Well, most things in life are multifactorial.

I met with Dr. Green, a maternal-fetal medicine (MFM) specialist, Monday morning to discuss the possible reasons for Peter’s premature delivery and to make a plan help ensure that my future pregnancies make it into the third trimester.

Unfortunately, there are no simple answers.  Doctors don’t fully understand what causes labor at term, much less what causes preterm labor.  I often think it’s a miracle that so many babies are born in the narrow window of 39-41 weeks’ gestation.  Peter’s delivery at 27 weeks seemed so random, so fast, so unexpected.

There are several reasons I may have gone into labor early.  Most likely, the malformation of my uterus played a big roll.  Peter was stuck in the left half of my uterus with his head under my rib cage and feet down near my cervix.  He didn’t have room to swim and somersault like other fetuses, and as a result, he had a very short, hypocoiled umbilical cord when he was born.

The MFM specialist also mentioned that the loss of Peter’s twin at 9 weeks may have contributed to my preterm labor.  I have difficulty believing that, though.  I did not miscarry naturally when Hugh passed away in August 2008.    Why would Peter’s twin precipitate labor 19 weeks after his or her demise?  By that point, the twin was an insignificant relict left over from the first trimester.

Perhaps the summer heat contributed to the preterm labor, perhaps I should have been on pelvic rest.  Perhaps the chemicals I worked with while I was in graduate school at MIT complicated my pregnancy, perhaps the D&C I had in 2008 injured my cervix.  Perhaps the phase of the moon or the price of rice in Vietnam precipitated my labor.  I suppose we’ll never know for sure.  For the medical record, Dr. Green listed the cause of my preterm labor as “multifactorial” and supported my plan to get a formal diagnosis for my Mullerian anomaly.

The plan for my next pregnancy includes injections of 17-alpha-hydroxyprogesterone caproate (17P) to help prevent preterm labor, frequent ultrasounds to check the length of my cervix during the second trimester, and betamethasone or dexamethasone injections to assist fetal lung maturation at the first sign of cervical change.  Dr. Green did not recommend prophylactic placement of a cerclage, as my story does not fit the classic definition of cervical incompetence.

Notably, tocolytic agents were not included in the plan outlined by Dr. Green.  I suppose I should have queried her more on this subject.  I mentioned my surprise that nifedipine did not hold off Peter’s delivery longer.  After my mother went into preterm labor, she was on terbutaline and bed rest for a good three weeks before her water broke and my brother had to be delivered.  Studies have shown that 61-78 % of women given tocolytics for preterm labor do not deliver within 7 days, as compared with 39 % of women given a placebo.  I only stayed pregnant 24 hours after starting nifedipine.  I’ve often wondered whether terbutaline or magnesium sulfate would have done a better job suppressing my contractions.  Studies have shown, however, that nifedipine prolongs pregnancy as effectively as other tocolytic agents and is associated with less maternal and fetal toxicity.  Terbutaline is not routinely used at UMass Memorial any longer due to side effects, leaving magnesium sulfate and nifedipine as the tocolytic workhorses.  If I find myself in preterm labor again, I’ll definitely suggest use of magnesium sulfate for the first 48 hours, despite the extremely unpleasant maternal side effects I’ve heard about – vomiting, flushing, headache, lethargy, and blurry vision.  I was underwhelmed by nifedipine’s effectiveness as a tocolytic last time around.

And with that, two things should be obvious:

1)  The causes of preterm labor are poorly understood.  More research is needed to identify women at risk for preterm labor and to understand the mechanisms that precipitate uterine contractions and cervical changes.

2)  Alternative tocolytic agents should be developed for women who, like me, don’t respond well to the currently-used first-line therapies.

