularly pH and basedeficit in the umbilical artery.

An accepted “threshold” of arterialpH (ApH) is commonly quoted as<7.00, although a recent analysis of>50,000 consecutive cord samples sug-gested that it is at 7.1 that the risk ofencephalopathy, an accepted precursor

to cerebral palsy of intrapartum origin,begins to rise.1 The arterial base deficit(ABD) threshold has been quoted as 12mmol/L and Low et al2 found increasingbase deficit values to be associated withhigher complication rates.It is widely believed that the metabolic

component is crucial. Fetal asphyxia isdefined as “a condition of impaired gasexchange leading, if it persists, to pro-gressive hypoxemia and hypercapniawithsignificant metabolic acidosis.”3 In 1999,the International Cerebral Palsy TaskForce stated that cord blood metabolicacidosis (ApH<7.00, base deficit!12) isan essential requirement before cerebralpalsy can be attributed to intrapartumevents4; the American Congress of Ob-stetricians and Gynecologists alone re-quires the ABD to be at least 12 mmol/L.5

Further, the base deficit has been used asan outcome measure in trials examiningintrapartum interventions6,7 and as acriterion for cooling in the Total BodyHypothermia for Neonatal Encephalop-athy trial.8

The aim of this study is to examine therelationship among ApH, base deficit,

and outcome in acidemic neonates. Ourhypothesis is that, in acidemic neonates,base deficit does not add to the predictivevalue of ApH.

MATERIALS AND METHODS

DatasetThis was an observational cohort studyof nonanomalous term singleton de-liveries where complete and validatedcord blood gas analyses were recorded.

Details of all deliveries at a majorteaching hospital, including cord gasanalysis if performed, were prospec-tively recorded in a database. Cord gasesare taken at approximately half of alldeliveries. These are manually enteredafter birth: so to avoid potential trans-position errors, we merged outcomedata, using hospital number and date,with the output from the unit blood gasanalyzer.

Of appropriate deliveries from June 23,2005, through Dec. 31, 2009, where cordsamples were taken, we excluded allwhere only 1 vessel was sampled or anyvalues, eg, bases deficit, pH, or partialpressure of carbon dioxide (pCO2), were

From the Oxford Fetal Medicine Unit, Women’sCenter, John Radcliffe Hospital (Drs Knutzenand Impey), and United Kingdom MedicalCareers Research Group, Nuffield Departmentof Population Health, University of Oxford(Dr Svirko), Oxford, United Kingdom.

Received Nov. 12, 2014; revised Feb. 20, 2015;accepted March 25, 2015.

The authors report no conflict of interest.

Corresponding author: Liv Knutzen, MD. [email protected]

0002-9378/$36.00ª 2015 Elsevier Inc. All rights reserved.http://dx.doi.org/10.1016/j.ajog.2015.03.051

MONTH 2015 American Journal of Obstetrics & Gynecology 1.e1

Research ajog.org

Am J Obstetrics Gynecol 2015;213:3:373.e1-7

Conclusion: In acidemic neonates, the metabolic component does not predict those at risk of adverse outcomes once pH is taken into account. The apparently worse outcomes with a greater base deficit simply reflects greater degre of acidemia. The prognostic significance attached to the base deficit among acidemic neonates is questionable.

•  Repris par Eisenberg (Réa adulte) en 1987

•  Puis par Blickstein (Périnatalité) en 2007

•  Puis par Racinet en 2013...

•  Mais aucun ne prennent en compte l’effet

hydrolyse de l’hypercapnie

13

Élimination de la composante respiratoire (American Heart Association)

•  Mécanisme physico-chimique

•  Réaction cellulaire des mécanismes tampons du

maintien de l’équilibre entre la PCO2 et les ions HCO3

•  Chaque aiguë d’une tranche de 10 mmHg de PCO2

ions HCO3 de 1 mmol/L

14

L’effet hydrolyse

Anhydrase carbonique

H2O + CO2 H2CO3 H+ + HCO3

En pratique, deux situations sont possibles: •  Le pH est < à 7,00 et le pH eucapnique est ≤ 7,10

alors le DB est toujours > à 12 mmol/L: le diagnostic d’acidose métabolique est confirmé

•  Le pH est < à 7,00 et le pH eucapnique est > 7,10 alors le DB est toujours < à 12 mmol/L: le diagnostic d’acidose métabolique n’est pas retenu

•  Conclusion: l’acidose métabolique néonatale sévère peut être retenue tant que le pH eucapnique du sang artériel ombilical est ≤ à 7,10

Article original

Diagnostic de l’acidose metabolique a la naissance par ladetermination du pH eucapnique

Diagnosis of neonatal metabolic acidosis by eucapnic pH determination

C. Racinet a,f,*, G. Richalet b, C. Corne c, P. Faure c, J.-F. Peresse d, X. Leverve e,1

a Universite J-Fourier, Grenoble, Franceb Laboratoire de biologie medicale MEDIBIO, 48, avenue de Grugliasco, 38130 Echirolles, Francec Departement de biochimie, toxicologie et pharmacologie, CHU de Grenoble, BP217, 38043 Grenoble cedex 09, Franced Medi-Cedres, 48, avenue de Grugliasco, 38130 Echirolles, Francee Unite Inserm de bioenergetique fondamentale, appliquee, universite J.-Fourier, Grenoble, Francef Registre des handicaps de l’enfant et observatoire Perinatal-Isere, 23, avenue Albert-1er-de-Belgique, 38100 Grenoble, France

Gynecologie Obstetrique & Fertilite 41 (2013) 485–492

I N F O A R T I C L E

Historique de l’article :Recu le 27 juin 2013Accepte le 8 juillet 2013Disponible sur Internet le 27 aout 2013

Mots cles :Nouveau-neValeurs de referenceAcidemieAcidose metaboliqueAcidose respiratoireLactatemiePH eucapniqueDeficit de baseAsphyxie fœtale perpartumParalysie cerebrale

