The timing of birth has major consequences for a baby. Too early or too late can mean the difference between life and death. Or so we have come to believe; and it’s undoubtedly true at the extreme ends of preterm and postterm birth dates. Although few babies are born at these extremes of the normal length of pregnancy, much of our prenatal care is based on bringing babies to birth “in a timely fashion”—neither too early nor too late. But our understanding of “timely” is clouded, and some of our methods are self-defeating. By intervening in the natural timing of birth, we sometimes exacerbate the problems or create entirely new ones.
Normal human pregnancy is approximately 280 days, with a variation of about three weeks. There may be reason for concern if labor has not begun weeks after the due date, since placental function begins to slow after some point in gestation. Placental insufficiency can lead to poor fetal growth and, eventually, damage to the baby’s organ systems or even stillbirth. This is rare, but it is not necessarily connected to the calendar. The placenta can begin to fail at any point in pregnancy, and part of good prenatal care is monitoring growth and fluid levels so we can act before the baby’s reserves are drained. We induce labor—even advise a cesarean without labor—if the baby is in trouble, regardless of due dates. It is obvious that a baby is “better off out than in” if the placenta can no longer nourish him/her or if the uterus has become a dangerous place.
But induction of labor causes so many problems that it should be a rarity, performed only when the benefits can be proven to outweigh the risks. Induction multiplies the risk of cesarean section, forceps-assisted delivery, shoulder dystocia, hemorrhage, fetal distress and meconium aspiration. It is a major contributor to birth-related expenses and complications in the US. Yet it is so common that we almost think of it as normal. More than a third of American women were induced in 1999, and another third had labors augmented with Pitocin. (The FDA says that this is the lowest estimate and that the true incidence of induction is “widely under-reported.”)
Even with early pregnancy tests and ultrasounds, induction of labor remains one of the largest causes of prematurity. Ultrasonic estimation of gestational age is still an inexact science; the range of error increases as pregnancy advances. Artifact and technician inexperience can multiply the inaccuracy. Many practitioners seem unaware of this error range or, alternatively, are unwilling to second guess a due date “confirmed” by ultrasound, even when the woman’s history and clinical assessment indicate a later due date. Hence, the woman may be induced, even though the baby is clearly several weeks early. Some people discount the danger of early induction as long as the baby is within the last month of gestation. But even minor degrees of prematurity can cause harm. Babies born before full maturity can suffer from breathing difficulties or transient tachypnea, requiring separation in the hospital. They may be more prone to meconium aspiration. They are at risk for hypoglycemia and may have trouble maintaining body temperature. They are at increased risk for nursing difficulties and feeding disorders. They suffer from colic and digestive disturbances. These “minor problems” can affect the early bonding experience and make family adjustments more difficult. The incidence of child abuse is higher with “difficult” babies. As midwives we should aim for our families to experience the best emotional as well as physical health possible. A timely birth is a good step in this direction!
Preterm birth is rising in the United States. Some of this rise results from misjudged due dates and the fear of postdates pregnancy. Some reason that the risk of inducing an early baby is lower than the risk of allowing a pregnancy to continue past due, even when the due date is uncertain. This might be true if the perceived risk of postdates matched the actual risk. But it doesn’t!
Postdates, by itself, is not associated with poor pregnancy outcome. Extreme postdates or postdates in conjunction with poor fetal growth or developmental abnormalities does 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”—seems to come from one study based on data collected in 1958.(1)
The first question one should ask is whether neonatal mortality statistics from the 1950s 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 postdates 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 the stillbirth rate. One retrospective study of almost 1800 postterm (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 postterm and 0.75/1000 in the on-time 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 Post-term Pregnancy Trial Group (Hannah) of 1700 postdates 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, postterm 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 postdates 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 ‘at-risk’ 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 that 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.
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 prepregnancy 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!
Bacterial Vaginosis (BV) has been associated with a two to three times increased rate of preterm labor and delivery, urinary tract infections (UTIs), premature rupture of the membranes (PROM) and endometritis.(10) Because about 50% of women show no symptoms, universal screening for BV was proposed over a decade ago. (Screening and treatment is a current World Health Organization recommendation.) Screening is simple and there are several effective prescription treatments. But BV has a tendency to recur and is sometimes resistant to chemical treatment.
