Recurrent Early Pregnancy Loss - 4 - Anatomic Causes

The next factors for recurrent early pregnancy loss we should discuss are anatomic causes, specifically, uterine abnormalities. Uterine abnormalities probably account for about 10% of the cases of recurrent early pregnancy losses. The most common ones are congenital malformations of the uterus (Mullerian abnormalities), uterine ‘neoplasms’ or ‘growths’, and iatrogenic causes (acquired damage of the uterine cavity). Common threads for the contribution of uterine abnormalities to early pregnancy loss are diminished numbers of adequate implantation sites, disruption of normal uterine blood supply, and alteration of the ‘normal’ intrauterine immune response by inflammation and in some cases infection. Let me explain …

Early in the embryonic development of the female genital tract, the uterus begins as separate structures on both side of the pelvis. In normal circumstances, as development progresses, these separate structures move to the midline and fuse, forming a single uterus, cervix and vagina. In 1 out of every 200 to 600 women, this process is interrupted during some point in the developmental process. The congenital malformations that result from this are called ‘Mullerian duct abnormalities.’ These abnormalities can range from complete lack of fusion of the Mullerian duct, resulting in two completely separate uteruses (uterus didelphys) with cervixes (and sometimes two vaginas); a partial lack of fusion, resulting in a uterus with two cavities and a single cervix (bicornuate uterus); or a uterus that has a single cavity that is divided in the midline to varying degrees by a fibromuscular wedge of tissue (septate uterus).

Under some circumstances, only one of the embryological precursors for the genital tract will develop forming a single (usually smaller) uterus (unicornate uterus) and cervix which deviates to the side of its origin. The latter are frequently associated with urinary tract abnormalities, such as an absent kidney, usually on the side which did not have normal development of the Mullerian duct. Mullerian abnormalities result in smaller uterine cavities, fewer suitable implantation sites, and aberrations of vascularization (blood supply) that may contribute to both early and later pregnancy losses. Indeed, these abnormalities are frequently also accompanied by cervical incompetence which has been addressed in other posts. One other condition associated with a small, abnormally-shaped uterine cavity and high rate of unexplained first trimester losses is seen in women who were exposed to DES (diethyl stilbesterol) in utero. Fortunately, since the last DES used in reproductive age women was given in the early 1970’s, this is quickly becoming less of a problem.

The most common neoplasms (‘tumors’) of the uterus are fibroids (leiomyomata). These are characterized by an excessive proliferation of the smooth muscle cells and connective tissues that are normally present in the muscular wall of the uterus. The cause of fibroids is unknown. They are generally ‘benign’ (not cancer) and can be located just beneath the intraabdominal surface of the uterus (subserosal fibroids), within the muscular wall (intramural fibroids), or beneath the inner lining (endometrium) of the ueterus (submucosal). At times they can project either into the abdomen or into the uterine cavity on ‘stalks’ and these are referred to as ‘pedunculated fibroids.’ Uterine fibroids can distort and/or decrease the volume of the uterine cavity, compromise implantation or growth of the placenta by stretching and thinning the endometrium or by stealing blood supply, and if located in proximity to the cervix, may distort the internal cervical opening (os) sufficiently to cause cervical incompetence as well.

Endometrial polyps result from localized overgrowth (proliferation) of the endometrium and also produce a stalked projection into the uterine cavity. Both endometrial polyps and intrauterine fibroids (pedunculated or not), in addition to causing distortion of the uterine cavity, are often sites of chronic inflammation and/or infection and this may be the means by which they contribute to early pregnancy losses. Under these circumstances they may function as a ‘natural’ analog to an intrauterine device (IUD), by preventing proper implantation or disturbing the delicate immunologic balance of early pregnancy, interrupting the growth of the developing embryo.

During our surgical care for patients, we may also induce damage to the endometrium that can lead to recurrent pregnancy loss. These are classified under the ‘iatrogenic’ causes for recurrent pregnancy loss. For example, many patients who have early pregnancy losses (or who have undergone elective termination of pregnancy in the past) will undergo dilatation and curettage (D&C) procedures to complete the evacuation of the pregnancy tissues from the uterus. If a D&C is performed too aggressively, or if an intrauterine infection is present as either the cause or the result of a pregnancy loss at the time a D&C is performed, the result can be scarring of the endometrial cavity, termed Asherman’s syndrome. At times this scarring can be so extensive (especially if infection was present at the time of the procedure), the woman will stop having periods altogether. Damage to the endometrial cavity can also result during the surgical removal of endometrial polyps or intrauterine fibroids, even when these procedures are performed through an operating scope (hysteroscopy). Again, regardless of the cause, when such damage or scarring is present, the common threads of poor implantation sites, decreased blood supply, and inflammation can raise their ugly heads to interrupt early pregnancies on a repetitive basis...