Keywords:NewbornReference valuesAcidemia

R E S U M E

L’acidose metabolique represente un critere essentiel pour etablir une relation causale entre uneasphyxie fœtale perpartum et une encephalopathie neonatale et/ou une paralysie cerebrale. Les moyensde diagnostic utilises a ce jour (mesure du pH et calcul du deficit de base ou dosage du lactate) sontimprecis et peu specifiques.Objectif. – L’etude avait pour seul objectif, a partir d’une cohorte de nouveau-nes issus d’une populationa bas risque (n = 867), de selectionner le meilleur marqueur de l’acidose metabolique parmi lesparametres sanguins ombilicaux du pH, des gaz du sang et de la lactatemie.Materiel et methode. – Les donnees ont ete obtenues a partir d’un automate de gazometrie. Puis parl’etude des correlations simples et partielles entre les donnees, on a cherche a definir le meilleurparametre pour caracteriser une acidose metabolique.Resultats. – Les resultats montrent une legere modification de tous les parametres en comparaison desparametres adultes : acidemie (pH a 7,28 ! 0,01), hypercapnie (56,5 ! 1,59 mmHg) et hyperlactatemie(3,4 ! 0,05 mmol/L). Tous les parametres sont correles entre eux (p < 0,001), en particulier lapCO2 represente le principal pourvoyeur d’acidemie. Sept cas (0,81 %) ont montre une acidemie severe(pH < 7,00) avec hypercapnie marquee. La correction de cette composante respiratoire par la methoded’EISENBERG aboutit au pH eucapnique revelant que six cas sur sept etaient dus a une acidose respiratoirepure. Les correlations partielles permettent d’affiner les resultats, demontrant que le lactate n’est passpecifique de l’acidose metabolique.Discussion et conclusion. – Il est demontre que les criteres ACOG-AAP d’acidose metabolique sontincomplets, imprecis et generateurs d’erreurs par exces. Il en est de meme pour le lactate, dont lasignification a ete revisee et remet en cause la conception erronee qu’il existe une acidose lactique,marqueur specifique d’hypoxie. Il apparaıt que le pH eucapnique, temoin de la part metabolique d’uneacidemie, represente le marqueur le plus fiable d’une acidose metabolique. Nous proposons un schemadecisionnel simple pour definir une acidose metabolique en cas d’acidemie inferieure a 7,00.

! 2013 Publie par Elsevier Masson SAS.

A B S T R A C T

The identification of a metabolic acidosis is a key criterion for establishing a causal relationship betweenfetal perpartum asphyxia and neonatal encephalopathy and/or cerebral palsy. The diagnostic criteriacurrently used (pH and base deficit or lactatemia) are imprecise and non-specific.

* Auteur correspondant.Adresse e-mail : [email protected] (C. Racinet).

1 In memoriam.

Disponible en ligne sur

www.sciencedirect.com

1297-9589/$ – see front matter ! 2013 Publie par Elsevier Masson SAS.http://dx.doi.org/10.1016/j.gyobfe.2013.07.020

Article original

Diagnostic de l’acidose metabolique a la naissance par ladetermination du pH eucapnique

Diagnosis of neonatal metabolic acidosis by eucapnic pH determination

C. Racinet a,f,*, G. Richalet b, C. Corne c, P. Faure c, J.-F. Peresse d, X. Leverve e,1

a Universite J-Fourier, Grenoble, Franceb Laboratoire de biologie medicale MEDIBIO, 48, avenue de Grugliasco, 38130 Echirolles, Francec Departement de biochimie, toxicologie et pharmacologie, CHU de Grenoble, BP217, 38043 Grenoble cedex 09, Franced Medi-Cedres, 48, avenue de Grugliasco, 38130 Echirolles, Francee Unite Inserm de bioenergetique fondamentale, appliquee, universite J.-Fourier, Grenoble, Francef Registre des handicaps de l’enfant et observatoire Perinatal-Isere, 23, avenue Albert-1er-de-Belgique, 38100 Grenoble, France



Historique de l’article :Recu le 27 juin 2013Accepte le 8 juillet 2013Disponible sur Internet le 27 aout 2013

Mots cles :Nouveau-neValeurs de referenceAcidemieAcidose metaboliqueAcidose respiratoireLactatemiePH eucapniqueDeficit de baseAsphyxie fœtale perpartumParalysie cerebrale

Keywords:NewbornReference valuesAcidemia

R E S U M E

L’acidose metabolique represente un critere essentiel pour etablir une relation causale entre uneasphyxie fœtale perpartum et une encephalopathie neonatale et/ou une paralysie cerebrale. Les moyensde diagnostic utilises a ce jour (mesure du pH et calcul du deficit de base ou dosage du lactate) sontimprecis et peu specifiques.Objectif. – L’etude avait pour seul objectif, a partir d’une cohorte de nouveau-nes issus d’une populationa bas risque (n = 867), de selectionner le meilleur marqueur de l’acidose metabolique parmi lesparametres sanguins ombilicaux du pH, des gaz du sang et de la lactatemie.Materiel et methode. – Les donnees ont ete obtenues a partir d’un automate de gazometrie. Puis parl’etude des correlations simples et partielles entre les donnees, on a cherche a definir le meilleurparametre pour caracteriser une acidose metabolique.Resultats. – Les resultats montrent une legere modification de tous les parametres en comparaison desparametres adultes : acidemie (pH a 7,28 ! 0,01), hypercapnie (56,5 ! 1,59 mmHg) et hyperlactatemie(3,4 ! 0,05 mmol/L). Tous les parametres sont correles entre eux (p < 0,001), en particulier lapCO2 represente le principal pourvoyeur d’acidemie. Sept cas (0,81 %) ont montre une acidemie severe(pH < 7,00) avec hypercapnie marquee. La correction de cette composante respiratoire par la methoded’EISENBERG aboutit au pH eucapnique revelant que six cas sur sept etaient dus a une acidose respiratoirepure. Les correlations partielles permettent d’affiner les resultats, demontrant que le lactate n’est passpecifique de l’acidose metabolique.Discussion et conclusion. – Il est demontre que les criteres ACOG-AAP d’acidose metabolique sontincomplets, imprecis et generateurs d’erreurs par exces. Il en est de meme pour le lactate, dont lasignification a ete revisee et remet en cause la conception erronee qu’il existe une acidose lactique,marqueur specifique d’hypoxie. Il apparaıt que le pH eucapnique, temoin de la part metabolique d’uneacidemie, represente le marqueur le plus fiable d’une acidose metabolique. Nous proposons un schemadecisionnel simple pour definir une acidose metabolique en cas d’acidemie inferieure a 7,00.

! 2013 Publie par Elsevier Masson SAS.

A B S T R A C T

The identification of a metabolic acidosis is a key criterion for establishing a causal relationship betweenfetal perpartum asphyxia and neonatal encephalopathy and/or cerebral palsy. The diagnostic criteriacurrently used (pH and base deficit or lactatemia) are imprecise and non-specific.

* Auteur correspondant.Adresse e-mail : [email protected] (C. Racinet).

1 In memoriam.


www.sciencedirect.com

1297-9589/$ – see front matter ! 2013 Publie par Elsevier Masson SAS.http://dx.doi.org/10.1016/j.gyobfe.2013.07.020

Clinical expert series

Neonatal metabolic acidosis at birth: In search of a reliable marker§

Acidose metabolique neonatale a la naissance : a la recherche d’un marqueur

pertinent

C. Racinet a,b,*, P. Ouellet c,d, F. Charles e, T. Daboval f,g

a UGA Grenoble, Domaine Universitaire, 621, avenue Centrale, 38400 Saint-Martin-d’Heres, Franceb Childhood Disabilities and Perinatal Data Register (RHEOP), 23, avenue Albert-1er-de-Belgique, 38000 Grenoble, Francec Department of Surgery, Sherbrooke University, Sherbrooke, Quebec, Canadad Vitality Health Care Network, zone 4, Edmundston, New Brunswick, Canadae Regional Hospital Center of Toulon-La Seyne/Mer, Toulon, Francef University of Ottawa, Ottawa, Canadag Department of Pediatrics, Children’s Hospital of East Ontario, Ottawa, Canada


