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Placental transfusion as an alternative
Preventing Neonatal Transfusion
Neonatal Transfusion
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Eileen Nicole Simon, Nurse http://conradsimon.org/
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eileen.n.simon{at}verizon.net Eileen Nicole Simon
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Dear Editor Placental transfusion ought to be considered as possibly the safest alternative to neonatal transfusions. Although clamping of the umbilical cord has been practiced for hundreds of years, until about 20 to 25 years ago most textbooks of obstetrics still taught that the newborn should be breathing on its own before the cord is clamped, and many advocated waiting until pulsations of the cord had stopped. Immediate clamping of the cord is now recommended to prevent circulatory overload, polycythemia, and jaundice. This is certainly an opinion-based practice, as plentiful evidence exists that placental transfusion is important for the changes in cardiac and pulmonary circulation that must take place in the transition from fetal to neonatal respiration. The evidence is mostly part of forgotten history which would be better to remember than have to repeat. Some important findings of thoughtful and well educated researchers of the past include: 1. Before the cause of erythroblastosis fetalis was known, Zimmerman and Yannet in 1933 summarized a large number of case reports in German that pointed out that kernicterus was caused by bilirubin staining of subcortical nuclei already injured by sepsis or oxygen deprivation.[1] 2. Experimental asphyxia of monkeys later revealed what Myers in 1972 described as a "monotonous rank order" of brainstem structures damaged by asphyxia at birth.[2] This same rank order of brainstem structures were stained by bilirubin injections that had no adverse effect anywhere in the brains of monkeys not subjected to asphyxia.[3,4] 3. Pulsations of the umbilical arteries would appear to control the amount of placental transfusion, thus leaving the cord unclamped should not produce any overload. Desmond and co-workers in 1959 observed that pulsations of the umbilical cord stump in the newborn nursery could be related to the degree of distress a newborn was suffering.[5] Especially when an infant is born pale and not breathing, shouldn't it be important to leave the child attached to its maternal lifeline? Placental transfusion may be important to close the fetal shunts in the heart and redirect blood flow to the lungs, where filling of the capillaries may stimulate opening of the alveoli.[6,7] There is much more to discuss, especially the importance of brainstem nuclei for autonomic functions, which are often disturbed in cases of neonatal distress. References 1. Zimmerman HM, Yannet H. Kernikterus: Jaundice of the nuclear masses of the brain. Am J Dis Child 1933;45:740-759. 2. Myers RE. Two patterns of perinatal brain damage and their conditions of occurrence. Am J Obstet Gynecol 1972;112:246-276. 3. Lucey JF, Hibbard E, Behrman RE, Esquivel FO, Windle WF. Kernicterus in asphyxiated newborn monkeys. Exp Neurol 1964;9:43-58. 4. Windle WF. Brain damage by asphyxia at birth. Sci Am 1969;221:76- 84. 5. Desmond MM, Kay JL, Megarity AL. The phases of "transitional distress" occurring in neonates in association with prolonged postnatal umbilical cord pulsations. J Pediatr 1959;55:131-151. 6. Jäykkä S. A new theory concerning the mechanism of the initiation of respiration in the newborn: A preliminary report. Acta Paediatrica 1954;43:399-410. 7. Mercr JS, Skovgaard RL. Neonatal transitional physiology: a new paradigm. J Perinat Neonatal Nurs 2002;15:56-75. |
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George M. Morley, Retired Obstetrician / Gynecologist
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obgmmorley{at}aol.com George M. Morley
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Dear Editor For obstetricians and midwives, preventing (sometimes massive) blood loss and thus avoiding maternal transfusion are basic principles of practice. Therefore, the introductory statement in this article from Hammersmith Hospital is quite astounding: “Sick neonates are one of the most heavily transfused groups of patients in modern medicine.” The authors do not attempt to explain or prevent this incredible situation – that modern newborns are as prone, or much more prone to suffer massive post-partum or intra-partum hemorrhage than are their mothers! At any other age, iron deficiency anemia that progresses to the point of requiring blood transfusion usually means that the CAUSE of the blood loss has not been diagnosed and adequately treated. HOW IS IT POSSIBLE FOR MODERN NEONATES TO LOSE SO MUCH BLOOD THAT TRANSFUSION IS NEEDED FOR THEIR SAFE SURVIVAL? The answer to this question has been written “in stone” for over two hundred years: 1773: "The common method of tying and cutting the navel string in the instant the child is born is likewise one of those errors in practice that has nothing to plead in its favour but custom." A Treatise on the Management of Pregnant and Lying-In Women" by Charles White, published in 1773. 