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Recurrent Early Pregnancy Loss - 3 - Chromosomal Causes

Although 50% or more of sporadic pregnancy losses in first trimester are the result of CHROMOSOMAL ABNORMALITIES, these probably account for less than 5% of recurrent early pregnancy losses. There is also usually a difference in the type of chromosomal abnormalities found under these situations. In sporadic losses, the most common causes are ‘nondisjunction events’ in the final cell division that is supposed to equally divide the chromosomal pairs and create eggs or sperm (gametes) that contain only half (23 chromosomes = 22 different ‘autosomes plus 1 ‘sex chromosome’) the normal chromosomal complement (46 chromosomes = 22 pairs of different ‘autosomes’ plus 2 ‘sex chromosomes’, one from each parent).

In nondisjunction events, a pair of chromosomes (autosomes or sex chromosomes) may stick together, resulting in one gamete (egg or sperm) with one too many (24) and one with too few (22) chromosomes. Doing the simple math, if either such gamete combines with a normal gamete containing 23 chromosomes from the other parent, the resulting embryo will have either 45 (a monosomy) or 47 (a trisomy) chromosomes. These events can occur with any of the autosomes or sex chromosomes and most result in lethal combinations of genetic material and pregnancies that are lost early in gestation. However, there are situations in which the pregnancy might survive, the best known being Down syndrome (extra number 21 chromosome), Turner’s syndrome (single X chromosome), other sex chromosomal abnormalities such as 47XXY or 47XYY, and trisomies 18 or 13. In reality, even most of these combinations are lost in first trimester, many are lost in mid or late pregnancy, and almost all trisomy 18 or 13 babies are lost shortly after birth if they manage to survive to delivery.

Chromosomal abnormalities that lead to recurrent pregnancy losses, on the other hand, are usually not monosomies or trisomies resulting from nondisjunction. Instead, they result from gametes that have either too much or too little chromosomal material as a consequence of a parent having a chromosomal ‘rearrangement.’ Under these circumstances a parent has the correct total amount of genetic material, but may have two whole chromosomes (either the same or different chromosomes) stuck together, may have a portion of one chromosome exchanged with a portion of another chromosome (balanced translocations), or have rearrangements of a portion of one chromosome within the chromosome in which that genetic material was originally located (usually these are ‘inversions’). The problem with parents who have ‘chromosomal rearrangements’ is that they have a harder time producing gametes with the correct amount of genetic material. Fortunately, most parents with balanced translocations or inversions will eventually ‘get it right’ but it may be only after many pregnancy losses. Even then, because of ‘crossing over’ events that occur during chromosomal replication, they could end up with a baby that has the ‘right number’ of chromosomes but a very small amount missing (microdeletions) or extra that can still lead to serious problems. Parents who have whole chromosomes stuck together on the other hand cannot produce normal gametes.

Diagnostic testing for parental chromosomal rearrangements is fairly simple, but expensive. It is often one of the first diagnostic tests offered to a couple with recurrent early pregnancy loss, although the yield is low because these account for such a small percentage of the problems. Ideally, both parents should be tested, but if resources are limited, it is often best to start with the mother’s chromosome studies (karyotype) since for reasons beyond the scope of this discussion, if a parental chromosomal rearrangement is the culprit, she is the more likely contributor to the problem under many circumstances. If the products of conception from an early loss have chromosome studies performed and reveal that a parental chromosome rearrangement is likely, parental karyotype testing really should be advanced in the diagnostic studies. Although nothing can be done to correct the problem, genetic counseling is warranted so that parents can be appraised of their risks and their options for a successful pregnancy.