A R T I C L E I N F O

Article history:Received 18 March 2016Accepted 11 April 2016Available online 20 May 2016

Keywords:NeonateRespiratory acidosisMetabolic acidosisBirth-related eucapnic neonatal pH

Mots cles :Nouveau-neAcidose respiratoireAcidose metaboliquePH eucapnique neonatal a la naissance

A B S T R A C T

Objective. – A newborn may present acidemia on the umbilical artery blood which can result fromrespiratory acidosis or metabolic acidosis or be of mixed origin. Currently, in the absence of a satisfactorydefinition, the challenge is to determine the most accurate marker for metabolic acidosis, which can bedeleterious for the neonate.Methods. – We reviewed the methodological and physiological aspects of the perinatal literature tosearch for the best marker of NMA.Results. – Base deficit and pH have been criticized as the standard criteria to predict outcome. Theproposed threshold of pathogenicity is not based on convincing studies. The algorithms of various bloodgas analyzers differ and do not take into account the specific neonatal acid–base profile.Conclusion. – Birth-related neonatal eucapnic pH is described as the most pertinent marker of NMA atbirth. The various means of calculating this value and the level below which it seems to play a possiblepathogenic role are presented.

! 2016 Elsevier Masson SAS. All rights reserved.

R E S U M E

Objectif. – Un nouveau-ne peut presenter une acidemie dans le sang cordonal, resultant d’une acidoserespiratoire ou d’une acidose metabolique (ANM) ou bien d’une acidose mixte. Devant l’utilisationpersistante de definitions non satisfaisantes, il paraıt necessaire de determiner quel est le meilleurmarqueur d’une ANM, car celle-ci peut se reveler pathogene pour le nouveau-ne.Methode. – Nous avons revu les aspects methodologiques et les bases physiologiques de la litteratureperinatale pour construire un marqueur fiable de l’ANM.Resultats. – Le deficit de base et le pH ne sont pas des marqueurs fiables du pronostic neonatal. Le seuilpropose pour les valeurs pathogenes ne repose pas sur des etudes convaincantes. Les algorithmes utilisespar les divers analyseurs de gaz du sang different et ne prennent pas en compte le profil specifique acido-basique du nouveau-ne.Conclusion. – Le pH eucapnique neonatal a la naissance est decrit comme le marqueur le plus pertinentde l’AMN. Les diverses methodes de calcul et le niveau au-dessous duquel il paraıt pouvoir jouer un rolepathogene sont presentes.

! 2016 Elsevier Masson SAS. Tous droits reserves.

DOI of original article: http://dx.doi.org/10.1016/j.gyobfe.2016.04.011§ Voir, dans ce meme numero de Gynecologie Obsterique & Fertilite, l’avant-propos signe par E. Simon : Interpretation du pH au cordon a la naissance : le piege de

l’hypercapnie [Interpretation of umbilical cord pH at birth: the trap of hypercapnia]. Gynecol Obstet Fertil 2016;44. http://dx.doi.org/10.1016/j.gyobfe.2016.04.011.

* Corresponding author. UGA Grenoble, Domaine Universitaire, 621, avenue Centrale, 38400 Saint-Martin-d’Heres, France.E-mail address: [email protected] (C. Racinet).

Available online at

ScienceDirectwww.sciencedirect.com

http://dx.doi.org/10.1016/j.gyobfe.2016.04.0051297-9589/! 2016 Elsevier Masson SAS. All rights reserved.




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Valeurs normales du nouveau-né pH 7,28 PCO2 54,0 mmHg HCO3 24,5 mmol/L

they do not take into account the hypercapnic portion thatcontributes substantially to acidemia (information on PCO2 valuesis lacking in the majority of articles).

Our goal is to obtain a reliable method of diagnosing NMA thatwould be a true instantaneous picture at time zero (T0) of themetabolic part of newborn acid–base status, to measure fetalresponse to labor, and to identify any potential abnormalities thatmay result from labor, because this knowledge may help identifyterm infants at risk of morbidity, or later may have a recognizedmedical-legal importance in case of CP [4].

It is important to underline that the infant is born in an acid–base state close to respiratory decompensation [8],1 which isnormal and indicative of an unavoidable birth-related biochemicalstress that most newborns can tolerate with no subsequent harm.This biochemical snapshot is indispensable for correctly inter-preting the antepartum history of any neonatal distress.

Newborn biochemical conditions are not taken into account inany of the available algorithms: they all refer to adult standards.This results in overestimation of BD, which—despite uncertaintyrelated to the absence of consensus between manufacturers on thealgorithms used—assigns a threshold of pathogenicity that was notcalculated with reference to neonatal conditions. We believe thatthis fully warrants our reviewing the situation and our recom-mendations.

We have considered the primary methods used to diagnose andquantify NMA that might affect the child in the future, and none ofthem appears to be satisfactory.

Starting from the basic premise that pH is the universallyacknowledged marker of acidemia, but is not specific because by itcannot specify whether it originates from a respiratory ormetabolic cause, but still seems to be the best predictor ofneonatal outcomes, we believe that the concept of birth-relatedneonatal eucapnic pHua best fulfills this need for specificity in asimple, objective, and precise way, resulting in BD estimation nolonger being of practical interest. Based on our clinical experience,we confirm that birth-related neonatal eucapnic BD adds nothingof value over and above knowledge of the birth-related neonataleucapnic pH because their correlation is nearly linear (r = !0.98).1

It can be calculated using two possible methods, at the user’sdiscretion:

" direct use of the Charles-Racinet diagram;" or the Excel form to calculate the newborn’s eucapnic pH.

This recommendation calls for all researchers in obstetrics andperinatal medicine to converge towards a redefinition of thepathogenic threshold of NMA.

Pending results of additional studies, we estimate that a birth-related neonatal eucapnic pH of umbilical artery blood < 7.11 ismore specific than a pH < 7.0 to define severe NMA. Its presence isnecessary to strongly support a position that fetal intrapartumhypoxia might be the root of neonatal encephalopathy andeventually cerebral palsy. Conversely, this level of acidemia isnot sufficient to confirm the diagnosis of perinatal asphyxia, whichmust be based on accumulated evidence from clinical practice,laboratory tests, and brain imaging.

Disclosure of interest

The authors declare that they have no competing interest.

Appendix A. Supplementary data

Supplementary data associated with this article can be found, inthe online version, at http://dx.doi.org/10.1016/j.gyobfe.2016.04.005.

References

[1] Saling E. Das Kind im Bereich der Geburtshilfe. Stuttgart: Georg Thieme Verlag;1966.

[2] MacLennan A, for the International Task Force on Cerebral Palsy. A template fordefining a causal relationship between acute intrapartum events and cerebralpalsy: international consensus statement. BMJ 1999;319:1054–9.

[3] The American College of Obstetricians and Gynecologists. Neonatal encepha-lopathy and neurologic outcome, second edition, executive summary. ObstetGynecol 2014;123(4):896–901.

