First Trimester Screening and Twins

Below is a series of excellent questions and my responses related to first trimester screening from a woman who has an IVF pregnany and twins...

• At Fri Jun 27, 06:53:00 AM 2008, Anonymous said…

Hi: How reliable is first trimester screening (FTS) in twins pregnancy? I was told it is not and some said it is. We are trying to make a decision if we will pursue chorionic villus sampling (CVS). I am 36 and I would be 1 month away from 37 when it is my due date. I am now 11 weeks almost 12. I did the FTS and the ultrasound looks good. The genetic counselor said the blood test will not be as accurate as in singleton pregnancy. The spaces on the necks (nuchal translucencies) on both babies are normal and look good. We conceived using IVF (1st cycle). It is unexplained infertility. I had natural pregnancy once but miscarried during 7-8 weeks (no heart beat detected). No family history of birth defect on either side. I am Asian if this matters and my husband is white (British/ French). I really appreciate your opinion. Thank you.

• Tue Jul 01, 01:05:00 PM 2008, Anonymous said…
Dr. T.
I left comment earlier on 6/27 about reliable in FTS in twin. I just got the test results for FTS:

IVF/ICSI cycle
36 yrs (asian) weight 165 lbs
Gest Age: 11.3 wks
IDDM: no DS HX: NO
NT: 1.3 mm and 1.5 mm
CRL: 49.3mm and 48.3 mm
Nuchal Translucency: 1.08 MoM/ 1.25 Mom
PAPP-A: 3.00 MoM
hCG - 1.36 Mom

Down Syndrome: Screening Risk 1:660 Age Risk 1:130
Risk Cutoff: 1:50
Trisomy 18: Screening Risk - can't accurately estimated in twin
Age Risk 1:470
Risk Cutoff: 1:100

We were told by the genetic counselor and another doctor who does CVS that our position is good base on the FTS result. We would do amniocentesis at 16 weeks, but if there would be an unfortunate result, would that be too late to do selective reduction which it could be 18 weeks by the time we get the result?

I would appreciate any comment based on your expertise. These tests are very confusing and driving us crazy. Thank you so much for having such an informative blog for all Moms-to-be.
W.

• At Tue Jul 01, 05:51:00 PM 2008, Kenneth F. Trofatter, Jr., MD, PhD said…

To W: Those are very good first trimester results. Personally, I have found combined first trimester screening (NT measurements plus maternal serum markers) to be very helpful in twins. Below is an abstract from a recent article that gives you some idea of its value. I would suggest an MSAFP only (and perhaps another ultrasound) at 16 weeks and then a good genetic sonogram at 18-20 weeks. If all that checks out fine, you probably do not need to have any invasive procedure done and with those first screening results, we would not ordinarily recommend a CVS at all. Of course, regardless of what we suggest, the final choice is yours!

It is not too late to do selective reduction at 18 weeeks or even later, but the risks do go up with gestational age. If you have an amnio done and you are seriously considering selective reduction if one of the babies is chromosomally abnormal, consider having a FISH study done from which you can get a result back in about 72 hours. I am NOT recommending it in your case at this time, but if you elect to proceed with the amnio,that is an option to consider.

Best of luck and please let us know how things turn out. By the way, at the time of the genetic sonogram, ask your doctors to evaluate your cervical length as well! Infertility patients are notorious for having unsuspected cervical incompetence, especially with multiple gestations!

Thanks for reading and good luck to you for the rest of the pregnancy!
Dr T

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Chasen, et al., First-trimester risk assessment for trisomies 21 and 18 in twin pregnancy. Am J Obstet Gynecol 2007;197:374.e1-3.

OBJECTIVE: Our objective was to describe performance of first-trimester combined risk assessment in twin pregnancies. STUDY DESIGN: Twin pregnancies that underwent risk assessment in our ultrasound unit from 2003-2006 were included. Adjusted risks for trisomies 21 and 18 that were based on age, nuchal translucency (NT), and biochemistry were provided for each twin. Detection rates for Down syndrome and trisomy 18 were calculated for age/NT, and age/NT/biochemistry at a screen-positive rate of 5% of pregnancies. RESULTS: Five hundred thirty-five pregnancies were included. Median maternal age was 34 years, with 47% of women > or = 35 years old. There were 7 fetuses in 6 dichorionic pregnancies with Down syndrome and 3 fetuses in 3 pregnancies with trisomy 18. For a 5% false-positive rate, age/NT identified 83.3% of Down syndrome and 66.7% of Trisomy 18 pregnancies. Adding biochemistry resulted in 100% detection rates for both conditions. CONCLUSION: The addition of biochemistry may enhance first-trimester risk assessment in twin pregnancies. Further studies with larger numbers of affected pregnancies are needed.