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Recurrent Early Pregnancy Loss - 2 - Hormonal Causes

To begin our discussion of actual causes of recurrent early pregnancy loss, let’s start with the one that is probably the most commonly touted, though still the least well-understood (and to me the MOST confusing) – HORMONAL CAUSES. Now, let me also begin by saying, we will not be addressing the most severe hormonal abnormalities that lead to primary infertility problems. I will leave that discussion to the real experts in that area – the specialists in Reproductive Endocrinology. Instead, let’s focus the discussion today on more subtle abnormalities that are associated with decreased likelihood of a successful pregnancy once conception has taken place.

If you look back at my second post about the young couple who had an early pregnancy loss (technically given the unflattering terminology of a ‘missed abortion’), I asked her a series of questions upon which to direct my later discussion of potential causes. One of first issues I tried to sort out was the normalcy of her menstrual cycles in terms of regularity, timing, and bleeding. She reported that she always had regular menstrual cycles with bleeding beginning about every 28-29 days and she had had these from the age of 13 when she first started having periods. Without doing a mega workup for hormonal abnormalities, it is highly likely that she has none, if what she reported to me is true. She is probably ovulating regularly and in midcycle and the second part of the cycle, the ‘luteal phase’, is probably characterized by normal production of and response to the hormone progesterone. Progesterone is necessary for the final preparation of the uterine lining (the endometrium) to accept and nurture the early growth of the fertilized egg. On the otherhand, it is also likely that the woman who reports irregular cycles, or cycles that are unusually short or long in duration DOES have some degree of hormonal imbalance.

The simplest way of thinking about this in terms of its negative effects on a successful pregnancy is that the abnormal cycles indicate that the patient is either not ovulating at the appropriate time (around day 14, counting from the first day of the last period) or, if she is, she has inappropriate production or action (in terms of timing, amount, or effect) of the hormone progesterone that is made by the ovary (the corpus luteum at the site from which the egg was hatched) during the second half of the menstrual cycle and the early weeks of pregnancy. Unusually long cycles usually reflect a delay in ovulation and are more common in women with thyroid disorders, excess amounts of the pituitary hormone prolactin (hyperprolactinemia) from any cause, and women who have ‘polycystic ovary syndrome’ that may be accompanied by hyperandrogenemia (increased levels of male hormones), elevated levels of luteinizing hormone (LH, another pituitary hormone that stimulates androgen production in the ovary), and insulin resistance. Unusually short cycles usually indicate an inadequate progesterone effect on the endometrium (often called “luteal phase defects’) and may result from too little progesterone production or from an endometrium that is less responsive to the hormone.

In any individual, one or more of these hormonal imbalances may exist. And, regardless of the specific contribution of each to early pregnancy loss, the common thread is that they disrupt the 'window of receptivity' by impairing the successful attachment, implantation, or early growth of a fertilized egg in the endometrium. There is only a very limited period of time in its development during which the fertilized egg (at this point the ‘blastocyst’) can attach to the endometrium and if the timing is off, or the endometrial response to progesterone is inadequate, and it is not ready to receive the blastocyst, hold onto it, and allow it to invade, and grow, then the pregnancy will not be successful. Hormones can influence every step of this process by their effects on the production and types of adhesion molecules present in the endometrium (necessary for attachment), regulation of the maternal immune response (permitting and promoting trohpblastic invasion), and by the production of growth factors that facilitate invasion and differentiation of the early embryonic and placental tissues.

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Recurrent Early Pregnancy Loss - 1 - Implantation

In our last post we discussed the high frequency of early pregnancy losses in first conceptions that probably results from a naive maternal immune response to the fetal tissues; and also the high frequency of chromosomal abnormalities as the most common cause of sporadic early pregnancy losses in otherwise healthy women who have successfully carried a pregnancy. But, what about the scenario our patient had concerns about – the patient who has or is at risk for repetitive early pregnancy losses?

Although uncommon, about one out of every 100-200 women will have recurrent early losses without a successful pregnancy and another small percentage will have recurrent losses only after initially having successful outcomes (these women have been termed ‘secondary aborters’). A woman who has had one clinically recognized miscarriage is probably at no greater risk than any woman in the general population for having another (15-20%). However, if she has had two spontaneous losses in a row, the risk rises to about 35% for a third; and, if she has three consecutive losses, the risk is about 50%. Before looking at some factors that can contribute to early pregnancy loss, let’s review the ‘normal’ sequence of events that lead to a ‘successful’ pregnancy.