[4] Racinet C, Hoffmann P. Perinatal asphyxia and cerebral palsy: medico-legalimplications. Bull Acad Natl Med 2010;194(6):891–901.

[5] Papille LA, Committee on fetus and newborn. Hypothermia and neonatalencephalopathy. Pediatrics 2014;133(6):1146–9.

[6] MacLennan AH, Thompson SC, Gecz J. Cerebral palsy: causes, pathways, andthe role of genetic variants. Am J Obstet Gynecol 2015. http://dx.doi.org/10.1016/j.ajog.2015.05.034.

[7] CLSI. Blood gas and pH analysis and related measurements; approvedguidelines, Second edition. CLSI document C46-A2, Wayne, PA: Clinical andLaboratory Standards Institute; 2009.

[8] Racinet C, Richalet G, Corne C, et al. Diagnosis of neonatal metabolic acidosis byeucapnic pH determination. Gynecol Obstet Fertil 2013;43:485–92.

[9] Ramin SM. Umbilical cord blood acid-base analysis at delivery; 2015, http://www.update.com.

[10] Schistig R, Grogono AW, Severinghaus JW. Human pCO2 and standard baseexcess compensation for acid-base imbalance. Crit Care Med 1998;26(7):1173–9.

[11] Davenport HW. ABC de l’equilibre biochimique acido-basique. Masson; 1973.[12] McIntyre KM, Lewis AJ. Textbook of advanced cardiac life support. In: Carveth

SW, editor. American Heart Association. Dallas; 1983.[13] Eisenberg MS, Cummins RO, Ho MT. Code blue: cardiac arrest and resuscita-

tion. Philadelphia: Saunders; 1987.[14] Blickstein I, Green T. Umbilical cord blood gases. Clin Perinatol 2007;3(3):451–9.[15] Henderson LJ. Concerning the relationship between the strength of acids and

their capacity to preserve neutrality. Am J Physiol 1908;21:173–9.[16] Brackett NC, Cohen JJ, Schwartz WB. Carbon dioxide titration curve of normal

man. Effect of increasing degrees of acute hypercapnia on acid-base equilibri-um. N Engl J Med 1965;272(1):6–12.

[17] Mokarami P, Wiberg N, Olofsson P. An overlooked aspect on metabolic acidosisat birth: blood gas analysers calculate base deficit differently. Acta ObstetGynecol Scandin 2012;91:574–9.

[18] Low JA, Lindsay BG, Derrick EJ. Threshold of metabolic acidosis associated withnewborn complications. Am J Obstet Gynecol 1997;177(6):1391–4.

[19] Schwartz WB, Relmann AS. A critique of the parameters used in the evaluationof acid-base disorders: whole blood buffer base and standard bicarbonatecompared with blood pH and plasma bicarbonate concentration. N Engl J Med1963;268–325:1382–8.

[20] Knutzen L, Svirko E, Impey L. The significance of base deficit in acidemic termneonates. Am J Obstet Gynecol 2015. http://dx.doi.org/10.1016/j.ajog.2015.03.051.

[21] Georgieva A, Moulden M, Redman C. Umbilical cord gases in relation to theneonatal condition: the EveREst plot. Eur J Obstet Gynecol Reprod Biol 2013;168:155–60.

[22] Olofsson P. Determination of base excess in umbilical cord blood at birth:accessory or J excess? Am J Obstet Gynecol 2015;213:259–61.

[23] Cahill AG. Umbilical artery pH and base deficit in obstetrics. Am J ObstetGynecol 2015;213(3):257–8.

C. Racinet et al. / Gynecologie Obstetrique & Fertilite 44 (2016) 357–362362




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CorrespondenceJK Muraskas in response to the article by C. Racinet et al. Neonatal��metabolic acidosis at birth: In search of a reliable marker.

Correspondence

JK Muraskas in response to the article byC. Racinet et al. Neonatal metabolic acidosis atbirth: In search of a reliable marker. GynecolObstet Fertil 2016; 44: 357–62

Reponse de JK Muraskas a l’article de C. Racinet et al. Acidosemetabolique neonatale a la naissance : a la recherche d’un marqueurpertinent. Gynecol Obstet Fertil 2016 ; 44 : 357–62

Neonatal encephalopathy is clinically defined as a syndrome ofdisturbed neurologic function in infants > 35 weeks gestation andoccurs in 1–3 per 1000 term births [1]. Approximately 10% ofcerebral palsy is directly related to the intrapartum period and thefocus all too often is the last 2 hours of a 7000 hour termpregnancy [2]. Current guidelines suggests that physicians shouldobtain both cord blood arterial and venous samples in all high riskpregnancies and especially in cases of low 5 minute Apgar scores,severe fetal growth restriction, maternal thyroid disease, intra-partum fever, multi-fetal gestations, or abnormal fetal heart ratetracings [3]. Universal collections of cord blood gases at everydelivery have been adopted at some institutions. According to theAmerican College of Obstetricians and Gynecologist/AmericanAcademy of Pediatrics task force on neonatal encephalopathy andcerebral palsy, fetal umbilical artery acidemia is defined asumbilical artery pH less than 7.0 and/or base deficit greater than!12 mmol/L [4,5]. Studies have found that moderate and severenewborn complications occurred in 10% of term newborn with anumbilical artery base deficit between 12 and 16 mmol/L and in40% of those with umbilical artery base deficit greater than16 mmol/L [6]. The use of umbilical cord venous blood gases(when arterial sample cannot be obtained) and measurement ofumbilical artery lactate levels have recently been described inpredicting fetal acidemia [7,8].

In the last issue (June) of French Journal GynecologieObstetrique & Fertilite, Racinet et al. propose calculation of abirth related neonatal eucapnic umbilical arterial pH thatrepresents the residual acidity related solely to the metaboliccomponent. Two critical points the authors bring to light arethat respiratory acidosis is usually not harmful to the newbornbrain and different blood gas analyzers use different calculationalgorithms which may result in different base deficit results.Every 10 mmHg increase in PCO2 will decrease pH by 0.08 units.Many cord arterial pH < 7.00 have a significant reversiblerespiratory component with no evidence of anaerobic metabo-lism. Many clinicians might be unaware of the fluid compart-ments influence on base deficits. The majority of neonatalintensive care units in the United States report in vitro bloodbase deficit although it is usually labeled only as a base deficitwithout a subscript identifier. The Siggaard Andersen alignmentnomogram approximates the blood base deficit. The in vivoextracellular fluid base deficit is a corrected form of blood base

deficit for which allowances have been made for the fact ofblood makes up only 37% of the extracellular fluid volume. Theauthors identify in vivo base deficit as birth related neonataleucapnic base deficit that measures acidity at a normal newbornPCO2. The Charles-Racinet diagram is based on the Henderson-Hasselbalch equation and every 10 mm rise in CO2 increasesHCO3 by 1 mmol/L demonstrating linear correlation.

