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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”. Gynecol Obstet Fertil 2016;44:357–62
Gyne´cologie Obste´trique & Fertilite´ 44 (2016) 730–731
Available online at
ScienceDirect www.sciencedirect.com
Correspondence 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’’. Gynecol Obstet Fertil 2016;44:357–62 Re´ponse de E. Saling et S. Schmidt a` l’article de C. Racinet et al. : « Neonatal acidosis at birth: In search of a reliable marker ». Gynecol Obstet Fertil 2016;44:357–62 A forgotten biochemical parameter for the assessment of the biochemical state of the newborn Claude Racinet et al. in their remarkable publication about: ‘‘Neonatal acidosis at birth: In search of a reliable marker’’ [1] have discussed the problems concerning the best suitable assessment of the biochemical state of the newborn infant. This motivated us to remember that during our concerned activities in the 1960s we introduced a particularly suitable parameter 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 offers advantages because of its simplicity. More details: the calculation of pH values from fetal and newborn blood during fetal blood analysis (FBA) and of blood samples from umbilical cordblood (UA) is the basis for our knowledge of fetal pathophysiology [2,3] (Fig. 1). While the normal range of fetal pH values during the progress of labor was defined, the pattern of blood gas changes during disturbances, an initial rise of the carbondioxide partial pressure, due to diminished gas transfer is leading to respiratory acidosis [2,3]. An improved understanding of fetal hemodynamics led to the concept of fetal metabolic acidosis and rise of lactid acid concentration. This phenomenon is caused by a centralisation of circulation during fetal distress and consequent anerobic glycolysis, the socalled ‘‘oxygen-conservation adaptation of the fetal circulation’’ [4,5]. Later erroneously called ‘‘brain spairing effect’’.
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 of carbon 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 acidosis is 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 http://dx.doi.org/10.1016/j.gyobfe.2016.10.009 1297-9589/ß 2016 Elsevier Masson SAS. All rights reserved.
Correspondence / Gyne´cologie Obste´trique & Fertilite´ 44 (2016) 730–731
The pattern of both initial respiratory acidosis responsible for an initial decrease of the pH and the consequent rise of lactid acid is demonstrated in the attached figure, which has been published decades ago [2,3]. The evaluation of early and late newborn morbidity and mortality detected the importance of a monitoring of metabolic disturbances as a valid predictive factor for newborn outcome [6]. Early on Saling and Turowsky evolved a pH meter for measurement 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 of the metabolic proportion and furthermore has the great advantage to provide information within the same parameter area, namely the 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 labor successfully for many years and was welcomed by the clinicians because of the simplicity of practical orientation about the proportions between the respiratory and the metabolic parts from which the latter was of particular prognostic interest. Other authors advised automated blood gas machines, that calculate 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 SiggaardAnderson based on measurements of: pH/pCO2 mmHg/cHb g/dL. Different algorithms have been used for ‘‘standard BE’’ and ‘‘oxy BE’’ in reference to the influence of concentration of hemoglobine and the oxygenation status [7]. A lack of standardisation of base excess (BE) is problematic because of its confounding difficulties in the comparability both during external quality control and scientific evaluations. Due to this difficulty direct measurements of lactate acid have been proposed and standardised and is used for clinical assessments in Scandinavian countries [8]. The normal range has been defined by a Swedish Group [9]. While enzymatic lactate measurements were time consuming and cumbersome, newly developed ‘‘lactate electrodes’’ are introduced in clinical routine – in recent years electrodes for lactate measurements are available in clinics in Sweden. The cost factor though has to be taken into account as it potentially inhibits the widespread use for the application of this technology.
