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Low fetal oxygen saturation at birth and acidosis
Low fetal oxygen saturation at birth and acidosis To the Editor:
The article by Arikan et al (Obstet Gynecol 2000;95: 565–71) deviates from the scientific method, ignoranes perinatal feto-placental physiology, and promotes an unethical and harmful procedure on newborns. The study subjected about 2000 newborns to immediate cord clamping and failed to include a control group of newborns whose cords were allowed to close physiologically. The most frequent cause of fetal hypoxia is cord compression, and because the fetal oxygen supply is dissolved in blood, the cord-compressed, hypoxic fetus is correspondingly hypovolemic and the placenta is engorged with fetal blood volume. Hypovolemic shock, regardless of the oxygenation of the blood supply, produces metabolic acidosis in poorly perfused tissues. Tissue acidosis and hypoxia will be reflected in umbilical arterial blood only to the extent that those tissues are well perfused, and despite laminar flow in the inferior vena cava through the foramen ovale, some mixing of umbilical and caval blood occurs, especially with caval constriction in hypovolemia. At birth without cord clamping, massive placental transfusion of oxygenated, nonacidotic blood rapidly corrects any hypovolemia, hypoxia, and acidosis, and quickly establishes the pulmonary circulation so that newborn pulmonary respiration can first supplement, then replace placental oxygenation and removal of excess CO2. Such newborns, following a 30% to 5% boost in blood volume, are routinely pink and crying at the 5-minute Apgar score. The effect of immediate clamping is seen in Table 6 of the article, where 5-minute Apgar scores show minimal improvement over 1-minute scores, emphasizing that all newborn resuscitation should be done with the placental circulation intact. If cord blood studies are needed, they may be obtained from pulsating cord vessels with fine, sterile needles. The authors should consider a further study of 2000 newborns who are allowed to close their cords physiologically and compare these with the original newborns in relation to neonatal pallor, anemia, hypotension, metabolic acidosis, hypothermia, oliguria, hypoxia, respiratory distress syndrome, oxygen therapy, plasma volume expansion, and blood transfusion. The results will confirm that immediate occlusion of the cord at birth is much more harmful in producing hypoxia and acidosis than is cord compression in utero.
VOL. 96, NO. 1, JULY 2000
G. M. Morley, MB, ChB Beverly Hills, Michigan 48025 In reply:
Assessing the status of the newborn by clamping the cord and sampling cord blood immediately after birth is a common and accepted practice.1–3 In the event that cord blood analysis is desired or deemed necessary3 (eg, Apgar scores under 7),1 a segment of cord (10 to 20 cm) should be doubly clamped immediately after birth, as described by ACOG.1–3 At our center, midwives conduct labor,4 clear the airway, milk-out and clamp the cord. Vigorous neonates are immediately bonded with their mothers. The cord is usually clamped within the first 30 seconds and this was not changed in our study. We have defined this as immediate clamping to emphasize that late cord clamping was not performed. It is not reasonable to claim that the beneficial autotransfusion effect is completely hindered in our study. Like many other centers throughout the world, we transfer depressed neonates to neonatology care. Resuscitating these neonates while the placental circulation is intact is certainly not the standard of care. The author’s suggestion that the neonates with low base excess values5 presented in Table 6 had minimally improved Apgar scores only because of early clamping is pure speculation. In fact, only one of those neonates had persisting Apgar score under 7 at 5 minutes. Collecting blood samples during intact placental perfusion is an interesting suggestion, but it is difficult to practice. The benefit of late cord clamping for all neonates is not proved. Late cord clamping increases fetal blood volume and hematocrit, may reduce the rate of respiratory distress, and may be useful in premature neonates. However, late cord clamping can cause hypervolemia, polycythemia, hyperviscosity, and hyperbilirubinemia. It may also cause an increase of systemic and pulmonary vascular resistance, adverse effects on left ventricular performance, and neonatal drug exposure (eg, local anesthetics). Late cord clamping is not a standard procedure in term neonates, and should even be avoided at cesarean if the neonate is elevated. Moreover, it may cause technical problems in depressed or operatively delivered neonates requiring resuscitation. Finally, the increasing practice of immediate bonding makes it necessary to investigate possible adverse effects of late cord clamping due to elevation of the neonate (reverse flow). On the basis of present medical knowledge, we believe that it is not justified to promote late cord clamping for all neonates. We find Morley’s remarks concerning ethics surprizing and would emphasize that our study design was approved by the Institutional
