The gentlebirth.org website is provided courtesy of
Ronnie Falcao, LM MS, a homebirth midwife in Mountain View, CA
Dirty Dozen List of Endocrine Disruptors
12 Hormone-Altering Chemicals and How to Avoid Them
This article for Family Physicians discusses the hazards of endocrine disruptors during pregnancy.
By George M. Morley, MB., CH. B
July 1998 * OBG Management
While exploring the feasibility of saving placental blood for autologous NICU transfusion, the author found a disturbingly obvious alternative: If cord clamping is delayed to permit normal placental transfusion, the need for newborn transfusion often could be eliminated.
During the third stage of natural labor, placental respiration continues
for a time. The newborn also receives a placental transfusion that optimizes
its blood volume. Physiologic closure of the cord vessels terminates this
transfusion. When the cord is clamped before these vessels close, the amount
of placental transfusion usually is reduced, sometimes markedly, particularly
if the infant's lungs are not yet ventilated. Clamping after the vessels
have closed insures hemostasis and does not affect cord physiology. In
current practice, the cord usually is clamped as soon as is convenient,
regardless of physiology. An ACOG bulletin recommends immediate clamping
to obtain an arterial pH.1
When this process is observed clinically, the umbilical arteries constrict first.2 While they are pulsating, placental respiration continues.3 Tensing of the cord vein indicates contraction of the uterus, which squeezes the placenta and forces a 30% to 50% increase in blood volume into the infant. Gravity also is a factor in this transfusion." Ventilation reflexively 'opens the pulmonary vasculature that accommodates the transfusion. Finally, the umbilical vein at the umbilicus constricts,2 usually after the child is pink .6 While this entire process typically lasts about 3 minutes, it may take longer or occur in less than 1 minute.2 Physiologic clamping is extremely effective in procuring, regulating, and retaining the neonate's blood volume.
The figure on page 34 shows a transfusion of about 100g (100 mL) for a term child with a final blood volume approximating 300 mL to 350 mL. However, between pathologic extremes, the normal range of transfusion is wide, and most newborns can tolerate a similar variation in blood volume.
The effects of high or low blood volumes vary by degree. Minor deficiencies
may result in a fall in the hematocrit or urine output. Pathologic over-transfusion
requires phlebotomy, while pathologic under-transfusion requires blood
or volume replacement.
In 1993, Kinmond and her colleagues noted that heterologous blood transfusion may be virtually avoided in preemies of 27 to 33 weeks by lowering the child 20 cm below the placenta for 30 seconds before clamping the cord. This gravity-enhanced method of placental transfusion produced healthier babies needing fewer blood draws and no heterologous transfusions.8
Kinmond et al. found no increased jaundice, plethora, hyperviscosity, or polycythemia using this method. Yet fear of late clamping persists because physicians have been conditioned to believe that these complications are caused by placental over-transfusion. Cord stripping has become tantamount to malpractice.
The prevailing view is that early clamping produces a correct blood
volume and prevents a pathologically high blood volume, if this view were
accurate, however, neonatal transfusion would be less common than it is.
Because placental transfusion patterns vary widely, it is futile to
attempt to give the newborn the "right" amount of blood by Clamping at
a set time after birth. However, it is extremely likely that the infant
will have less-than-optimal blood volume if the cord is clamped before
the lungs are ventilated.
Polycythemia (hematocrit >65%) is often produced by late clamping. Hemoconcentration normally follows placental transfusion. It also occurs during normal labor. Serum albumin and colloid osmotic pressure (COP) rise with the hematocrit. Pulmonary function requires a COP high enough to prevent pulmonary edema. At elective cesarean section with rapid cord clamping, this COP increase does not occur. Not surprisingly, wet lungs occasionally result.
Oligohydramnios results in vein compression, causing increased capillary pressure in the placenta, which leads to fluid loss, dehydration, and hemoconcentration. Amnioinfusion may correct this; otherwise, rapid fluid replacement at birth is needed to amend this pathologic polycythemia.
The multifaceted (and uncertain) hyperviscosity syndrome11-13 is based on the premise that increased viscosity (high hematocrit) results in decreased tissue perfusion.2,11 However, factors other than viscosity also affect tissue perfusion.
According to Poiseuille's law, the blood flow through vessels (liquid flow through tubes) is inversely proportional to the length of the tube and the viscosity of the liquid, and directly proportional to the pressure differential and to the fourth power of the radius of the tube. Therefore, if the radius is reduced from 3 to 2, flow is reduced 81:16, or by four-fifths; whereas, if viscosity is increased from 2 to 3, flow is reduced 1/2:1/3, or by one-sixth. Clearly, vasoconstriction reduces blood flow much more than a similar change in viscosity.