Labels: amniocentesis, chorionic villus sampling, first trimester screening, FISH

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Elevated FSH and Aneuploidy?

The reader whose comments are featured below has had two miscarriages associated with chromosomally abnormal babies. She also has several medical problems that may or may not decrease her chances for a successful pregnancy. I thought her questions were excellent and I tried to provide answers for those while expanding on several other issues about which she did not have questions. I have paraphrased or expanded some of her comments to improve clarity for other readers...

• At Sat Jun 14, 11:29:00 PM 2008, Polly Gamwich said…(and my responses follow her questions in italics):

Hi Doctor,

I am 31 years old. At age 29 I had two miscarriages, the first at 10 weeks due to Turner’s syndrome (45XO) and the second at 8 weeks due to XXYY. When I was 30 I had two chemical pregnancies. I have yet to have a live birth.

I have elevated FSH (12.3), am a compound heterozygote carrier for MTHFR polymorphisms and am currently being treated (with folic acid), and have Hashimoto's thyroiditis, currently being treated for hypothyroidism. I have four questions for you:

1. Am I more at risk of having a chromosomally abnormal baby, as a woman in her 40's might be because of my elevated FSH?

Increased FSH (follicle stimulating hormone) is associated with decreased ovarian reserve and that is associated with aging, as is the risk for producing an egg with an unbalanced chromosomal complement (aneuploidy), BUT the two do NOT appear to be related. Indeed two recent publications clearly show no direct relationship between the FSH level and aneuploidy risk (Massie, et al., Fertil Steril 2007;87;S7 and Thum, et al., Fertil Steril 2007;Oct 20 – epub ahead of print) (Note: FSH is made by the pituitary gland. Its production is regulated by a negative feedback loop secondary to estrogen produced by the ovaries. When estrogen levels are high, FSH levels decrease (are suppressed) and when estrogen levels are low, as occurs during the luteal phase (after ovulation) of the menstrual cycle, menopause, or premature ovarian failure, then FSH levels are elevated).

2. Why does your body allow you to even GET pregnant with chromsomally abnormal babies ... why doesn't it just pass the baby without implantation??

Most chromosomally abnormal babies do NOT make it successfully through the implantation process and of those that do, very few will survive the first trimester.

3. I've had all the testing there is (and more) and we're treating all the problems ... why would my risk of miscarriage go up after the 2nd miscarriage? (I've heard that if you've had two losses you have a better chance of having a healthy pregnancy, however if you have more than 2 miscarriagess you have a worse chance of having a healthy pregnancy ... I would assume this is assuming an untreated issue??)

That is only true if there is NO IDENTIFIABLE CAUSE for the losses. You DO have an identifiable cause - babies that had chromosomal abnormalities. So, that may just be a string of bad luck or there is a very small possibility you are at risk for recurrent aneuploidy for reasons we do not yet understand. I guess I would have several other concerns and these are related to your Hashimoto’s thyroiditis. Hashimoto’s disease is an autoimmune condition characterized by the presence of antibodies against your thyroid gland. Recent studies have confirmed that autoimmune thyroid disease is associated with unexplained infertility and recurrent implantation failure (Belver, et al., Hum Reprod. 2008 23:278-84).

Furthermore, sometimes the presence of one autoimmune condition can be an indicator of others since these result from imbalances in your immune response that cause you to attack your own tissues as if they are ‘foreign’ to your body. Some individuals will develop polyglandular autoimmune syndromes characterized not only by Hashimoto’s disease, but also by premature ovarian failure, type 1 diabetes, and autoimmune adrenal deficiency (Addison’s disease – 90% of which is the result of autoimmune adrenalitis). Other conditions thought to have an autoimmune basis, such as pernicious anemia and myasthenia gravis, may also be found under these circumstances. My question to you, in view of your Hashimoto’s disease and elevated FSH) is have you been screened for any other autoimmune conditions that could have a deleterious affect on your fertility?