The authors identify normal values for arterial cord blood gasand I have added the wide range of acceptable values [9]:

" pH 7.28 (7.18–7.38);" PCO2 53.8 mmHg (32.2–65.8);" PO2 15 mmHg (5.6–30.8);" HCO3 24.5 mmol/L (17–27);" base deficit 0–8 mmol/L.

A hypoxic ischemic insult progresses from a respiratoryacidosis over a 10–20 minute period to a mixed acidosis andthen a pure metabolic acidosis which cannot be timed [10]. Theinitial respiratory component is reversible with brain damageunlikely. This important manuscript by Racinet should be animpetus for further worldwide collaboration and research todefine newborn metabolic acidosis more precisely. Criticalclinical decisions on initiating hypothermia to blunt the neuro-toxic cascade of hypoxic ischemic encephalopathy and accusa-tions of professional liability with multimillion dollar lawsuits arebased on these parameters that might not reflect the actual fetalacid-base status. Further studies will be necessary to determine ifan eucapnic pH of umbilical arterial blood < 7.11 as proposed byRacinet is more precise than < 7.00 in defining newbornmetabolic acidosis.


The author declares that he has no competing interest.

References

[1] Muraskas JK, Kelly AF, Nash MS, Goodman JR, Morrison JC. The Role of fetalinflammatory response syndrome and fetal anemia in nonpreventable termneonatal encephalopathy. J Perinatol 2016;36:362–5.

[2] Muraskas JK, Morrison JC. A proposed evidence-based neonatal work-up toconfirm or refute allegations of intrapartum asphyxia. Obstet Gynecol2010;116:261–8.

[3] The American College of Obstetricians and Gynecologists. Umbilical cordblood gas and acid-base analysis. Committee opinion. Obstet Gynecol2006;108(5).

[4] The American College of Obstetricians and Gynecologists, American Academyof Pediatrics. Neonatal encephalopathy and cerebral palsy: defining the path-ogenesis and pathophysiology. Washington, DC: The American College ofPediatrics; 2003.

[5] The American College of Obstetricians and Gynecologists. Neonatal encepha-lopathy and neurologic outcome, second edition, executive summary. ObstetGynecol 2014;123(4):896–901.


Available online at



[6] Low JA, Lindsay BG, Derrick EJ. Threshold of metabolic acidosis associated withnewborn complications. Am J Obstet Gynecol 1997;177(6):1391–4.

[7] Cantu J, Szychowski JM, Li X, Biggio J, Edwards RK, Andrews W, et al. Predictingfetal acidemia using umbilical venous cord gas parameters. Obstet Gynecol2014;124:926–32.

[8] Truli MG, Stout MJ, Shanks A, Odibo A, Macones GA, Cahill A. Umbilical cordarterial lactate compared with pH for predicting neonatal morbidity at term.Obstet Gynecol 2014;124:756–61.

[9] Pomerance J. Interpreting umbilical cord blood gases: for clinicians caring forthe fetus or newborn, 2nd ed., BNMG Publications; 2012.

[10] Blickstein I, Green T. Umbilical cord blood gases. Clin Perinatol 2007;3(3):451–9.

J. MuraskasLoyola University Medical Center, Loyola University Stritch School of

Medicine, Neonatal and Maternal Fetal Medicine, 2160 S, 1st avenue,Russo Surgical Pavilion, Maywood, Illinois 60153, United States

E-mail address: [email protected]

Received 19 May 2016Available online 15 July 2016

Correspondence / Gynecologie Obstetrique & Fertilite 44 (2016) 455–456456




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The pattern of both initial respiratory acidosis responsible foran initial decrease of the pH and the consequent rise of lactid acid isdemonstrated in the attached figure, which has been publisheddecades ago [2,3].

The evaluation of early and late newborn morbidity andmortality detected the importance of a monitoring of metabolicdisturbances as a valid predictive factor for newborn outcome [6].

Early on Saling and Turowsky evolved a pH meter formeasurement of both actual and equilibrated pH(pCO2 = 40 mmHg) in the identical blood sample [2,3].

The result of this measurement leads to the differentiation ofthe metabolic proportion and furthermore has the great advantageto provide information within the same parameter area, namelythe actual pH and the so-called pH qu 40. We called it ‘‘pH act’’ and‘‘pH qu 40’’.

This solution was used in clinical routine during laborsuccessfully for many years and was welcomed by the cliniciansbecause of the simplicity of practical orientation about theproportions between the respiratory and the metabolic parts fromwhich the latter was of particular prognostic interest.

Other authors advised automated blood gas machines, thatcalculate the metabolic status using algorithms: base excess (BE)mmol/L.

Most equations which are used for calculation of ‘‘base excess’’are based on the Van Slyke equation described by Siggaard-Anderson based on measurements of: pH/pCO2 mmHg/cHb g/dL.

Different algorithms have been used for ‘‘standard BE’’ and ‘‘oxyBE’’ in reference to the influence of concentration of hemoglobineand the oxygenation status [7].

A lack of standardisation of base excess (BE) is problematicbecause of its confounding difficulties in the comparability bothduring external quality control and scientific evaluations. Due tothis difficulty direct measurements of lactate acid have beenproposed and standardised and is used for clinical assessments inScandinavian countries [8]. The normal range has been defined by aSwedish Group [9].

While enzymatic lactate measurements were time consumingand cumbersome, newly developed ‘‘lactate electrodes’’ areintroduced in clinical routine – in recent years electrodes forlactate measurements are available in clinics in Sweden.

The cost factor though has to be taken into account as itpotentially inhibits the widespread use for the application of thistechnology.

In conclusion, in considering the problems of standardisation ofthe calculation of base excess (BE) and focusing on cost balances, adirect measurement of pH qu 40 might still be the preferableoption for monitoring the metabolic status of the fetus andnewborn. In so far the publication from Racinet et al. could be thestart of a French initiative to recover and to improve thebiochemical assessment of the fetus and newborn.

An important supporting comment has been recently publishedin the corresponding letter from J.K. Muraskas [10].


The authors declare that they have no competing interest.

References

[1] Racinet C, Ouellet P, Charles F, Daboval T. Neonatal metabolic acidosis at birth:in search of a reliable marker. Gynecol Obstet Fertil 2016;44(6):357–62.

[2] Saling E. Das Kind im Bereich der Geburtshilfe. Stuttgart: Thieme; 1966.[3] Saling E. Foetal and neonatal hypoxia in relation to clinical obstetric practice.

London: Arnold; 1968.[4] Saling E. Die O2-Sparschaltung des fetalen Kreislaufes. Geburtshilfe Frauen-

heilk 1966;26:413–9.[5] Saling E. Oxygen-conserving adaptation of the foetal circulation. Mod Trends

Paediat 1970;3:51–68.[6] Saling E. Comments on past and present situation of the fetus during labor. J

Perinat Med 1996;4:7–11.[7] Zander R. The accuracy of calculated base excess in blood. Clin Chem Lab Med

2002;40(4):404–10.[8] Westgren M, et al. Lactat comparability with pH analysis at fetal blood sampling

a prospective randomised study. Brit J Osten Gynacol 1998;05:29–33.[9] Wiberg N, Kallen K, Herbst A, Olofson P. Relation between umbilical cord blood

pH, base deficit, lactat, 5-minute Apgar score and development of hypoxicischemic encephalopathy. Acta Obstet Gynecol Scand 2010;89(10):1263–9.