In clinical practice, late clamping produces a high hematocrit, 2, 9,14,15 high blood pressure, and vasodilatation to accommodate the large volume of blood.9,16 These latter two factors should increase tissue perfusion. In searching the literature, I was unable to find any documented case of hyperviscosity syndrome in which the cord was clamped late," although I did find many documented cases of late clamping involving normal newborns with high hematocrits. 2,9,15,17,18
There are, however, many documented cases of hyperviscosity syndrome
with high hematocrits (e.g., cases involving gestational diabetes or postmaturity)
in which the cord was clamped before physiologic cord closure, thus creating
low blood volume, low blood pressure,16 and vasoconstriction coupled with
the polycythemia.11 The inadequate tissue perfusion is blamed on the high
hematocrit, when the root cause of the hyperviscosity syndrome is hypovolemic
vasoconstriction enforced to the fourth power.
The usual treatment of the infant with an Apgar score of 0 is immediate cord clamping, ventilation, and administration of CPR, intracardiac adrenaline, and plasma volume expansion. A more logical approach would be to strip in all available cord blood. A strong stimulus for cardiac systole is cardiac distention, and oxygenated blood is the ideal fluid. I have seen human plasma protein fraction restart a heart minutes after birth with the child surviving well.
When the infant has an Apgar score of 1 or 2 (cord pulsating), rapid placental transfusion is better accomplished by gravity. Stripping may be of benefit but occludes the arteries and interrupts placental oxygenation. A cord beating at a vigorous 120 bpm while child is in the uterus does not indicate distress. With an apneic infant outside the uterus, there is no reason to clamp such a cord; placental respiration is functioning well. However, pulmonary resuscitation on site obviously should be prompt.
In some cases of extreme fetal distress (e.g., severe oligohydramnios),
when general fetoplacental vasoconstriction has effectively emptied the
placenta and cord vessels, the cord at birth is visibly bloodless.
With neither placental function nor placental transfusion available, immediate
clamping is indicated for rapid fluid replacement.
The problem may be largely avoided by resuscitating the child with the placental circulation intact.9 This maintains newborn placental oxygenation and provides blood volume to establish pulmonary circulation. If need be, a cord pH sample may be obtained without clamping by inserting a fine, sterile needle into a pulsating cord artery.
The newborns at high risk from a lack of placental transfusion are:
Premature babies. Multiple studies of premature births have noted the correlation between infant respiratory distress syndrome and low blood volume or low red cell mass. 2,8,9,15,19,20,23,24
Infants delivered by cesarean section. Such children seldom receive transfusions resulting from the uterus squeezing the placenta. Blood loss into the placenta due to gravity is common.9,21,25 The increased incidence of infant respiratory distress syndrome in C-section babies was eliminated when a full placental transfusion was given.9,21
Compromised newborns. Cord compression in utero results in fetal hypoxia and fetal hypovolemia, with oxygenated blood being pooled in the placenta.22,26,27 At birth, the asphyxiated child is typically ashen and limp. The logical way to resuscitate such newborns is to allow the massive placental transfusion of oxygenated blood to proceed while the airway is cleared and the lungs ventilated. Every effort should be made to reduce rather than clamp a cord around the neck." A normal blood volume at birth should aid recovery of a compromised child. ~~~~~~~~~~ (insert) Clamp the cord with good reasonÖ The vast research literature on placental transfusion recognizes no physiologic norm and has few controls and no standard definitions. Groups of newborns clamped at varying times after birth are averaged and compared. The conclusions (e.g., 60% of the transfusion occurs within the first 30 to 60 seconds before clamping is said to avoid over transfusion. Contradictions abound, as the following cases illustrate.
A child who cries when the head is delivered may achieve an optimal blood volume even if the cord is clamped at birth. The uterine contraction that delivers the infant may deliver a massive placental transfusion into the child at the same time.
Conversely, an apneic child delivered by c/s and held 20 cm above the flaccid uterus may suffer massive gravitational hemorrhaging into its placenta. The blood loss is made permanent at 30 seconds by the clinician adhering to the "average."
Individual newborns cannot be treated on the basis of what appears to happen to the average child. Only one paper defended third stage cord physiology.1 Understanding what is normal is essential for diagnosing and correcting abnormal neonatal blood volumes.
~~ References: 1. Gunther M. The transfer of blood between baby and placenta in the minutes after birth. Lancet 1975;I:1277-1280 ~~~~~~~~~~~~~~~~ Conclusion
Normal blood volume is not produced by a cord clamp. The newborn and placenta reach physiologic, hemodynamic equilibrium without interference, The placental transfusion is massive, silent, and invisible, but as normal and physiologic as is crying at birth. An adequate blood volume is needed to perfuse the lungs, gut, kidneys, and skin that replace the placenta's respiratory, alimentary, excretory, and thermal functions. During the third stage of labor, a large portion of placental blood is shifted to these organs, While the normal, term child tolerates immediate clamping, lack of placental transfusion increases morbidity in "at risk" births. Many neonatal morbidities such as the hyperviscosity syndrome, infant respiratory distress syndrome, anemia, and hypovolemia correlate with early clamping. To avoid injury in all deliveries, especially those of neonates at risk, the cord should not be clamped until placental transfusion is complete.