4. I get pregnant on every cycle I attempt (4 months we've tried - we've had 4 pregnancies and 4 miscarriages) ... will I have more miscarriages than the average women because my babies seem to implant whether they are healthy or not?

No. I do not think you are unique in that regard. You have just had a rough time with the conception side of things at least as reflected in those babies that were shown to be chromosomally abnormal. In that regard, if it has not been done already, your husband should have a careful semenanalysis performed because there is a possibility he is contributing to the situation as well. I wrote a post on the contribution of the male partners to pregnancy loss and infertility earlier in the year. Also, you might be a good candidate for either IVF and/or prenatal genetic diagnosis (PGD) to help improve your chances of having an implantation of a chromosomally NORMAL embryo!
Thank you,
Polly
Great questions and thanks for writing. Best of luck to you.
Dr T

• At Tue Jun 17, 10:33:00 AM 2008, Polly Gamwich said…

Dr. Trofatter,

Thank you so much for your response. Your articles are excellent and your compassion and respect for women is overwhelming - thank you.

And in my case, of the things that you suggested, I wanted you to know that you're right on. I wanted to follow up to your June 14th response with this:

We are actually testing my eggs (not our embryos - unfortunately, we can't/won't do PGD on embryos for moral/religious reasons) because we were so worried about chromosomal abnormalities being caused by the eggs. We have done one IVF retrieval and we retrieved 6 eggs, 5 were mature: Based on CGH polar body testing of the eggs: 3 were abnormal, 1 was normal and 1 was inconclusive - the good news is - I DO HAVE NORMAL EGGS IN THERE SOMEWHERE! (and note: we did do oocyte vitrification ... I'm curious if you have any articles on that - we know it's not proven, but without being able to do PGD on embryos, it was the best option for us.)

We've been suffering through miscarriages for two years and our Reproductive Endocrinologists still have yet to do a traditional semenanalysis. We're having one done in a few weeks. But we have had the Sperm DNA Defragmentation (SDFA) test done on my husband and it came back 50% abnormal - I guess that means that either the DNA is bad or the ability for the DNA to appropriately work with the egg's DNA is affected - is this what the post you refer to is about? Anyhow, my husband has been taking antioxidant supplements for three months and we will retest his semen soon. If this turns out to be a problem, we'll move to in vitro fertilization with intracytoplasmic sperm injection.

I just thought I'd close the loop on some of your statements/comments/questions.

Again, Doctor, I really appreciate your dedication to your field and the support you provide to so many women.

Take care,
Polly

Note: Oocyte vitrification is a relatively new cryopreservation technique in which the ice formation is totally avoided (Bagchi, et al., Expert Rev Med Devices 2008;5:359-70). Using this technique, mature or immature oocytes are retrieved following ovarian stimulation and then cryopreserved for further attempts at in vitro fertilization. Recent studies have demonstrated that not only is the technique successful in achieving pregnancy, “the results indicate that the mean birth weight and the incidence of congenital anomalies are comparable to that of spontaneous conceptions in fertile women or infertile women undergoing in-vitro fertilization treatment…” (Chian, et al., Reprod Biomed Online. 2008;16:608-10).
Dr T

Labels: autoimmune thyroiditis, FSH, oocyte vitrification, recurrent aneuploidy, recurrent pregnancy loss

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Grand Rounds 4.39 at Marianas Eye

Thanks to Dr. David Khorram at Marianas Eye for hosting and all the effort put into this week's Grand Rounds 4.39. The variety, breadth, and presentation of the offerings (not to mention the great photos at the bottom of the page) make a quick trip to his "island in the South Pacific" a very worthwhile investment in time.