Under ideal circumstances, a woman with regular menstrual cycles (every 28 days) produces an egg (ovulates) around day 14 (counting from the first day of the last menstrual bleeding). The egg contains 23 ‘normal’ chromosomes and begins the trip down the fallopian tube where it becomes fertilized (ideally within less than 24 hours of being ‘hatched’) by a sperm, also containing 23 ‘normal’ chromosomes, producing a ‘fertilized’ egg, or zygote, with 46 chromosomes. Over the next two days, the zygote undergoes rapid cell divisions, entering the uterine cavity as a relatively homogeneous mass of about 16 cells called the morula. Once in the uterus, the cell mass begins to ‘differentiate’ (separate into cells that will eventually form the baby and those that will eventually form the placenta) into a structure called the blastocyst which must then attach to a favorable location on the inner lining of the uterus (the endometrium) within about 48 hours. Over the next week (and prior to the time of the next expected menstrual period), the blastocyst solidifies its attachments to the endometrium and, while continuing to differentiate into tissues that will eventually form the placenta or the baby, literally buries itself in the endometrial lining.

The cells (trophoblasts) that will develop into the placenta first anchor the blastocyst to the endometrium, eventually burrowing further into maternal tissues in which there are lakes of blood, an early source of nutrients for the developing pregnancy. Over the next 6 weeks (the embryonic period), not only will all major internal and external structures of the baby develop, but the trophoblasts will begin an extremely important 'second wave’ of invasion that involves a dangerous journey through the relatively ‘hostile’ environment of the maternal endometrial tissues where they are exposed to both nonspecific and specific mediators of the mother’s immune response. At the end of this long journey, under 'normal' circumstances, the trophoblasts will have successfully invaded and replaced (remodeled) the lining and muscular wall of the endometrial portion of the mother’s ‘spiral arterioles’ assuring the developing placenta of a continuous source of maternal blood in which to ‘bathe’ and, thereby, providing the placenta (and hence the baby) a source of oxygen and nutrients to continue its growth.

Factors that contribute to recurrent early pregnancy loss can result from problems occuring at ANY of the stages (and more that haven’t been mentioned) detailed above; and in our next post, we will begin the discussion of specific areas of concern to which evaluation and treatment might be directed.

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Thanks Dr. Blackman at Blog, MD for Grand Rounds 3.26

Many thanks to Dr. Sam Blackman at Blog, MD for the quality effort he made in putting together this week's Grand Rounds 3.26. My recent posts on Early Pregnancy Loss 1 and 2 address a common issue which, nevertheless, can be very traumatic for a couple and should always be handled with utmost care and understanding by the provider. Thanks again for including me, Dr. Sam! There are many couples out there who will appreciate the comments.

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Early Pregnancy Loss - 2

...When things had gotten quieter in the room, I went back to talk with the couple about our findings (see my last post). I could see the thousand questions she had on her lips and told them, “Let me just talk with you for a few minutes, and then I will answer any other questions you might have.” Asking my own questions first, I found out that this was her first pregnancy (in fact her husband was her first sexual partner); she always had regular menstrual cycles with periods every 28-29 days since age 13; she had no significant medical problems; she was on no medications other than prenatal vitamins; there was no family history of congenital birth defects, syndromic problems, inborn errors of metabolism, unexplained mental retardation, or chromosomal abnormalities; she did not smoke or use street drugs, but did occasionally “have a beer”; there was no family history of recurrent miscarriages, autoimmune diseases, or clotting disorders. I did not go into detail with her about why I needed this information, but told her that it would help me to counsel her with regard to what might have happened to her current pregnancy.

Then, to answer the first question I knew was on her mind, I told her, “Based on what you have just told me, it is very unlikely there was anything that you have done, eaten, smoked, or drank that caused this pregnancy loss.” “Then why did this happen to me,” she asked. “I know this will not make things any easier today,” I responded, “but, even if people don’t like to talk about them, early pregnancy losses are very common.” I then went on to explain. Across the board, at least 20 to 30% of all pregnancies miscarry. The most common reason for this in someone who has previously had one or more successful pregnancies is a fetal chromosomal abnormality (I did explain what that meant before going on). Most babies with chromosomal abnormalities don’t survive the first trimester, and even the ones folks are most familiar with, like Down syndrome, usually are lost in early pregnancy.