1801: “Another thing very injurious to the child, is the tying and cutting of the navel string too soon; which should always be left till the child has not only repeatedly breathed but till all pulsation in the cord ceases. As otherwise the child is much weaker than it ought to be, a portion of the blood being left in the placenta, which ought to have been in the child.” Erasmus Darwin, Zoonomia, 1801 Placental transfusion and blood loss caused by immediate cord clamping (ICC) have been verified repeatedly over the centuries. Depending on birth circumstances, ICC may leave 30% - 50% or more of a child’s natural blood volume in its placenta. Every “at risk” neonate that is handed to a waiting neonatology team has had its cord clamped immediately. Following full (physiological) placental transfusion, some hemo- concentration occurs and normal hemoglobin levels are in the 18 – 20g/dl range. The threshold indication for RBC transfusion is <10g/dl; assuming that these anemic neonates have restored their blood volumes to normal by hemodilution, the inevitable conclusion is that they did, indeed, lose half of their red cell mass and half of their natural blood volume at birth. In the adult, a rapid hemorrhage of this magnitude would be uniformly fatal; there is good reason for these modern ICC neonates to be sick. Perhaps the most relevant recent article was published in the BMJ in January 1993. Kinmond et al, in a double blind study, allowed preemies 27 – 32 weeks gestation to receive some placental transfusion by gravity drainage for 30 seconds after delivery. None of the placental transfused group required blood transfusion while the immediately clamped control group needed significant transfusion. The placental transfusion group was not “sick,” requiring an average of 3 days in supplemental oxygen compared to 10 days in the control group. Another recent relevant study (from Hammersmith) is “The Origin and Timing of … Neonatal Encephalopathy” (Cowan et al. The Lancet, March 2003); this featured over 300 immediately clamped neonates that were already compromised during birth. All had post-partum ISCHEMIC brain lesions, the obvious origin of the brain ischemia being massive blood loss at birth. The incidence of blood transfusion in these neonates was not reported, but anemia and/or blood transfusion is frequent in such infants. ICC may subject any neonate to a massive hemorrhage into its placenta. ICC is practiced routinely in most hospitals in the western world, especially on compromised neonates. The only effective treatment of hypovolemic shock is immediate replacement of blood volume, preferably with whole blood. Thus the need for neonatal blood transfusion can be eliminated by NOT clamping the cord and by allowing placental transfusion to proceed normally; the neonate attains physiological hemodynamic equilibrium with its placenta. The result is a physiological (healthy) blood volume and a healthy neonate. The neonate that receives a full placental transfusion at birth has enough iron to prevent anemia during the first year of life. Neonatal heterologous transfusion with all its “finite risks and costs” is readily and very safely avoided by allowing physiological cord closure. Complete medical references and explanations of the above are
available at: |
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Frances M Cowan, Neonatal neurologist Imperial College and Hammersmith Hospital, Irene Roberts
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f.cowan{at}imperial.ac.uk Frances M Cowan, et al.
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Dear Editor Dr Morley implies that early cord clamping is the main cause of anaemia and blood transfusion in preterm infants and of hypoxic-ischaemic encephalopathy in full term infants. He sites references from a time long before neonatal intensive care was available and when preterm infants who would require transfusion would not have survived. The reason preterm neonates require transfusion is not, in the main, because they have bled into their placental circulation at birth. The majority are not anaemic at birth but gradually become so because they do not get the normal transfer of iron in the third trimester, they have frequent episodes of sepsis and, above all, they undergo frequent blood sampling. Dr Morley gives no evidence that these infants are anaemic at birth and makes no reference to the potential dangers of polycythaemia from placental transfusion. Our article [1] does not address the value of delayed cord clamping. However there are no data to suggest that this is a useful approach in the management of sick VLBW infants; we do not dispute however that placental transfusion may be useful in reducing transfusion in a proportion of well moderately preterm infants who in any case have a low transfusion requirement. There is no evidence that early cord clamping causes neonatal encephalopathy in the full term neonate. In our hospital it is routine for infants to have cord blood sampling for pH and base excess. Neonatal encephalopathy is a rare event. The infants in our study [2] did not have a post-partum origin for their brain lesions and neither was there, in the vast majority, evidence of intrapartum blood loss, postnatal hypovolaemia or anaemia or the need for blood transfusion. We strongly disagree with Dr Morley’s contention that early cord clamping causes hypovolaemia, which in turn causes neonatal encephalopathy in the term infant and anaemia in the very low birth weight infant. References 1. Murray NA & Roberts IA. Neonatal transfusion practice. Arch Dis Child 2004;89:F101-7. 2. Cowan F et al. Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 2003; 361:736-42. |
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