However, women may be able to discourage BV with some simple home methods. Numerous studies have shown that when natural vaginal Lactobacilli levels drop, BV invades. Lactobacilli inhibit the growth of Mobiluncus, Gardnerella vaginalis, Bacteroides and anaerobic cocci even in a petri dish.(11) Colonizing (or recolonizing) with Lactobacilli is key to vaginal health. According to Skarin and Sylwan, “The paucity of vaginal Lactobacillus is pivotal in allowing overgrowth of many other organisms of the vagina.”(12) Lactobacilli grow best in an acidic environment. A healthy vagina is acidic and naturally resists infection by “bad” bacteria—including strep.
In fact, pH alone—the acid/alkaline level measured by nitrazine or litmus paper—is a marker for prematurity risk. Retrospective and prospective studies show that high vaginal pH (a low acid, or alkaline, state) is predictive of preterm labor and preterm rupture of membranes. Viehweg, et al. state: “Measurements of the vaginal pH value are able to verify an alkalinization of the vagina caused by atypical vaginal flora…. In contrast to normal pregnancies there is a relation between a pathological pH value > 4.5 and consequent preterm birth in pregnancies with preterm labor.”(13) In the Multicenter Bacterial Vaginosis (BV) Trial—a prospective study—21,554 women were screened for vaginal pH and outcome. Women with a vaginal pH of 5.0 or greater had a significantly increased risk of preterm birth and/or low birth weight.(14)
Several alkaline organisms other than Gardnerella (BV) are implicated in PROM. Women with high levels of these alkaline-producing bacteria had over 300% increase in rate of PROM. In an article on pPROM, Ernest, et al. note: “Numerous infectious organisms that change the normal vaginal milieu have been associated with preterm PROM. Because these organisms alter vaginal pH, the use of pH was evaluated as a potential marker for women at increased risk for preterm PROM…. Those with a mean vaginal pH above 4.5 had a threefold increased risk of preterm PROM as compared with those with a mean pH of 4.5 or lower.”(15)
Testing pH level is simple, fast, inexpensive and non-intrusive. Women can do it themselves by touching a strip of nitrazine paper to their vaginal walls. Nitrazine or litmus paper is available in most drug stores. The urine test strips used by most midwives also assess pH.
Cultivating Good Bacteria
How can a woman GET an acidic vagina? The old time vinegar douche is an acidic wash and effective treatment for BV and yeast. Vinegar’s mild cleansing action is stronger against undesirable bacteria than against Lactobacilli, and it has a short residual effect, which helps encourage rapid regrowth of Lactobacilli. (In pregnancy, a woman should seek her caregiver’s advice and use only a low-pressure, low-level douche.)
An infusion of two tablespoons of hydrogen peroxide kills BV and helps Lactobacilli colonize. But recent research shows that Lactobacilli themselves are the source of most of the acid produced in a healthy vagina! They create their own optimum growth pH. “Lactobacilli bacteria, not epithelial cells, are the primary source of lactic acid in the vagina,” according to an article in Human Reproduction (16)
So… a woman can get an acidic vagina by GROWING the Lactobacilli. How? By planting them—just like any good gardener!
Researchers are working on a two-pronged approach to using Lactobacilli as a natural antibiotic. Some are trying to analyze, isolate and replicate the effective ingredient, while others are working on methods to establish optimum vaginal growth. Pharmaceutical companies want to create a Lactobacilli super pill, but I think we women should do our own home gardening!
Many methods have been advised for colonizing the vagina directly. Wearing a tampon soaked in yogurt is an old folk remedy used for yeast infections (it works!). The yogurt can be used like a cream or gently squeezed in with a bulb syringe.
Many strains of Lactobacilli exist. You can purchase acidophilus compounds and special “probiotics” at some pharmacies and most health food stores. But good yogurt contains live cultures, is readily available, inexpensive and proven to be effective. In the Tasdemir study, pregnant women with bacterial vaginosis were treated with commercial yogurt. The yogurt was administered daily with a 10-ml syringe for seven days and then was repeated after a one-week interval. All the women showed clinical improvement on the third day of treatment. A month after the second treatment, 90% of the women had no signs or symptoms of bacterial vaginosis. The researchers concluded: “Commercially available yogurt may restore the microenvironment and pH of the vagina,” cure BV and “prevent prematurity.”(17)
In another study, from Japan, women with BV were treated with intravaginal application of 5 ml of commercial yogurt. In the initial cultures, 29 strains of bacteria were detected. The women were evaluated and recultured three days later. There was significant decrease in discharge and vaginal redness, and the vaginal pH was lowered significantly (acidified). All 14 strains of Gram-negative bacteria disappeared! The researchers concluded that “the Lactobacillus therapy was effective in both clinical and bacteriological responses.”(18) In other words, improvement occurred in both the SYMPTOMS and the cultures.