In her case, though, there is probably another explanation. This was most likely her very first conception and a much higher percentage of first pregnancies (perhaps 50-90%) miscarry, even if the baby is not chromosomally abnormal. At the risk of oversimplification, I explained to her that since the baby is only half herself, it is then ‘foreign’ to her body. And, using the analogy of organ transplantation, I told her that if I placed a kidney in her body from someone who was only half ‘matched’ with her, without using very potent immunosuppressive drugs, her body would reject the kidney in a very short period of time. From what we know, it appears that the mother’s immune system does have to be able to recognize that the baby is ‘foreign’ but then, rather than rejecting the baby, it must actually ‘learn’ to promote and nurture its growth. To successfully carry a baby, the mother has to become ‘immunized’ to pregnancy.

Then she asked, “What can I do so that this doesn’t happen again?” I told her that what happened this time may actually reduce the risk of a miscarriage with the next pregnancy. She did not have any factors to put her at risk to have repetitive miscarriages. Because this was her first miscarriage, and because of what I had told her about the risk for the same for someone having their first pregnancy, an extensive medical ‘work up’ for this was not warranted at this time. “Once this is all over,” I said, “give your body about 3 months to recover, continue taking your prenatal vitamins, and then, when you are ready, go ahead and try again. Most of the time things work out the next time around.” “And, what if they don’t,” she asked? “We’ll cross that bridge when we come to it,” I said; and, besides, that will be a good topic for another post………….

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Early Pregnancy Loss - 1

One of my sonographers came out of an exam room the other day with a vaginal transducer (ultrasound probe) held out in front of her, still sheathed in a lubricated condom, and lightly streaked with old blood. The expression she had on her face is one that I have seen hundreds (probably thousands) of times over the years and so I simply preempted her report to me with the simple question, “How far along was she supposed to be today?” Not surprised at all by my ‘insight’, she responded just as straightforwardly, “Well, she is supposed to be 12 weeks, but the baby is only 8 weeks size and does not have a heartbeat.” “Does she know?” I asked (thinking wishfully, but also anticipating the response). “No,” I was told, “All they wanted to know is if it is a boy or a girl, and I told them the doctor would have to talk with you about that.” My sonographers do their jobs and know their roles all to well. The MD after my name means that I am the one responsible for the Morbid Discussion that has to take place to inform a couple that they have a pregnancy that didn’t make it through the first trimester.

I went into the room, introduced myself, and picked up another transducer to ‘lay my hands’ on the patient before giving them the bad news. They were a young couple, neither one more than 19 years old, and had “just gotten married the week before,” probably because of the unplanned pregnancy. But, they were also very excited about the prospects of being parents, and almost immediately asked me the same question they asked my sonographer, “Is it a boy or girl?” I told them that “I can’t tell because the baby is too small” and at that point, as so often happens, they opened the door with the question that almost always inevitably follows, “Does that mean there is something wrong?” Then, in a routine I have had too many opportunities to rehearse through the years, with the transducer focused on the tiny embryo so that they could see the baby on the viewing screen, I told them, “You are supposed to be 12 weeks by your last period and the baby appears to have stopped growing at about 8 weeks. Here (using the pointer) is where we should easily be able to see the baby’s heart beating, even if the baby was only 8 weeks, and there is no heart beat. I’m so sorry.”

At that point, also as so often happens under these circumstances, she sat straight up in the bed, the tears streaming out of her eyes and, hoping she had misunderstood my words, she asked, “Does that mean there is something wrong with my baby?” “Yes,” I responded, handing her the box of tissues we always keep in close proximity to the exam table, “The baby is not alive, you have lost this baby, and we are 100% certain of that diagnosis. I am very sorry.” Since most patients are in a ‘state of shock’ after hearing this news, and are not receptive to any kind of ‘input’, I also said at that point, “Let me give the two of you a few minutes alone together and then we can talk about all this…”

I left the exam room, still within earshot of the heart-wrenching sounds of anguish that I have never gotten used to after all these years; the conversation we had when I returned will be continued in our next post…

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Constipation in Pregnancy - 2

Since constipation can be a chronic and ongoing concern in pregnancy, it is worth revisiting at least once with a few additional comments. Actually, the writer referred to in the previous post had some more specific follow-up questions and my responses touched on issues that were omitted from that post...