[10] Muraskas JK. Correspondence letter. Obstet Gynecol Fertil 2016;44:357–62.

E. Saling*,1, S. SchmidtInstitute of Perinatal Medicine, Rudower Str. 48, 12351 Berlin

(Neukoelln), Germany

*Corresponding authorE-mail address: [email protected] (E. Saling)

1Internet: http://www.saling-institut.de.

Received 13 October 2016Accepted 13 October 2016

Available online xxx

Correspondence / Gynecologie Obstetrique & Fertilite xxx (2016) xxx–xxx2

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GYOBFE-3006; No. of Pages 2

Please cite this article in press as: Saling E, Schmidt S. E. Saling and S. Schmidt in response to the article by C. Racinet et al.: ‘‘Neonatalacidosis at birth: In search of a reliable marker’’. Gynecol Obstet Fertil 2016;44:357–62. Gynecologie Obstetrique & Fertilite (2016),http://dx.doi.org/10.1016/j.gyobfe.2016.10.009

Correspondence

E. Saling and S. Schmidt in response to the articleby C. Racinet et al.: ‘‘Neonatal acidosis at birth: Insearch of a reliable marker’’. Gynecol ObstetFertil 2016;44:357–62

Reponse de E. Saling et S. Schmidt a l’article de C. Racinet et al. :« Neonatal acidosis at birth: In search of a reliable marker ». GynecolObstet Fertil 2016;44:357–62

A forgotten biochemical parameter for the assessment of thebiochemical state of the newborn

Claude Racinet et al. in their remarkable publication about:‘‘Neonatal acidosis at birth: In search of a reliable marker’’ [1] havediscussed the problems concerning the best suitable assessment ofthe biochemical state of the newborn infant.

This motivated us to remember that during our concernedactivities in the 1960s we introduced a particularly suitableparameter for an exemplary clinical use namely the so-called pH

qu 40 which curiously did not find enough acceptance but which –now as before – from logical clinical point of view offersadvantages because of its simplicity.

More details: the calculation of pH values from fetal andnewborn blood during fetal blood analysis (FBA) and of bloodsamples from umbilical cordblood (UA) is the basis for ourknowledge of fetal pathophysiology [2,3] (Fig. 1). While the normalrange of fetal pH values during the progress of labor was defined,the pattern of blood gas changes during disturbances, an initial riseof the carbondioxide partial pressure, due to diminished gastransfer is leading to respiratory acidosis [2,3].

An improved understanding of fetal hemodynamics led to theconcept of fetal metabolic acidosis and rise of lactid acidconcentration.

This phenomenon is caused by a centralisation of circulationduring fetal distress and consequent anerobic glycolysis, the so-called ‘‘oxygen-conservation adaptation of the fetal circulation’’[4,5]. Later erroneously called ‘‘brain spairing effect’’.

Gynecologie Obstetrique & Fertilite xxx (2016) xxx–xxx

Fig. 1. Pattern of parameters of acid base balance and blood gases during rapidly progressive intrauterine fetal disturbances: during the fall of oxygen partial pressure a rise ofcarbon dioxide leads to a respiratory acidosis. This causes a fall of the actual pH values. With a rise of lactid acid concentration due to anaerobic glycolysis a metabolic acidosisis induced. This is indicated by a fall of pH after equilibration of the blood samples at a pCO2 of 40 mmHg, the by us so-called pH qu 40. Figure according to Saling [2,3].

DOI of original article: http://dx.doi.org/10.1016/j.gyobfe.2016.04.005

G Model

GYOBFE-3006; No. of Pages 2

Please cite this article in press as: Saling E, Schmidt S. E. Saling and S. Schmidt in response to the article by C. Racinet et al.: ‘‘Neonatalacidosis at birth: In search of a reliable marker’’. Gynecol Obstet Fertil 2016;44:357–62. Gynecologie Obstetrique & Fertilite (2016),http://dx.doi.org/10.1016/j.gyobfe.2016.10.009

Available online at



Correspondence (Article in Press)E. Saling and S. Schmidt in response to the article by C. Racinet et al.:Neonatal acidosis at birth: In search of a reliable marker’A forgotten biochemical parameter for the assessment of the biochemicalState of the newborn.




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Article original

Le pH eucapnique neonatal a la naissance : application a une cohortede 5392 nouveau-nes

Neonatal eucapnic pH at birth: Application in a cohort of 5392 neonates

C. Racinet a,e,*, J.-F. Peresse d, G. Richalet b, C. Corne c, P. Ouellet f,g

a Universite Grenoble-Alpes, domaine universitaire, 621, avenue Centrale, 38400 Saint-Martin-d’Heres, Franceb Laboratoire de biologie medicale MEDIBIO, 48, avenue de Grugliasco, 38130 Echirolles, Francec Laboratoire des maladies metaboliques et depistage neonatal, institut de biologie et pathologie, CHU de Grenoble, 38043 Grenoble, Franced Medicedres, 48, avenue de Grugliasco, 38130 Echirolles, Francee Registre des handicaps de l’enfant, observatoire perinatal, 23, avenue Albert-1er-de-Belgique, 38100 Grenoble, Francef Departement de chirurgie, universite de Sherbrooke, Sherbrooke, Quebec, Canadag Reseau de sante Vitalite, zone Nord-Ouest, Edmundston, Nouveau-Brunswick, Canada



Historique de l’article :Recu le 17 mai 2016Accepte le 15 juillet 2016Disponible sur Internet le 30 aout 2016

Mots cles :Acidose metabolique neonataleAcidose respiratoirepH eucapnique neonatal a la naissanceEncephalopathie neonataleParalysie cerebrale