REFERENCES, [NOTE - Many of these are older studies. It seems that interest in supporting resuscitation with the cord intact declined as obstetricians stopped providing care for the baby and neonatal teams took over newborn resuscitation. Even though the studies are older, you can still go to the citation page and follow the link to "Related Articles." It's interesting to note that more recent research has followed on the heels of this article. This is doctors improve obstetrics for mothers and babies! ]
1. American College of Obstetricians and Gynecologists. Umbilical Artery Blood Acid-Base Analysis. Washington, D.C.: ACOG; 1995. Educational bulletin 216.
2. Linderkamp O. Placental transfusion: determinants and effects. Clinics in Perinatology 1982;9:559-592.
3. Gunther M. The transfer of blood between baby and placenta in the minutes after birth, Lancer 1957;i:1277-1280.
4. Yao AC, Lind J. Effect of gravity on placental transfusion. Lancet 1969;ii:505-508.
5. Botha MC. The management of the umbilical cord in labour. S.A. J Obstet Gynecol 1968,August:30-33
6. Philip GS, Teng SS. Role of respiration in effecting placental transfusion at cesarean section Biol Neonate 1977;31:219-224.
7. Darwin E. Zoonomia. Vol III 3rd ed London, 1801:302.
8, Kinmond S, et al. Umbilical cord clamping and preterm infants: a randomized trial, BMJ 1993;306:172175.
9. Peltonen T. Placental transfusion-advantage and disadvantage. EurJ Pediatr 198 1; 137 141-146,
10. Saigal S, Usher RH Symptomatic neonatal plethora. Biol Neonate 1977;32:62-72.
11. Mentzer W. Polycythemia and the hyperviscosity syndrome in newborn infants. Clinics in Haematology 1978;7(1):63-74.
12. Oh W. Neonatal polycythemia and hyperviscosity. Pediatric Clinics in North America 1986;33:523-532.
13. Weinburger MM, Oleinick A. Neonatal polycythemia, Clinical Research 1971;29:209.
14. Usher R, Shephard M, Lind J. Blood volume in the newborn infant and placental transfusion. Acta Paediatr Scand 1963; 52:497-512,
15. Moss AJ, Monset-Couchard M. Placental transfusion: early versus late clamping of the umbilical cord Pediatrics 1967;40(1):109-126.
16. Arcilla RA, Oh W, Lind J, et al. Portal and atrial pressures in the newborn period. Acta Paediatr Scand 1966;55:615-625
17. Nelle M, et al. The effect of Leboyer delivery on blood viscosity and other herriorrheologic parameters in term neonates. A m J Obstet Gynecol 1993; 169(1):189-193
18 Linderkamp 0, et al. The effect of early and late clamping on blood viscosity and other hemorrheologic parameters in full-term neonates, Acta Paediatr Scand 1992;81(10):745-750.
19. Inall JA, Bluhm MM, et al. Blood volume and hematocrit studies in respiratory distress syndrome of the newborn. Arch Dis Childb 1965;40:480-484.
20. Brown EG, Krouskop RW, McDonnell FE. Blood volume and blood pressure in infants with respiratory distress. J Pediatrics 1975;87(6):1133-1138,
21. Landau DB. Hyaline membrane formation in the newborn: hematogenic shock as a possible etiologic factor, Missouri Med 1953;50:183.
22. Faxelius G, Raye J, et al. Red cell volume measurements and acute blood loss in high-risk infants. Pediatrics 1977;90(2):273-281,
23. Usher R, Saigal S, O'Neill A, Surainder Y, Chua L. Estimation of red blood cell volume in premature infants with and without respiratory distress syndrome. Biol Neonate 1975;26:241-248.
24. Linderkamp 0, et al. Association of neonatal respiratory distress with birth asphyxia and deficiency of red cell mass in premature infants. Eur J Pediatr 1978; 129:167-173
25. Yao AC, Wist A, Lind J. The blood volume of the newborn infant delivered by caesarean section. Acta Paediatr Scand 1967;56:585-592.
26. Linderkamp 0, Versmold HT, et al. The effect of intra-partum asphyxia on placental transfusion in premature and full-term infants. Eur J Pediatr 1978; 127:91-99.
27. Cashmore J, Usher RH. Hypovolemia resulting from a tight nuchal cord at birth, Pediatr Res 1973;7:339
|About the Midwife Archives / Midwife Archives Disclaimer|