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Published:December 26, 2016DOI:https://doi.org/10.1016/j.ajog.2016.12.027
      We appreciate the authors’ letter, which nicely articulates an important but often underappreciated fact: at very high levels, partial pressure of carbon dioxide (pCO2) has a significant impact on calculated base excess. Thus, in the presence of markedly elevated pCO2 values, the traditional distinction between short-term, clinically benign fetal respiratory acidemia and longer term, potentially important fetal metabolic acidemia cannot be made using base excess and pH alone. The elevations of pCO2 commonly seen in adult medicine are generally such that this effect is clinically insignificant. However, when using blood gas analysis in an attempt to determine the presence, severity, and duration of putative in utero oxygen deprivation, this effect often becomes important. Our use of standard base excess calculations reflects current clinical capabilities in most laboratories; our results simply confirm in clinical terms the authors’ mathematical observations.
      • Clark S.L.
      • Hamilton E.H.
      • Garite T.J.
      • et al.
      The limits of electronic fetal heart rate monitoring in the prevention of neonatal metabolic acidemia.
      • Racinet C.
      • Ouellet P.
      • Charles F.
      • Daboval T.
      Neonatal metabolic acidosis at birth: in search of a reliable marker.
      Various methods have been proposed to correct for this pCO2 effect. In addition to the authors’ previously published use of eucapnic pH, other investigators have distinguished the commonly performed blood base excess from extracellular fluid base excess and proposed the latter as a more accurate approach. All use mathematical models based on modifications of the Henderson-Hasselbalch and Van Slyke equations.
      • Racinet C.
      • Ouellet P.
      • Charles F.
      • Daboval T.
      Neonatal metabolic acidosis at birth: in search of a reliable marker.
      • Rosen K.G.
      • Murphy K.W.
      How to assess fetal metabolic acidosis from cord samples.
      • Kellum J.A.
      Clinical review: reunification of acid-base physiology.
      • Corey H.E.
      Stewart and beyond: new models of acid-base balance.
      • Siggaard Andersen O.
      • Engle K.
      A new acid base nomogram.
      In our opinion, all of them are valid. Thus, we do not disagree with the premise of these authors and will certainly consider their generous proposal for collaboration.
      However, such collaboration would seem to us to be a very low priority for the following reasons. Even if one could perfectly correct calculation of base deficit to achieve a Platonic ideal, we are unsure just how useful this would be. While neonatal encephalopathy due to intrapartum events is rare with a pH >7.0 and a BD <–16, these are not absolute threshold values; current newborn cooling guidelines rely heavily on clinical indicia of hypoxia and recognize the need for cooling under certain circumstances with a pH as high as 7.15 and a BD as low as –10.
      American Academy of Pediatrics
      Committee on fetus and newborn. Hypothermia and neonatal encephalopathy.
      Thus, tweaking base excess values is unlikely to change either obstetric or neonatal management, or enhance our understanding of prenatal events leading to encephalopathy.
      As outlined in our study, we are of the opinion that the limits of utility of electronic fetal heart rate monitoring and cord blood gas measurements have been reached and clearly identified.
      • Clark S.L.
      • Hamilton E.H.
      • Garite T.J.
      • et al.
      The limits of electronic fetal heart rate monitoring in the prevention of neonatal metabolic acidemia.
      We have wrung just about all the useful information to be had out of these 2 valuable techniques and additional attempts at fine-tuning of these processes are not likely to yield information of significant clinical utility. Rather, we believe a refocus of research efforts on alternative or adjunctive techniques of assessment not based on heart rate and blood gas analysis will be necessary to make further significant impacts upon the prevention of perinatal neurologic impairment.

      References

        • Clark S.L.
        • Hamilton E.H.
        • Garite T.J.
        • et al.
        The limits of electronic fetal heart rate monitoring in the prevention of neonatal metabolic acidemia.
        Am J Obstet Gynecol. 2016; : 163.e1-163.e6
        • Racinet C.
        • Ouellet P.
        • Charles F.
        • Daboval T.
        Neonatal metabolic acidosis at birth: in search of a reliable marker.
        Gynecol Obstet Fertil. 2016; 44: 357-362
        • Rosen K.G.
        • Murphy K.W.
        How to assess fetal metabolic acidosis from cord samples.
        J Perinat Med. 1991; 19: 221-226
        • Kellum J.A.
        Clinical review: reunification of acid-base physiology.
        Crit Care. 2005; 9: 500-507
        • Corey H.E.
        Stewart and beyond: new models of acid-base balance.
        Kidney Int. 2003; 64: 777-787
        • Siggaard Andersen O.
        • Engle K.
        A new acid base nomogram.
        Scand J Clin Lab Invest. 1960; 12: 177-186
        • American Academy of Pediatrics
        Committee on fetus and newborn. Hypothermia and neonatal encephalopathy.
        Pediatrics. 2014; 133: 1146-1150

      Linked Article

      • Current base deficit is not a relevant marker of neonatal metabolic acidosis
        American Journal of Obstetrics & GynecologyVol. 216Issue 5
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          The article by Clark et al1 is a relevant attempt to assess the limits of electronic fetal heart rate monitoring to prevent neonatal metabolic acidosis (NMA), which is an intermediate biological marker of asphyxia and risk of neonatal encephalopathy. The challenge is to identify clinical information, biomarkers, and electrophysiological indicators that would best support clinical decision and better identify newborns who will benefit from therapeutic hypothermia to prevent postasphyxia cerebral damage.
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