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

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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

*************************************************************************************

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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Indications for Doppler Flow Velocimetry During Pregnancy

Recently, I received a phone call from our billing office reporting that an insurance company had declined to reimburse us for a claim that included charges for Doppler flow velocimetry for the indication of intrauterine growth restriction (IUGR). My response to the office personnel was simply that that is the most widely accepted indication we have for these procedures and that I would compose a letter of explanation to the insurance company, the contents of which are detailed below...

Doppler flow velocimetry (DFV) is a noninvasive method to assess resistance to, and velocity of, blood flow using ultrasound technology. In pregnancy, it has been proven to be a valuable adjunct to fetal assessment because often DFV abnormalities will precede detectable fetal abnormalities of growth, amniotic fluid, and placental insufficiency and can help assess the severity of fetal compromise when these abnormalities are suspected.

The principles underlying the most common indications for DFV are as follows:

Under normal conditions, the placenta offers little resistance to fetal and maternal blood flow, even during diastole (i.e., between heart beats); and, there is no preferential blood flow to the brain as reflected in normally high resistance, especially from late midtrimester on, at the expense of perfusion of other organs...

Under abnormal conditions, blood flow to the placenta may be reduced and accompanied by increased resistance to perfusion (fetal and/or maternal) and/or there is preferential blood flow to preserve ‘essential’ organs such as the brain (‘brain-sparing effect’) as manifested by low resistance Doppler patterns to these organs and eventually reduced perfusion (fetal blood flow redistribution) of ‘nonessential’ organs such as the kidneys.

Some factors that lead to aberrations in DFV patterns include:

• Abnormalities in placentation or of the umbilical cord
• ‘Placental insufficiency’ regardless of fetal size
• Fetal anemia resulting from maternal isoimmunization, viral infection (e.g., parvovirus B19 and CMV), twin-twin transfusion syndrome, fetal-maternal hemorrhage…
• Chromosomal abnormalities
• Cardiac and intracranial malformations

When indicated, DFV evaluation of the following may contribute valuable information with regard evaluation of the pregnancy, but should be performed by individuals trained and experienced in the performance and interpretation of the results:

Maternal:
Uterine arteries

Fetal:
Umbilical arteries
Middle cerebral arteries
Ductus venosus
Umbilical vein

Common indications for Doppler flow velocimetry studies include:

• Abnormalities of growth (both intrauterine growth restriction(IUGR) and excessive fetal growth (macrosomia)
• Fetal anomalies (e.g., cystic hygromas, cardiac, thoracic, diaphragmatic, neural tube, renal, and abdominal wall)
• Fetal hydrops
• Oligohydramnios (decreased fluid) and polyhydramnios (increased fluid)
• Poor OB history (e.g., preeclampsia, IUGR, previous stillborn…)
• Known maternal risk factors: hypertension, preeclampsia, diabetes, autoimmune disorders (overt and subclinical), thrombophilias (acquired and genetic)
• Abnormal maternal serum screening (e.g. elevated MSAFP and/or increased risk for fetal chromosomal abnormality)
• Multiple gestation
• Maternal trauma (fetal-maternal hemorrhage)
• Suspected placental abruption
• Known maternal isoimmunization
• Exposure to parvovirus B19

In recent years, DFV has become the primary means of screening related to fetal anemia. This is done by evaluating the peak systolic velocity (PSV) in the fetal middle cerebral artery. Its negative predictive value is so high that it has obviated the need for, and the expense of, repetitive invasive procedures when there is known maternal isoimmunization, Parvovirus B19 exposure, or other potential causes of severe fetal anemia such as trauma or placental abruption or placenta previa that might lead to fetal-maternal hemorrhage or fetal blood loss.

It is also the primary means of ruling out fetal anemia as a cause of hydrops fetalis and it is the mainstay in the assessment of multiple gestations as a means of screening and staging possible twin-to-twin transfusion syndrome. DFV of the fetal ductus venosus in early pregnancy has also proven useful in the identification of fetuses at risk for chromosomal abnormalities and major congenital heart defects. DFV of the branch pulmonary arteries can help predict the risk of fetal pulmonary hypoplasia in cases of premature and prolonged rupture of membranes.