Special appreciation, too, for the link to my recent post on "Asherman's Syndrome." As Dr. Khorram summarizes in the reference to my post, Asherman's syndrome is a condition related to scarring of the intrauterine cavity, usually as the result of a failed pregnancy and a D&C in the presence of infection, or another intrauterine surgical procedure, that can result in light (hypomenorrhea) or absent menstrual periods (amenorrhea), infertility, and recurrent pregnancy loss as well as other pregnancy complications. It is more common than most women realize and should be discussed as part of informed consent counseling with any woman prior to any intrauterine procedure. In a subsequent post, we continue the discussion of Asherman's syndrome with regard to diagnosis, treatment, and prevention. Thanks for reading and hope you enjoy!
Dr T

Labels: Asherman's syndrome

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Asherman's Syndrome: Diagnosis, Treatment, and Prevention

In our last post, we described the condition called “Asherman’s syndrome” wherein scarring of the intrauterine cavity can cause aberrations of menstrual bleeding (in the most extreme cases very light or absent periods), infertility, recurrent pregnancy loss, and other pregnancy complications. The extent of the scarring is correlated with the risks for these problems; however, some women will have minimal scarring and little if any aberration of menses and still be at risk for one or more of these complications. In today’s post we will briefly address the diagnosis, treatment, and prevention of Asherman’s syndrome…

The first step to establishing the diagnosis is maintaining a high index of suspicion. It is surprising to me, for example, how often a woman will present with recurrent pregnancy loss, where she has never been asked about specific events surrounding her management and complications related to previous pregnancies and/or these previous losses (i.e., postpartum hemorrhage, D&C for retained products of conception and the timing of the same with regard to the length of time from the delivery, D&C’s for missed or incomplete miscarriages and elective abortions, prolonged bleeding, fever, infection or evidence of infection on the pathology report, length of time between the death of the baby and the actual miscarriage or medical/surgical evacuation of the uterus, complications related to the D&C’s themselves, such as hemorrhage or uterine perforation). Yet, we know that the risk of intrauterine scarring (synechiae) increases with the number of D&C’s, the duration between fetal loss and the procedure itself, and any of the other complications noted above.

Clearly, if a patient has complete absence of menstrual bleeding, a history of an intrauterine procedure and/or infection, and documented ovulation, the diagnosis is readily apparent. However, since not all Asherman’s patients will have the most extreme presentation of the condition, and since ultrasound alone is unlikely to help establish the diagnosis under these circumstances, it is probably under-diagnosed, or at best the diagnosis is delayed in many instances. Occasionally, the diagnosis can be made using sonohysterography in which fluid is used to distend the uterine cavity while performing an ultrasound, or by hysterosalpingogram in which a radio-opaque dye is instilled into the uterus to outline its contour, but by far the most efficient and reliable approach is to perform hysteroscopy in which the uterine cavity is directly visualized with the aid of a special instrument that provides light and magnification.

Interestingly, in one prospective study in which hysteroscopy was performed routinely following D&C’s for uterine evacuation of early pregnancy, intrauterine adhesions were found in 16% of women after one procedure and 32% after three or more (Friedler, et al., Hum Reprod 1993;8:442-44)! Similarly, Westendorp and colleagues (Hum Reprod 1998;13:3347-50) found that 40% of women who underwent a D&C for retained placenta longer than 24 hours after delivery, or who required a repeat D&C for incomplete abortions, had intrauterine adhesions present by hysteroscopy three months after the intervention and almost half of these had moderate to severe disease (Grade III and IV).

Although treatment for Asherman’s syndrome has had various approaches, successful treatment relies on the lysis (breakdown) of the adhesions and restoration of some degree (the more the better) of normal-appearing and functioning endometrium (the inner lining of the uterus). The gold standard at present involves surgical removal of adhesions under direct visualization using operative hysteroscopy. The success depends on the experience and skill of the surgeon and in the most severe cases (complete obliteration of the uterine cavity by scar tissue), the procedure can be quite difficult. Even in skilled hands, the risk of recurrence of scar tissue following the initial operation is very high and many surgeons try to minimize this risk by avoiding surgical techniques (such as electrocautery) that will further promote scarring. Following the procedure itself, patients are often placed on high doses of estrogen to stimulate the endometrium and in some cases, balloons, catheters, or other forms of stents are placed into the uterine cavity to help prevent adherence of the walls. Another option is to have repeated in-office hysteroscopic lysis of adhesions once the primary procedure has been performed.

