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Jun
01

A Timely Birth: Part 2

Author // Gail Hart

Postdates alone are not associated with poor pregnancy outcome. Extreme postdates or postdates in conjunction with poor fetal growth or developmental abnormalities do show an increased risk of stillbirth. But if growth restriction and birth defects are removed, there is no statistical increase in risk until a pregnancy reaches 42 weeks and no significant risk until past 43 weeks. The primary “evidence” of a sharp rise in stillbirth after 40 weeks—often misquoted as “double at 42 weeks and triple at 43 weeks”—seem to come from one study based on data collected in 1958.(1)


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The first question one should ask is whether neonatal mortality statistics from the 1950’s should be compared to modern statistics, since labor anesthetics and forceps rates were very different. Early labor monitoring was scanty and prenatal monitoring not yet developed. The McClure-Brown report shows a rise in stillbirth from 10/1000 at 40 weeks to about 18/1000 at 42 weeks. Yes, that is nearly double. But think about those numbers. Even the beginning point is nearly ten times the modern mortality rate. Either modern delivery methods are vastly different or something is wrong with the data collection. This study should be updated by research conducted at least in this century! Modern statistics show an almost flat rate of stillbirth from 40 weeks to 42, with a slight rise at 43 weeks (all numbers being close to 1/1000).(2)

There is a creeping overreaction in dealing with postdate pregnancies. It is true that the stillbirth and fetal distress rates rise more sharply after 43 weeks, but it is also true that less than ten percent of babies born at 43 weeks suffer from postmaturity syndrome (over 90% show no signs). We should react to this rise by monitoring postdate pregnancies carefully and inducing if problems arise. But the rise in problems at 43 weeks does not imply a similar risk at 42 and 41 weeks. Postmaturity syndrome is a continuum. It becomes more likely as weeks progress past the due date but does not start on the due date. And the risks need to be compared to the risks of interventions. Induction, as already noted, is not risk free. In addition to the risks of prematurity, induced labors have higher rates of cesarean section, uterine rupture, cord prolapse, meconium aspiration, fetal distress, neonatal jaundice, maternal hemorrhage and even the rare but disastrous amniotic fluid embolism.

Large studies have shown that monitoring pregnancy while waiting for spontaneous labor results in fewer cesareans without any rise in stillbirth rate. One retrospective study of almost 1800 post term (past 42 weeks) pregnancies with reliable dates compared this group with a matched group delivering “on time” (between 37 and 41 weeks). The perinatal mortality was similar in both groups (0.56/1000 in the post term and 0.75/1000 in the on-times group). The rates of meconium, shoulder dystocia and cesarean were almost identical. The rates of fetal distress, instrumental delivery and low Apgar were actually lower in the postdate group than in the on-time group.(3) This is only one of several studies showing postdate pregnancies can be monitored safely until delivery or until indications arise for induction. Even the famous Canadian Multicenter Postterm Pregnancy Trial Group (Hannah) of 1700 postdate women showed no difference in perinatal outcome among women who were monitored past their due date, as compared with those who were induced at term.(4)

In some studies, post term births have shown a higher cesarean rate for suspected fetal distress. However, when a group of researchers conducted a case-matched review of nearly 300 postdate pregnancies, they concluded that the increased rate of obstetric and neonatal interventions “does not appear to be a result of underlying pathology associated with post-term pregnancy.” They suggest that “a lower threshold for clinical intervention in pregnancies perceived to be ‘atrisk’ may be a significant contributing factor.” In other words, the perceived risk is greater than the actual risk and can become a self-fulfilling prophecy!(5) When monitoring demonstrates the fetal growth, activity and amniotic fluid levels remain within expected norms, the baby can safely wait for spontaneous labor to begin. Spontaneous labor gives the greatest chance for vaginal birth, even though the baby may be slightly larger than if the mother were induced at 40 weeks.


Preventing Prematurity

Few medical treatments have been proven to truly prevent preterm birth. (Avoiding iatrogenic prematurity is most effective, of course!) Some of the most promising avenues are readily available to midwives, and we should share this research with our clients.

The following are some factors shown to be associated with preterm birth and some strategies for lowering the risks:

Overwork, job fatigue, stress Women in high-stress jobs or who work long hours on their feet have nearly three times the risk of preterm rupture of membranes leading to preterm birth. In a study of 3000 primips, those who worked in “high fatigue jobs” had a risk of preterm premature rupture of membranes (pPROM) of 7% compared to 2% for those who didn’t work outside the home.(6) Although many women must work until the end of pregnancy, changing to less fatiguing jobs, if possible, will lower their risk of preterm birth.

Poor nutrition in pregnancy, low weight gain Low maternal weight gain is the single risk factor that crosses all racial and economic indicators. A woman with a low pregnancy weight and/or a low rate of gain before 20 weeks is at high risk for preterm birth. A balance of protein and carbohydrates provides the best nutrition. According to the Cochrane Database, restricted carbohydrate diets may raise the risk of preterm birth without having any effect on the incidence of macrosomia.

Vitamin C supplements Low levels of vitamin C have been implicated for several decades as contributors to prematurity and preterm rupture of membranes.(7) In a study of 2064 pregnant women, those who had total vitamin C intakes of <10th percentile of the average intake prior to conception had twice the risk of preterm birth due to preterm rupture of membranes (relative risk, 2.2).(8)

Low levels of vitamin C may also be implicated in the risk of preeclampsia, which leads to preterm birth, as well as, frequently, induced labor. Researchers tested women for plasma vitamin C levels. Women who consumed less than 85 mg of vitamin C doubled their risk of developing preeclampsia (odds ration 2.1). Women who consumed the lowest amounts had almost four times the risk of those who consumed the highest.(9)

It is theorized that oxidative stress plays a role in preeclampsia, and we are learning that optimum levels of vitamin C protect against oxidative stress. We don’t know yet the optimum level of vitamin C or the best recommendation for supplements, but it has been proposed that 300 mg to 500 mg is probably needed. Many American women consume less than 85 mg daily!