What is the definition of constipation during pregnancy? In other words, when is a woman considered constipated?
The ‘standard’ definition of constipation is having a bowel movement less than 3 times per week, however, in my experience, even that cannot be defined as ‘constipation’ unless it is accompanied by hard, dry stool that requires straining to eliminate. Patients with constipation will frequently complain that their bowel, particularly, the rectum, feels “full” and doesn’t feel completely empty even after they have strained to pass a small amount of stool. They will also often complain of feeling “bloated” and have abdominal discomfort and cramping as the result of retained gas and stool. So, ‘constipation’ is not a disease as much as it is a complex of these symptoms.

Incidentally, although we did not discuss this in my previous responses, constipation, even if it is not a disease, it can be the result of certain common medications, especially narcotics, or a more serious underlying medical condition such as irritable bowel syndrome, bowel cancer, diabetes, multiple sclerosis, hypothyroidism, or certain autoimmune or neurological disorders, to mention just a few. If you are not only constipated, but have persistent abdominal pain, severe abdominal distention, constipation that alternates with diarrhea, bloody stools, dark and tarry stools, unexplained weight loss, long thin ‘pencil-like’ stools, fever, or other systemic symptoms, you should be discussing these findings with a physician rather than attempting to just treat your constipation, because these may be indicators of much more serious medical conditions.

What happens if a pregnant woman has been constipated for a while, and stool softeners or laxatives aren't working?
Under these circumstances, milk of magnesia, mineral oil, or an enema with a solution that does not cause a lot of irritation may be necessary. It is unusual that fiber, fluid, and exercise won’t work. Indeed, consultation with a gastroenterologist may be necessary at that point to rule out a true bowel motility problem that might be associated with a neurologic abnormality or another of the more serious medical conditions mentioned above.

I have had some patients with premature labor who have been so impacted with hard, dry stool in their rectums that we had to manually break this up and extract the stool before their contractions would stop. I can recall one case that was so severe that we had to perform the procedure under anesthesia because the woman was in such bad pain. I have had other patients in active labor at term where the fetal head would not descend into the pelvis until we had digitally ‘disimpacted’ them.

Can constipation affect the pregnancy at all other than what you mentioned in your last response?
“Constipation” by itself is a relatively benign condition, even if it does make you miserable. There are ‘old wives tales’ that when you are constipated, toxins will build up and be dangerous for you and a baby, but I doubt there is any truth to that. If constipation is associated with preterm contractions, THAT IS a serious condition, and the straining that a woman has to do to eliminate her stool can accelerate that process as it is exactly the type of ‘bearing down’ we ask a woman to do when she is ready to deliver a baby. Such straining might also weaken the woman’s pelvic floor, increasing her risk for long-term problems related to “pelvic floor relaxation and dysfunction” such as urinary incontinence, uterine prolapse, rectal prolapse, and pain with intercourse. Another, and perhaps greater concern I would have with regard to ‘pregnancy risk’ is that one of the more serious medical conditions mentioned above might be overlooked if the patient’s complaints were simply written off as ‘pregnancy-related.’

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Constipation in Pregnancy

A writer recently requested some information regarding "constipation in pregnancy." Having just gotten over the consequences of my Norovirus infection, I thought I might welcome a little constipation in my life, even if it isn't one of our more 'moving' topics (sorry, I couldn't help myself). Regardless, here are my responses to her questions...

What are some causes of constipation during pregnancy?
One of the primary causes of constipation in pregnancy is the hormone progesterone. Progesterone is the hormone that dominates the second half of a woman’s menstrual cycle after she ovulates. It is made early in the pregnancy by persistence of the site on the ovary (the corpus luteum) from which the egg that made the baby is produced. By the end of the first trimester, the placenta takes over production of large amounts of progesterone. One of the major effects of progesterone is to cause relaxation of ‘smooth muscles.’ Organs that contain smooth muscle are the blood vessels, the uterus, and the bowel. Progesterone decreases the strength and the frequency of bowel contractions that are necessary to move food, fluids, and wastes through the bowel. The slower the motility of the bowel, the greater the opportunity for absorption of fluid and foods. Unfortunately, by the end, if the remaining waste becomes very dehydrated, the stool becomes compact and hard, making it more uncomfortable to pass, sometimes getting to the point where a woman will not have a bowel movement for 5 or more days. This is constipation and it can be very uncomfortable. Other causes are iron and calcium supplements, poor fluid and fiber intake, and too little exercise during pregnancy.