R E S U M E

Objectif. – Appliquer le nouveau concept de pH eucapnique neonatal a la naissance (pH euc [n]), etcomparer son apport par rapport aux criteres classiques d’acidose metabolique severe.Methodes. – Etude faite sur une cohorte de 5392 nouveau-nes de 2010 a 2014 dans une maternite deniveau 1. Les donnees cliniques (poids de naissance, age gestationnel, mode d’accouchement, scored’APGAR) ont ete recueillies sur les dossiers archives. Les donnees biologiques retenues ont ete le pH, laPCO2, le DB, la lactatemie sur le sang arteriel et veineux du cordon. Le pH euc (n) et le DB euc (n) ont etecalcules a partir du pH et de la PCO2 par l’equation de Henderson-Hasselbalch appliquee dans lediagramme de Charles-Racinet et/ou dans un module Excel.Resultats. – Les donnees etablissent la frequence de l’acidemie neonatale < 7,00 a 0,62 % des naissances.La cohorte etudiee presente 32 cas d’acidose metabolique neonatale severe selon les criteres ACOG-AAP(2014) et 26/29 cas selon ceux de McLennan (2015), dont 80 % sont nes apres cesarienne ou extractioninstrumentale. Le calcul du pH eucapnique neonatal a la naissance n’a pas confirme la severite del’acidose metabolique dans 55 % des cas en fonction d’un seuil fixe a 7,11. Aucun des nouveau-nes des sixaccouchements spontanes n’a ete transfere. Cinq cas ont ete transferes en neonatologie sur desconsiderations cliniques de mauvaise adaptation neonatale (le pH euc < 7,11 etait egalement distribuechez les transferes et les non transferes, p = 0,76, de meme que pour les pH, p = 0,20) et ont presente desissues normales.Discussion et conclusion. – La seule determination du pH ne fournit une information que sur le degred’acidemie mais non sur les composantes metabolique et/ou respiratoire. Or, il existe a la naissance uncertain degre d’hypercapnie qui n’est pas pris en compte dans les recommandations pour determiner laseverite d’une acidose metabolique (The American College of Obstetricians and Gynecologists, 2014 ;MacLennan et al., 2015). Le nouveau concept de pH eucapnique neonatal a la naissance permet deprendre en compte exclusivement la composante metabolique. Il devrait permettre d’affiner lesindications d’hypothermie cerebrale et ainsi d’ameliorer son efficacite. Sur le plan medicolegal, en cas deparalysie cerebrale, il permet souvent de refuter une acidose metabolique attribuee a des evenementsperpartum souvent accuses a tort de generer des lesions cerebrales.


* Auteur correspondant. 189, chemin de l’Enclos, 38320 Brie-et-Angonnes, France.Adresse e-mail : [email protected] (C. Racinet).



http://dx.doi.org/10.1016/j.gyobfe.2016.07.0081297-9589/! 2016 Elsevier Masson SAS. Tous droits reserves.

Article original

Le pH eucapnique neonatal a la naissance : application a une cohortede 5392 nouveau-nes

Neonatal eucapnic pH at birth: Application in a cohort of 5392 neonates

C. Racinet a,e,*, J.-F. Peresse d, G. Richalet b, C. Corne c, P. Ouellet f,g

a Universite Grenoble-Alpes, domaine universitaire, 621, avenue Centrale, 38400 Saint-Martin-d’Heres, Franceb Laboratoire de biologie medicale MEDIBIO, 48, avenue de Grugliasco, 38130 Echirolles, Francec Laboratoire des maladies metaboliques et depistage neonatal, institut de biologie et pathologie, CHU de Grenoble, 38043 Grenoble, Franced Medicedres, 48, avenue de Grugliasco, 38130 Echirolles, Francee Registre des handicaps de l’enfant, observatoire perinatal, 23, avenue Albert-1er-de-Belgique, 38100 Grenoble, Francef Departement de chirurgie, universite de Sherbrooke, Sherbrooke, Quebec, Canadag Reseau de sante Vitalite, zone Nord-Ouest, Edmundston, Nouveau-Brunswick, Canada



Historique de l’article :Recu le 17 mai 2016Accepte le 15 juillet 2016Disponible sur Internet le 30 aout 2016

Mots cles :Acidose metabolique neonataleAcidose respiratoirepH eucapnique neonatal a la naissanceEncephalopathie neonataleParalysie cerebrale

R E S U M E

Objectif. – Appliquer le nouveau concept de pH eucapnique neonatal a la naissance (pH euc [n]), etcomparer son apport par rapport aux criteres classiques d’acidose metabolique severe.Methodes. – Etude faite sur une cohorte de 5392 nouveau-nes de 2010 a 2014 dans une maternite deniveau 1. Les donnees cliniques (poids de naissance, age gestationnel, mode d’accouchement, scored’APGAR) ont ete recueillies sur les dossiers archives. Les donnees biologiques retenues ont ete le pH, laPCO2, le DB, la lactatemie sur le sang arteriel et veineux du cordon. Le pH euc (n) et le DB euc (n) ont etecalcules a partir du pH et de la PCO2 par l’equation de Henderson-Hasselbalch appliquee dans lediagramme de Charles-Racinet et/ou dans un module Excel.Resultats. – Les donnees etablissent la frequence de l’acidemie neonatale < 7,00 a 0,62 % des naissances.La cohorte etudiee presente 32 cas d’acidose metabolique neonatale severe selon les criteres ACOG-AAP(2014) et 26/29 cas selon ceux de McLennan (2015), dont 80 % sont nes apres cesarienne ou extractioninstrumentale. Le calcul du pH eucapnique neonatal a la naissance n’a pas confirme la severite del’acidose metabolique dans 55 % des cas en fonction d’un seuil fixe a 7,11. Aucun des nouveau-nes des sixaccouchements spontanes n’a ete transfere. Cinq cas ont ete transferes en neonatologie sur desconsiderations cliniques de mauvaise adaptation neonatale (le pH euc < 7,11 etait egalement distribuechez les transferes et les non transferes, p = 0,76, de meme que pour les pH, p = 0,20) et ont presente desissues normales.Discussion et conclusion. – La seule determination du pH ne fournit une information que sur le degred’acidemie mais non sur les composantes metabolique et/ou respiratoire. Or, il existe a la naissance uncertain degre d’hypercapnie qui n’est pas pris en compte dans les recommandations pour determiner laseverite d’une acidose metabolique (The American College of Obstetricians and Gynecologists, 2014 ;MacLennan et al., 2015). Le nouveau concept de pH eucapnique neonatal a la naissance permet deprendre en compte exclusivement la composante metabolique. Il devrait permettre d’affiner lesindications d’hypothermie cerebrale et ainsi d’ameliorer son efficacite. Sur le plan medicolegal, en cas deparalysie cerebrale, il permet souvent de refuter une acidose metabolique attribuee a des evenementsperpartum souvent accuses a tort de generer des lesions cerebrales.


* Auteur correspondant. 189, chemin de l’Enclos, 38320 Brie-et-Angonnes, France.Adresse e-mail : [email protected] (C. Racinet).



http://dx.doi.org/10.1016/j.gyobfe.2016.07.0081297-9589/! 2016 Elsevier Masson SAS. Tous droits reserves.

effectues par surcharge de travail ou etre retenus car ne concernantqu’un seul vaisseau.

On constate que le nouveau-ne presentait en moyenne uneacidemie (pH a 7,279 ! 0,008), une hypercapnie a 54,05 ! 0,22 mmHg,

une hypoxemie (PO2 a 14,79 ! 0,13 mmHg) et une hyperlactatemie a3,53 ! 0,02 mmol/L (Tableau 2).

Les correlations simples entre ces divers parametres etaienttoutes significatives (Tableau 3) sauf celles qui impliquaient laPO2. Il en est de meme pour certaines correlations partielles quisont presentees dans le Tableau 4. On note que la lactatemie etaitcorrelee fortement avec le pH mais aussi avec la PCO2, ce quicontredit la croyance repandue d’une specificite de l’hyperlacta-temie en faveur d’une acidose metabolique (voire d’une hypo-xemie).