Letters
155
The article by Arikan et al (Obstet Gynecol 2000;95: 565–71) deviates from the scientific method, ignoranes perinatal feto-placental physiology, and promotes an unethical and harmful procedure on newborns. The study subjected about 2000 newborns to immediate cord clamping and failed to include a control group of newborns whose cords were allowed to close physiologically. The most frequent cause of fetal hypoxia is cord compression, and because the fetal oxygen supply is dissolved in blood, the cord-compressed, hypoxic fetus is correspondingly hypovolemic and the placenta is engorged with fetal blood volume. Hypovolemic shock, regardless of the oxygenation of the blood supply, produces metabolic acidosis in poorly perfused tissues. Tissue acidosis and hypoxia will be reflected in umbilical arterial blood only to the extent that those tissues are well perfused, and despite laminar flow in the inferior vena cava through the foramen ovale, some mixing of umbilical and caval blood occurs, especially with caval constriction in hypovolemia. At birth without cord clamping, massive placental transfusion of oxygenated, nonacidotic blood rapidly corrects any hypovolemia, hypoxia, and acidosis, and quickly establishes the pulmonary circulation so that newborn pulmonary respiration can first supplement, then replace placental oxygenation and removal of excess CO2. Such newborns, following a 30% to 5% boost in blood volume, are routinely pink and crying at the 5-minute Apgar score. The effect of immediate clamping is seen in Table 6 of the article, where 5-minute Apgar scores show minimal improvement over 1-minute scores, emphasizing that all newborn resuscitation should be done with the placental circulation intact. If cord blood studies are needed, they may be obtained from pulsating cord vessels with fine, sterile needles. The authors should consider a further study of 2000 newborns who are allowed to close their cords physiologically and compare these with the original newborns in relation to neonatal pallor, anemia, hypotension, metabolic acidosis, hypothermia, oliguria, hypoxia, respiratory distress syndrome, oxygen therapy, plasma volume expansion, and blood transfusion. The results will confirm that immediate occlusion of the cord at birth is much more harmful in producing hypoxia and acidosis than is cord compression in utero.
VOL. 96, NO. 1, JULY 2000
G. M. Morley, MB, ChB Beverly Hills, Michigan 48025 In reply:
Assessing the status of the newborn by clamping the cord and sampling cord blood immediately after birth is a common and accepted practice.1–3 In the event that cord blood analysis is desired or deemed necessary3 (eg, Apgar scores under 7),1 a segment of cord (10 to 20 cm) should be doubly clamped immediately after birth, as described by ACOG.1–3 At our center, midwives conduct labor,4 clear the airway, milk-out and clamp the cord. Vigorous neonates are immediately bonded with their mothers. The cord is usually clamped within the first 30 seconds and this was not changed in our study. We have defined this as immediate clamping to emphasize that late cord clamping was not performed. It is not reasonable to claim that the beneficial autotransfusion effect is completely hindered in our study. Like many other centers throughout the world, we transfer depressed neonates to neonatology care. Resuscitating these neonates while the placental circulation is intact is certainly not the standard of care. The author’s suggestion that the neonates with low base excess values5 presented in Table 6 had minimally improved Apgar scores only because of early clamping is pure speculation. In fact, only one of those neonates had persisting Apgar score under 7 at 5 minutes. Collecting blood samples during intact placental perfusion is an interesting suggestion, but it is difficult to practice. The benefit of late cord clamping for all neonates is not proved. Late cord clamping increases fetal blood volume and hematocrit, may reduce the rate of respiratory distress, and may be useful in premature neonates. However, late cord clamping can cause hypervolemia, polycythemia, hyperviscosity, and hyperbilirubinemia. It may also cause an increase of systemic and pulmonary vascular resistance, adverse effects on left ventricular performance, and neonatal drug exposure (eg, local anesthetics). Late cord clamping is not a standard procedure in term neonates, and should even be avoided at cesarean if the neonate is elevated. Moreover, it may cause technical problems in depressed or operatively delivered neonates requiring resuscitation. Finally, the increasing practice of immediate bonding makes it necessary to investigate possible adverse effects of late cord clamping due to elevation of the neonate (reverse flow). On the basis of present medical knowledge, we believe that it is not justified to promote late cord clamping for all neonates. We find Morley’s remarks concerning ethics surprizing and would emphasize that our study design was approved by the Institutional
Letters
155