Excerpted from A Timely Birth by Gail Hart, Midwifery Today, Issue 72.

Copyright © 2004 Midwifery Today, Inc. All rights reserved. Reprinted with permission from Midwifery Today, Winter 2004, Number 72.

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References:

  1. McClure-Browne, J.C. 1963. Comparison of perinatal mortality rates versus gestational age through the past three decades. Postmaturity, Am J Obstet Gynecol 85: 573–82.
  2. Eden, R.D., et al. 1987. Perinatal characteristics of uncomplicated postdates pregnancies. Obstet Gynecol 69(3 Pt.1): 296–99.
  3. Weinstein, D., et al. 1996 Sep–Oct. Expectant management of post-term patients: observations and outcome. J Matern Fetal Med 5(5): 293–97.
  4. Hannah, M.E., et al. 1992 Jun 11. Induction of labor as compared with serial antenatal monitoring in post-term pregnancy. A randomized controlled trial. The Canadian Multicenter Post-term Pregnancy Trial Group. N Engl J Med 326(24): 1587–92. PMID: 1584259
  5. Luckas, M., et al. 1998. Comparison of outcomes in uncomplicated term and post-term pregnancy following spontaneous labor. J Perinat Med 26(6): 475–79. PMID: 10224605.
  6. Newman, B., et al. 2001 Feb. Occupational fatigue and preterm rupture of membranes. Am J Obstet Gynecol 184(3): 438–46. PMID: 11228500
  7. Woods, J.R., Jr., et al. 2001 Jul. Vitamins C and E: Missing links in preventing preterm premature rupture of membranes? Am J Obstet Gynecol 185(1): 5–10. PMID: 11483896.
  8. Siega-Riz, A.M., et al. 2003 Aug. Vitamin C intake and the risk of preterm delivery. Am J Obstet Gynecol 189(2): 519–25. PMID: 14520228
  9. Zhang, C., et al. 2002 Jul. Vitamin C and the risk of preeclampsia. Epidemiology 13(4):409–16. PMID: 12094095.
  10. McCoy, M.C., et al. 1995 Jun. Bacterial vaginosis in pregnancy: an approach for the 1990s. Obstet Gynecol Surv 50(6): 482–88.
    McGregor, J.A., and J.I. French. 2000 May. Bacterial vaginosis in pregnancy. Obstet Gynecol Surv 5(5 Suppl 1): S1–19.
  11. Skarin, A., and J. Sylwan. 1986 Dec. Vaginal Lactobacilli inhibiting growth of Gardnerella vaginalis, Mobiluncus and other bacterial species cultured from vaginal content of women with bacterial vaginosis. Acta Pathol Microbiol Immunol Scand [B]. 94(6): 399–403.
  12. Ibid.
  13. Viehweg, B., et al. 1997. [Usefulness of vaginal pH measurements in the identification of potential preterm births]. Zentralbl Gynakol 119 Suppl 1: 33–37. PMID: 9245123. German.
  14. Hauth, J.C., et al. 2003 Mar. Early pregnancy threshold vaginal pH and Gram stain scores predictive of subsequent preterm birth in asymptomatic women. Am J Obstet Gynecol 188(3): 831–35. PMID: 12634666.
  15. Ernest, J.M., et al. 1989 Nov. Vaginal pH: a marker of preterm premature rupture of the membranes. Obstet Gynecol 74(5): 734–38. PMID: 2812649.
  16. Boskey, E.R., et al. 2001 Sep. Origins of vaginal acidity: high D/L lactate ratio is consistent with bacteria being the primary source. Hum Reprod, 16(9): 1809–13.
  17. Tasdemir, M., et al. 1996. Alternative treatment for bacterial vaginosis in pregnant patients; restoration of vaginal acidity and flora. Arch AIDS Res 10(4): 239–41. PMID: 12347751.
  18. Chimura, T., et al. 1995 Mar. [Ecological treatment of bacterial vaginosis]. Jpn J Antibiot 48(3): 432–36. PMID: 7752457. Japanese.
  19. Reid, G., and J. Burton. 2002 Mar. Use of Lactobacillus to prevent infection by pathogenic bacteria. Microbes Infect 4(3): 319–24. PMID: 11909742.
  20. Reid, G., et al. 2001 Feb. Oral probiotics can resolve urogenital infections. FEMS Immunol Med Microbiol 30(1): 49–52. PMID: 11172991.
  21. Reid, G., and A. Bocking. 2003 Oct. The potential for probiotics to prevent bacterial vaginosis and preterm labor. Am J Obstet Gynecol 189(4): 1202–28.
    See also Elmer, G.W., et al. 1996 Mar 20. Biotherapeutic agents. A neglected modality for the treatment and prevention of selected intestinal and vaginal infections. JAMA 275(11): 870–76.
  22. Reid, G., and J. Burton. op cite.
  23. Andreeva, P., and A. Dimitrov. 2002. [The probiotic Lactobacillus acidophilus—an alternative treatment of bacterial vaginosis]. Akush Ginekol (Sofia) 41(6): 29–31. Bulgarian.



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