Even with all these precautions, recurrence of adhesions is extremely common and success, measured in terms of restoration of fertility, is relatively low. In moderate to severe Asherman’s syndrome, recurrence rates range between 20-40% and 40-50%, respectively (Valle, et al., Am J Obstet Gynecol 1988;158:1459-70; Yu, et al., Fertil Steril 2008;89:715-22). Conception and pregnancy success depends on the success of the lysis of adhesions, the degree to which a normal endometrium can be restored, damage done to the uterus by the procedure itself and, eventually, the site of implantation of a subsequent pregnancy. As also reported in the article by Yu and colleagues noted above, “…the chances of conception in women who remained amenorrheic (2 out of 11); 18.2%) were significantly lower than in those who continued to have menses (37 out of74; 50%)…the conception rate in women who had reformation of intrauterine adhesions (2 out of 17; 11.8%) was significantly lower than that of women who had a normal cavity (26 out of 44; 59.1%)."

And, as we pointed out in our previous post, even if conception occurs, a good outcome is not guaranteed. Probably no more than one-third of women with moderate to severe adhesions will successfully carry a pregnancy and of those, there is increased risk for cervical incompetence, intrauterine growth restriction, fetal loss (early and late), placenta accreta or placenta previa, premature delivery, preeclampsia, cesarean delivery, uterine rupture, peripartum hemorrhage and hysterectomy.

In closing, let us just mention a few thoughts on prevention of Asherman’s syndrome. Based on several reports, the risk of Asherman’s could be reduced significantly if pregnancy-related D&C procedures could be minimized or done less traumatically. To that end, in recent years, the prostaglandin drug, misoprostol, has been used effectively even in first trimester uterine evacuations and compared to D&C is clearly associated with a reduction in risk for adhesions (Tam, et al., J Am Assoc Gynecol Laparoscop 2002;9:182-5). When given the option of instruments to use for D&C, a plastic suction curette is probably (but not completely) less traumatic than a sharp metal curette and efforts should be made to reduce the degree to which the endometrium is denuded by either. Prophylactic antibiotics, although rarely used when a D&C is performed, unless there is frank evidence of infection, might be considered in patients who opt to defer uterine evacuation following fetal loss in preference to awaiting spontaneous abortion. I think if I learned nothing else from this review myself, it was the fact that the risk of Asherman’s appears to go up dramatically with the length of time from fetal death to uterine evacuation although the factors that contribute to this risk are not entirely clear.

Labels: Asherman's syndrome, cervical incompetence, IUGR, placenta accreta, placenta previa, recurrent pregnancy loss

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Asherman's Syndrome

Recently, several readers have requested information or had complications I suspect are related to "Asherman's syndrome." Two comments and my responses are included below...

Julia Mangan has left a new comment on your post "Request to My Readers...":

Thank you for all your work on the blog and answering our comments!
I would love for you to address Asherman's Syndrome at some point and the risks of D&C's.

So be it Julia! See my response to the reader below and the comments that follow addressing Asherman's syndrome.
Dr T

At Thu Jun 05, 09:33:00 AM 2008, Anonymous said…

I had a miscarriage at 11-12 weeks of pregnancy in Nov 2008 due to some unknown infection. I had slight spotting in the 5th and 6th week then again in 11th week… the spotting increased to bleeding and 2 days before the miscarriage I had fever, chills and vomiting…and had a very painful miscarriage and the doctor did a D&C.

Now I am trying again for the past 2 months. This month my period has been delayed by 5 days and I had spotting like its a beginning of period….However, I do not have any pregnancy symptom this time expect that my period is delayed…I am worried that the first miscarriage due to infection could have affected my fallopian tube although the doctor said in most cases it won’t…Why do I have spotting? Does it mean that my uterus not strong enough? Could a doctor please reply to my question….

At Sat Jun 07, 08:21:00 AM 2008, Kenneth F. Trofatter, Jr., MD, PhD said…
To anonymous June 5: If you have not had a normal period since the D&C, and are just spotting, I am concerned that you either are not yet ovulating normally, or that you might have developed "Asherman's syndrome." This is scarring of the lining of the uterus that can occur if you have a D&C that is preceded by infection inside the uterus. If you do not have a normal period within the next couple of months, you need to discuss this possibility with your doctor. If you develop Asherman's syndrome, it is very hard to get pregnant unless you get some help. Dr T

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J.G. Asherman described the syndrome that now bears his name in a 1948 publication in what was then known as the Journal of Obstetrics and Gynecology of the British Empire. The condition he termed “amenorrhea traumatica (atretica),” basically, the absence of menstrual bleeding following trauma (specifically, D&C – dilatation and curettage) to the inner lining of the uterus, was further defined in a subsequent paper in the same journal (1950;57:892-96). Earlier descriptions in case studies were discussed in the 1890’s by several physicians, including Heinrich Fritsch in 1894, and the condition can be found occasionally referenced as the Fritsch-Asherman syndrome.