731
In conclusion, in considering the problems of standardisation of the calculation of base excess (BE) and focusing on cost balances, a direct measurement of pH qu 40 might still be the preferable option for monitoring the metabolic status of the fetus and newborn. In so far the publication from Racinet et al. could be the start of a French initiative to recover and to improve the biochemical assessment of the fetus and newborn. An important supporting comment has been recently published in the corresponding letter from J.K. Muraskas [10]. Disclosure of interest 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 Frauenheilk 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, Ka¨llen K, Herbst A, Olofson P. Relation between umbilical cord blood pH, base deficit, lactat, 5-minute Apgar score and development of hypoxic ischemic 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. Schmidt Institute of Perinatal Medicine, Rudower Str. 48, 12351 Berlin (Neukoelln), Germany *Corresponding author E-mail address: [email protected] (E. Saling) 1
Internet: http://www.saling-institut.de. Received 13 October 2016 Accepted 13 October 2016 Available online 4 November 2016
Available online at
ScienceDirect www.sciencedirect.com
Correspondence 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’’. Gynecol Obstet Fertil 2016;44:357–62 Re´ponse de E. Saling et S. Schmidt a` l’article de C. Racinet et al. : « Neonatal acidosis at birth: In search of a reliable marker ». Gynecol Obstet Fertil 2016;44:357–62 A forgotten biochemical parameter for the assessment of the biochemical state of the newborn Claude Racinet et al. in their remarkable publication about: ‘‘Neonatal acidosis at birth: In search of a reliable marker’’ [1] have discussed the problems concerning the best suitable assessment of the biochemical state of the newborn infant. This motivated us to remember that during our concerned activities in the 1960s we introduced a particularly suitable parameter 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 offers advantages because of its simplicity. More details: the calculation of pH values from fetal and newborn blood during fetal blood analysis (FBA) and of blood samples from umbilical cordblood (UA) is the basis for our knowledge of fetal pathophysiology [2,3] (Fig. 1). While the normal range of fetal pH values during the progress of labor was defined, the pattern of blood gas changes during disturbances, an initial rise of the carbondioxide partial pressure, due to diminished gas transfer is leading to respiratory acidosis [2,3]. An improved understanding of fetal hemodynamics led to the concept of fetal metabolic acidosis and rise of lactid acid concentration. This phenomenon is caused by a centralisation of circulation during fetal distress and consequent anerobic glycolysis, the socalled ‘‘oxygen-conservation adaptation of the fetal circulation’’ [4,5]. Later erroneously called ‘‘brain spairing effect’’.
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 of carbon 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 acidosis is 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 http://dx.doi.org/10.1016/j.gyobfe.2016.10.009 1297-9589/ß 2016 Elsevier Masson SAS. All rights reserved.
Correspondence / Gyne´cologie Obste´trique & Fertilite´ 44 (2016) 730–731
The pattern of both initial respiratory acidosis responsible for an initial decrease of the pH and the consequent rise of lactid acid is demonstrated in the attached figure, which has been published decades ago [2,3]. The evaluation of early and late newborn morbidity and mortality detected the importance of a monitoring of metabolic disturbances as a valid predictive factor for newborn outcome [6]. Early on Saling and Turowsky evolved a pH meter for measurement 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 of the metabolic proportion and furthermore has the great advantage to provide information within the same parameter area, namely the 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 labor successfully for many years and was welcomed by the clinicians because of the simplicity of practical orientation about the proportions between the respiratory and the metabolic parts from which the latter was of particular prognostic interest. Other authors advised automated blood gas machines, that calculate 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 SiggaardAnderson based on measurements of: pH/pCO2 mmHg/cHb g/dL. Different algorithms have been used for ‘‘standard BE’’ and ‘‘oxy BE’’ in reference to the influence of concentration of hemoglobine and the oxygenation status [7]. A lack of standardisation of base excess (BE) is problematic because of its confounding difficulties in the comparability both during external quality control and scientific evaluations. Due to this difficulty direct measurements of lactate acid have been proposed and standardised and is used for clinical assessments in Scandinavian countries [8]. The normal range has been defined by a Swedish Group [9]. While enzymatic lactate measurements were time consuming and cumbersome, newly developed ‘‘lactate electrodes’’ are introduced in clinical routine – in recent years electrodes for lactate measurements are available in clinics in Sweden. The cost factor though has to be taken into account as it potentially inhibits the widespread use for the application of this technology.
731
In conclusion, in considering the problems of standardisation of the calculation of base excess (BE) and focusing on cost balances, a direct measurement of pH qu 40 might still be the preferable option for monitoring the metabolic status of the fetus and newborn. In so far the publication from Racinet et al. could be the start of a French initiative to recover and to improve the biochemical assessment of the fetus and newborn. An important supporting comment has been recently published in the corresponding letter from J.K. Muraskas [10]. Disclosure of interest 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 Frauenheilk 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, Ka¨llen K, Herbst A, Olofson P. Relation between umbilical cord blood pH, base deficit, lactat, 5-minute Apgar score and development of hypoxic ischemic 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. Schmidt Institute of Perinatal Medicine, Rudower Str. 48, 12351 Berlin (Neukoelln), Germany *Corresponding author E-mail address: [email protected] (E. Saling) 1
Internet: http://www.saling-institut.de. Received 13 October 2016 Accepted 13 October 2016 Available online 4 November 2016