How common is it?
More than 50% of all pregnant women suffer some degree of constipation. It is probably only second to headaches among common pregnancy complaints. Think of it as ‘nature’s way’ of getting the mother to absorb the most food and fluid from her diet she possibly can to help nourish her baby and maintain the pregnancy - at a cost!

When does it typically occur? How long can it last?
It can begin early in the first trimester, but usually becomes more of a problem only from 20 weeks on when, not only are there high progesterone levels, but the uterus enlarges to the point that it can impede movement through the bowel by its sheer size and position in the pelvis. Some people are unusually prone to constipation because of poor fluid or fiber intake in their diets, so it can be a chronic problem throughout the pregnancy.

What are some ways to prevent this?
Drink plenty of fluids (8-12 glasses per day); take in plenty of fiber – 15 grams or more per day (fruits, vegetables, whole grains, beans);and, although iron and calcium are important minerals for both mothers and their babies, they can both worsen constipation. Get some exercise (unless you have a reason to be at bedrest). This will improve bowel motility.

How can it be treated? Fluids, fiber, bulk laxatives (such as Metamucil and Citrucil). Avoid irritant laxatives, mineral oils, and irritating enemas since these might also cause the uterus to contract prematurely. Add some daily, non-jarring exercise to your routine.

When is there cause for concern?
If you haven't had a bowel movement in 4-5 days, you should notify your provider of your dilemma. When the stool becomes very hard and distends the bowel, then pain and bleeding can occur. This can be a serious problem if a woman has large hemorrhoids (enlarged veins in the rectum and anus) which could tear and bleed quite heavily. Also, when the bowel gets over-distended or ‘impacted’ in its lowest portion, it can release chemicals that try to force the bowel to contract. These same chemicals, in close proximity to the uterus can make the smooth muscle of the uterus also contract and actually precipitate premature labor!

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Norovirus Infections and Pregnancy

Sorry, guys, I have been out of commission over the past week. Between the very unfriendly Norovirus that has been going around (don’t ask for details) and playing catch-up at work following the fun with Noro, I have not had the time or the energy to write. There is not a lot published regarding Norovirus infections and pregnancy, but they are believed to cause about 50% of all cases of gastroenteritis (abdominal pain, vomiting, and diarrhea) and, therefore, frequently occur in pregnant women.

Noroviruses are small, RNA viruses that do not appear to readily cross the placenta or directly affect the baby. These infections are often called ‘stomach flu’ and are also often mistaken for ‘food poisoning.’ They are usually accompanied by headaches, low-grade fever (less than that typically seen with the flu), chills, lethargy (tiredness), weakness, and muscle aches. The course of infection is usually limited to 2-3 days, but the nausea, vomiting (more common in children) and diarrhea (more common in adults) can result in dehydration and electrolyte imbalances very quickly. The latter are where our pregnant women get into trouble. With dehydration and electrolyte imbalances, pregnant women are at increased risk for preterm labor and for developing urinary tract infections (which may also contribute to preterm labor).

Noroviruses are spread by the ‘fecal-oral route’ in contaminated water and foods and can be passed directly between individuals. Onset of symptoms usually occurs within 24-48 hours after exposure. They are the source of very rapid and widespread outbreaks in close quarters such as schools, daycare centers, nursing homes, restaurants, hotels, and cruise ships and this is what has often led to the mistaken accusation of ‘food poisoning’ in those situations. Common contaminated sources of infection are raw or undercooked shellfish, swimming pools and lakes, wells and municipal water supplies, ice machines, and ill individuals who handle food sources. There are several different strains of Noroviruses and despite the fact that individuals develop ‘immunity’ to the viruses, the immunity often is not permanent and reinfection with the same or different strains readily occurs. Noroviruses are believed to cause about 300 deaths per year in the U.S., but these serious complications usually occur in very young children and elderly and debilitated individuals.

If you are pregnant and develop symptoms related to viral gastroenteritis, you should let your provider know. If you have a low-grade fever and if you are able to ‘keep up with your fluids’ during the acute phase of the illness, it is unlikely that you will develop serious complications related to the pregnancy. If you cannot keep up with the fluids, develop a high fever, begin having contractions or other symptoms of a more serious problem, let your provider know about these immediately. If you have a sick child at home with a Norovirus infection, wash your hands frequently, but don’t be surprised if you join them in their misery despite your best efforts. And when you feel well again, come back and visit me here!

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