So, what is Asherman’s syndrome; under what conditions does it come about; what problems does it cause; how is it diagnosed; and, what can be done about it? To help understand this condition, let’s first discuss the uterine anatomy. The innermost lining of the uterus is called the endometrium. It contains the tissues (blood vessels and glands) that proliferate in the early stages (estrogen-dependent) of the menstrual cycle and then becomes conditioned (decidualized) following ovulation (progesterone-dependent) to facilitate the implantation of the egg should it become fertilized on its journey down the fallopian tube. If fertilization does not occur (or the embryo does not implant), the upper portion of the endometrium (the functional layer) sheds and regresses with the bleeding that accompanies the menstrual period. Normally, when tissues are damaged and bleed, they tend to adhere to each other in the presence of blood clot and begin to form scar tissue. However, one very important characteristic of the innermost endometrial layer is that this does NOT usually occur – in other words, one key role of the endometrium must be to keep the inside of the uterus from sticking together and closing up!

In Asherman’s syndrome, on the other hand, that’s exactly what happens – the uterine cavity becomes obstructed by scar tissue (intrauterine synechiae) and if this is severe enough, there may not be sufficient endometrium remaining to cycle normally, resulting in very light periods (hypomenorrhea) or even the complete absence of periods (amenorrhea). There are several conditions that are together associated with more than 90% of all cases of Asherman’s syndrome (Schenker, et al., Fertility Sterility 1982;37:593-610): pregnancy, intrauterine infection, and trauma (usually by D&C) to the endometrium. This triad of conditions can lead to an intense inflammatory response and denuding of the endometrium into the deeper (basalis) layer, or into the stromal connective tissue, or the muscle (myometrium) of the uterus itself, which do not have the same regenerative capabilities as the innermost layer of the endometrium, nor the same capacity to prevent activation of pathways that can lead to the formation of scar tissue. Although Asherman’s syndrome probably complicates no more than about 1% of D&C's done electively and in the absence of infection, it has been estimated to occur in about 25% of these procedures that are done one to four weeks following pregnancy (Buttram, et al., In J Fertil 1977;22:98-103) and as many as 30% of missed spontaneous abortions with the length of time between fetal demise and the D&C itself being directly correlated with the risk of adhesion formation (Adoni, et al., Int J Fertil 1982;27:117-18).

Of the three conditions, the presence of infection perhaps contributes the most to the onset of adhesion formation. The result, in the most severe cases, is that the entire uterine cavity may be completely fused together. In the developing world, chronic endometritis from pelvic tuberculosis (Netter, et al., Am J Obstet Gynecol 1956;71:368-75) and schistosomiasis (Krolikowski, et al., Obstet Gynecol 1995;85:898-9) are major causes of intrauterine synechiae. Other uterine procedures, such as removal of fibroids (myomectomies) and even cesarean section have been associated with Asherman’s syndrome, but these are less common causes.

Other than light or absent periods, the primary complications related to Asherman’s syndrome are recurrent miscarriages and infertility. Patients at risk for or suspected of having Asherman’s syndrome, who still have pain occurring at the expected time of menstruation in the absence of significant or any menstrual flow, may have obstruction of the cervix by scar tissue and are then at risk for accumulating menstrual blood and tissues within the uterine cavity (hematometra) and also may develop endometriosis as a secondary consequence of this. In addition to the risk of miscarriage when pregnancy occurs, women with intrauterine adhesions are at risk for later pregnancy complications related to abnormalities of placentation, either small placentas with poor blood supply or a placenta accreta (placentation into the deeper basalis layer and the myometrium). These conditions increase risk for cervical incompetence, poor fetal growth (intrauterine growth restriction), fetal demise, preeclampsia, early delivery, cesarean section, uterine rupture, postpoartum hemorrhage, and peripartum hysterectomy.

In our next post on this subject, we will discuss the diagnosis, treatment, and prevention of Asherman’s syndrome….

Labels: Asherman's syndrome, intrauterine synechiae

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