Enfin, le DB est parfaitement correle avec le pH euc (n)(r = "0,97) et s’avere donc sans interet pratique car il n’apporteaucune valeur ajoutee a celle du pH euc (n) (Tableau 3).Inversement le pH eucapnique n’est absolument pas correle avecla PCO2, ce qui confirme bien son caractere specifique de la fractionmetabolique d’une acidemie.

Calcul du pH euca pnique néonata l à la naissa nce Normales à l a na issance

pH 7,28 PCO2 53,8 m mHg HCO3 24,5 mm ol/L Gazométrie art. ombilicale

pH 6,92 PCO2 100 mmHg

Résultas HCO3 anticipé

(Selo n PCO2 réelle) 29,12 mmol/L

HCO3 ré el (Selo n l’équa tion HH)

20,0 mmol/L HCO3 eu capniq ue néonatal

16,8 mmol/L Défic it de ba se (in vivo) (Eucapniq ue néonatal)

7,7 mEq/L pH euc apnique néonatal à

la n aissa nce ca lculé 7,12

Fig. 1. Ecran du module Excel pour le calcul automatise du pH eucapnique a lanaissance et des variables liees, apres introduction des valeurs du pH mesure et dela PCO2 (ref : Racinet et al., 2016 [17]). Afin de palier au besoin urgent d’un outilaccessible et facile a utiliser, nous proposons une fonction Excel qui permetd’afficher la valeur du pH eucapnique neonatal a la naissance sans aucun calculintermediaire. Ce fichier est disponible en hyperlien. Une application pour iPhone etAndroıde est aussi disponible.

Fig. 2. Diagramme de Charles-Racinet aux valeurs normales du nouveau-ne. pH7,28, PCO2 53,8 mmHg, HCO3 24,5 mmol/L (ref : Racinet et al., 2016 [17]).

Tableau 4Correlation partielle des divers parametres de l’equilibre acido-basique a lanaissance sur une cohorte de 5392 nouveau-nes a la clinique des Cedres (Echirolles,France).

(Couples de parametres),avec neutralisation del’effet d’un 3e parametre

Coefficient decorrelation

(PCO2 – pH), lactates "0,85 (p < 0,001)(PCO2 – Lactates), pH "0,58 (p < 0,001)(Lactates – pH), PCO2 "0,82 (p < 0,001)(Lactates – pH euc [n]), PCO2 "0,82 (p < 0,001)

pH euc (n) : pH eucapnique neonatal a la naissance.

Tableau 1Repartition des naissances vivantes et des prelevements sanguins arteriels a lanaissance effectues au cordon pendant les annees 2010 a 2014 (MEDIBIO et cliniquedes Cedres, Echirolles, France).

Annee Naissances vivantes(dont paires de jumeaux)

Prelevements effectues(% des naissances)

2010 1356 (12) 953 (70)2011 1233 (9) 1106 (90)2012 1287 (8) 1159 (90)2013 1321 (13) 1181 (89)2014 1282 (11) 993 (77)Total 6479 (53) 5392 (83)

Tableau 2Valeurs moyennes ! ecart-type de la moyenne du pH, des gaz du sang et de lalactatemie dans le sang arteriel cordonal a la naissance chez 5392 nouveau-nes de2010 a 2014 (MEDIBIO et clinique des Cedres, Echirolles, France).

pH PCO2

(mmHg)PO2

(mmHg)La"

(mmol/L)

7,279 ! 0,008 54,05 ! 0,22 14,79 ! 0,13 3,53 ! 0,02

Tableau 3Matrice de correlation entre les parametres mesures et calcules dans le sang arterieldu cordon de 5392 nouveau-nes de la clinique des Cedres (Echirolles, France) de2010 a 2014.

pH PCO2 PO2 DB Lactate pH euc

pHPCO2 0,80a

PO2 0,27a 0,42a

DB "0,74a "0,20a "0,04Lactate "0,76a 0,38a "0,10 "0,83a

pH euc 0,58a 0,003 "0,13 "0,97a 0,76a

pH euc : pH eucapnique.a Ces resultats montrent des liaisons significatives a p < 0,05.

C. Racinet et al. / Gynecologie Obstetrique & Fertilite 44 (2016) 468–474 471

Diagramme CHARLES-RACINET Valeurs normales du nouveau-né pH 7,28 PCO2 54,0 mmHg HCO3 24,5 mmol/L

Racinet C, Ouellet P, Charles F, Daboval T. Neonatal metabolic acidosis at birth: in search of a reliable criterion (Gynéc Obst et fertilité, 2016;40:357 – 562)

54,0

Cas pH 6,92 PCO2 100 mm Hg

x A

X N

x 7,08

6,92

100

B 16,8 C

54,0

B = A+N-R = 6,92+7,28-7,08 = 7,12

DB (eucapnique) = 24,5 - C = 7,7 mmol/L

N: Gazométrie ombilicale normale: (7,28 PCO2 54,0)

A: pH actuel (6,92) à PCO2 100

R: pH à la ligne tampon (7,08)

B: pH eucapnique (7,12)

C: HCO3(eucapnique 16,8)

x

7,28

7,12

R




pertinent








A B S T R A C T



R E S U M E






Available online at



https://itunes.apple.com/ca/app/neonatal-eucapnic-ph/id1167486332?l=fr&mt=8




pertinent








A B S T R A C T



R E S U M E






Available online at



Module excel Calcul du pH eucapnique néonatal à la naissance

Normes à la naissance pH 7,28 pCO2 53,8 mmHg HCO3 24,5 mEq/L

Gazométrie artère ombilicale pH 6,92 pCO2 100 mmHg

Résultats HCO3 aCendu

(Selon la pCO2 actuelle) 29,12 mmol/L

HCO3 actuel (Selon l'équaJon HH)

20,0 mmol/L HCO3 eucapnique néonatal

16,8 mmol/L Déficit de base

eucapnique néonatal 7,7 mmol/L

pH eucapnique néonatal à la naissance

7,116

pHR 7,084

COMMUNICATION




RÉSUMÉ





891

COMMUNICATION




RÉSUMÉ





891

Bull. Acad. Natle Méd, 2010;194:6:891 – 901

•  Les causes de la PC sont surtout anténatales: - Échec de la technologie perpartum - Échec de la césarienne préventive

•  Inflation des primes d’assurances professionnelles

souvent attribuable à une mauvaise gestion de l’accouchement, à une réalisation trop tardive d’une césarienne

•  L’hypercapnie est toujours présente en cas d’acidémie sévère à la naissance

•  Le pH euc(n) est un ancien concept revisité •  Plus spécifique d’une acidose métabolique si l’on

fixe un seuil à pH = 7,11 que les critères habituels •  Confirmer par une approche multicentrique la

valeur de 7,11 pour affiner sa valeur prédictive d’une morbidité néonatale

•  L’absence de gazométrie de l’artère ombilicale conduit à des spéculations entre défense – couronne plus que n’importe quel autre test de laboratoire

Conclusions

Merci de votre attention

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