But yogurt doesn’t need to be planted directly into the vagina, in order to grow there. Several studies have shown that simply EATING it will result in increased vaginal Lactobacilli! The Lactobacilli colonize the intestinal tract and migrate to the vagina and urinary tract system. (Urinary tract infections are also risk factors for preterm labor and newborn infections.) Researchers say: “The instillation of Lactobacillus GR-1 and B-54 or RC-14 strains into the vagina has been shown to reduce the risk of urinary tract infections and improve the maintenance of a normal flora. Ingestion of these strains into the gut has also been shown to modify the vaginal flora to a more healthy state. In addition, these strains inhibit the growth of intestinal, as well as urogenital, pathogens, colonize the gut and protect against infections.”(19)
In one study, ten women with a history of BV, yeast and urinary infections, drank a Lactobacilli solution in milk twice daily. The Lactobacilli were molecularly typed for identity. One week later, the researchers were able to culture the tagged Lactobacilli from the vaginas of every participant. (And six of the cases of BV were resolved within the week). This is one of several studies that have proved that the oral route can seed the vagina.(20)
Of course, the quality of the yogurt is crucial. If it doesn’t contain live cultures, it’s useless! Make sure it’s really yogurt and not simply a form of milk pudding!
These once-alternative ideas have become mainstream. The American Journal of Obstetrics and Gynecology published an article in March 2003 stating, “Certain Lactobacilli strains can safely colonize the vagina after oral and vaginal administration, displace and kill pathogens including Gardnerella vaginalis and Escherichia coli and modulate the immune response to interfere with the inflammatory cascade that leads to Pre-term Birth.”(21)
In sum, cultivating a healthy vaginal “floriculture” can reduce the incidence of preterm birth and lower the rate of bladder infection and UTIs.(22) A healthy colony of Lactobacilli guards the mother and baby against yeast and E. coli infections.(23) It also may offer protection against Group B Strep. Adding live-culture yogurt to the diet—or treating with “probiotics”—is an effective natural method to treat subclinical vaginal infections. It can also treat intestinal infections, which may trigger preterm birth. I agree with the conclusion of these researchers: “The lack of systemic side effects makes it a drug of choice in the treatment of pregnant women.”
No magic pill exists to assure a timely birth—a baby born at its healthiest point in gestation, neither too soon nor too late. Born ready to breathe, eager to nurse, primed to learn and love. Good health, good nutrition, good living habits and the avoidance of stress go far to ensure the baby will thrive until his birth date. As we learn more about normal pregnancy, we gain new tools to help both mother and baby achieve optimum health. This new research may help tip the balance in favor of better health—and a timely birth.
- 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.
- Eden, R.D., et al. 1987. Perinatal characteristics of uncomplicated postdates pregnancies. Obstet Gynecol 69(3 Pt.1): 296–99.
- Weinstein, D., et al. 1996 Sep–Oct. Expectant management of post-term patients: observations and outcome. J Matern Fetal Med 5(5): 293–97.
- 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
- 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.
- Newman, B., et al. 2001 Feb. Occupational fatigue and preterm rupture of membranes. Am J Obstet Gynecol 184(3): 438–46. PMID: 11228500
- 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.
- 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
- Zhang, C., et al. 2002 Jul. Vitamin C and the risk of preeclampsia. Epidemiology 13(4):409–16. PMID: 12094095.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- Chimura, T., et al. 1995 Mar. [Ecological treatment of bacterial vaginosis]. Jpn J Antibiot 48(3): 432–36. PMID: 7752457. Japanese.
- Reid, G., and J. Burton. 2002 Mar. Use of Lactobacillus to prevent infection by pathogenic bacteria. Microbes Infect 4(3): 319–24. PMID: 11909742.
- Reid, G., et al. 2001 Feb. Oral probiotics can resolve urogenital infections. FEMS Immunol Med Microbiol 30(1): 49–52. PMID: 11172991.
- 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.
- Reid, G., and J. Burton. op cite.
- Andreeva, P., and A. Dimitrov. 2002. [The probiotic Lactobacillus acidophilus—an alternative treatment of bacterial vaginosis]. Akush Ginekol (Sofia) 41(6): 29–31. Bulgarian.