That brings me to my first reason why the March of Dimes deserves your charity and support: it is funding research to address these two points.  Example research grants include:

Iain L. Buxton, PharmD, University of Nevada School of Medicine in Reno, is studying variant versions of a protein structure in uterine muscle cells to see if any of these variants are linked with preterm labor. These structures appear to help keep the uterus relaxed during pregnancy. This study could improve identification of women at high risk of premature delivery and, ultimately, allow early treatment to prevent it.

Stephen Lye, PhD, Mount Sinai Hospital, University of Toronto, Canada, is investigating how inflammatory proteins (cytokines) produced by the uterus may contribute to the chain of events that results in term or preterm labor. Because these events occur early in labor, they may be targets for new drugs to prevent preterm labor.

Sam Mesiano, PhD, Case Western Reserve University in Cleveland, Ohio, is seeking to identify genes and other factors that help trigger labor, at term or prematurely. A better understanding of biological events that normally start labor may lead to development of novel drugs to prevent premature delivery.

Jeffrey Murray, MD, University of Iowa, Iowa City, is conducting a comprehensive search of the entire human genome for gene variants that contribute to spontaneous preterm delivery. He also is seeking to identify environmental factors that may interact with such variants to cause prematurity. Identifying the complex causes of spontaneous prematurity is essential to learning how to predict it reliably and prevent it.

Kristina M. Adams Waldorf, MD, University of Washington in Seattle, is studying how uterine stretching may trigger preterm labor, as a step toward developing drug treatments to prevent stretch-induced labor. Uterine stretching appears to be an important stimulus of preterm labor in pregnancies with twins and other multiples and in pregnancies with excess amniotic fluid.

[Apologies for all the big words.  This post lived up to the name of my blog.]

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4 Responses to Well, most things in life are multifactorial.

  1. Kristine says:

    I came across your blog while searching for hypocoiled umbilical cord. I just had my 20 week ultrasound the other day and was told our little girl’s cord is straight and that she is behind in growth. I also have a bicornuate uterus and lost her twin in the first trimester as well. The high risk OB that I am seeing only briefly mentioned the cord issue and said to come back at 28 weeks. Of course Googling this brings up nothing but potentially tragic outcomes and overall I feel pretty helpless at this point. I was wondering if you had any advice, as someone who has been through several of the same issues and now has a beautiful boy. I’m so incredibly frightened about losing our baby.

    • kristinlena says:

      I’ll be praying that your little girl keeps growing. Unfortunately, I think that’s all you can do at this point in your pregnancy.

      I didn’t learn that Peter’s cord was short and hypocoiled until after he was born, but I didn’t have any detailed ultrasounds after 18 weeks. Thankfully, his weight was 75 %ile for gestation at birth, so he was not growth restricted. To be honest, I wouldn’t worry so much about the umbilical cord as about your daughter’s growth at this point. You want her to weigh at least 800 grams at birth to avoid the challenges that accompany extremely low birth weight.

      Are you certain that you have a bicornuate uterus and not a septate uterus or uterus didelphys? Misdiagnoses are common among women with Mullerian anomalies. The best methods for diagnosing uterine anomalies are hysteroscopy/laparoscopy and MRI.

  2. Cara says:

    I’ve reached a point where I’m just trying to find more information about hypocoiled umbilical cord. It was never detected by ultrasound, and unfortunately our daughter passed during labor. Thank you for your post. I sometimes wish I had the symptoms of it, but there were no signs. No preterm labor, low birth weight or signs of slow growth.

    • kristinlena says:

      So sorry for your loss, Cara. Did you get your medical records – delivery note and placental examination report? In my case, the hypocoiled umbilical cord didn’t have any direct negative consequences. That’s to say, the hypocoiled cord didn’t cause the preterm labor. I did, however, eventually come to the epiphany that the short cord was probably related to the fact that I didn’t have a third stage of labor… the force of my water breaking and the cord pulling on the placenta caused a complete placental abruption during delivery, which was why Peter was in hypovolemic shock after delivery. Luckily, we got him out and into the care of the NICU team quickly.

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