DFV is no longer considered ‘experimental’ and it has become a ‘standard of care’ in the hands of specialist in Maternal-Fetal Medicine for the evaluation and management of complicated pregnancies.

Labels: Doppler flow velocimetry, fetal hydrops, isoimmunization, IUGR, oligohydramnios, polyhydramnios

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The Happy Hospitalist Hosts Grand Rounds 4.37

Thanks to The Happy Hospitalist for the effort and the humor put into this week's rendition of Grand Rounds. I am thankful and quite grateful that he chose to include my recent post on "Teen Pregnancy: We ARE Failing Our Children."

As pointed out in my post, this is a growing concern that appears to be under the radar screen of many health care professionals and is being completely (conveniently?) ignored (as is so often the case with medical issues facing women and children) by the individuals in high places that would be in the best postion to effect change. Reasons for the epidemic are not entirely clear, but solutions are going to take a practical, realistic, creative, and widespread integrated approach to a problem that will just NOT go away and threatens to undermine the fabric of generations to come...

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Teen Pregnancy: We ARE Failing our Children

What is wrong with these scenarios?!?....

Last Thursday night while I was in the hospital on call for our Residency Program, we had 8 patients on our Labor and Delivery unit. The mean maternal age was 17...

The next day, I was covering our ultrasound unit and three of the last patients I saw were age 14 (2) and age 15. I had seen a couple of 16 year olds earlier in the day. None knew when they had gotten pregnant, how many weeks gestation they might be, or even what that meant. All were “late entries to prenatal care” with estimates of gestational age between 25 and 33 weeks, thus missing any benefit of early counseling, screening, and medical care...

Within the past year, I saw an 11 and a half year old who also presented at 28 weeks gestation. Her mother was excited that her daughter was having a girl – all I could think about (while tactfully suppressing my blind rage) was finding the criminal who had gotten her pregnant...

Recently, I saw a 16 year old who presented for her initial visit and ultrasound at 33 weeks gestation. The baby had an abdominal wall defect called gastroschisis in which the intestines are outside the abdomen exiting through a small defect next to the umbilicus. When I tried to explain what the condition was all about to the patient and her family, she became angry at me, demanded to know what she could “do about it” (in the context of terminating the pregnancy) and then told me that she was going to go outside and smoke before she would “talk about it anymore.” Her mother handed her a cigarette as she was heading toward the door...

In almost every instance above, the father of the baby was significantly older than the mother...

While I was discussing these observations with one of our nurses on L&D, I was told that “60 girls in her daughter’s high school are currently pregnant...”

The children are not to blame. We have failed hem. We have all failed them – parents, social services, schools, counselors, religious leaders, government leaders, the criminal justice system, and health care providers. The annual summary from the National Center for Health Statistics and the Centers for Disease Prevention and Control for 2006 (most recent data) support my simple observations in the trenches that began a few years back. Teen pregnancy rose 3% in 2006, to 41.9 per 1000 females aged 15 to 19 years, the first increase after 14 years of steady decline (Martin, et al., Pediatrics 2008;121:788-801). From what we have seen recently in our own practice, I anticipate now that the rates for 2007 and 2008 will be even worse. It goes without saying that the rates among Blacks and Hispanics will probably be nearly twice those seen in the White populations.

We live in times when there has never in the history of humans been a greater disparity between the age of puberty and the social and economic demands that allow us to survive productively in this world. That also means that children are now reaching the age of ‘reproductive maturity’ when they are least likely to be in a position to control impulses, to understand the consequences of, and to make sensible decisions (or to resist sexual overtures of older and more experienced males) related to, sexual activity. The consequences are not only pregnancies and sexually transmitted disease but, in most cases, as has been shown repeatedly in the past, a loss of lifetime opportunities for success, a life spent in poverty, poor health, a long history of dependency on social welfare, limited access to an adequate health care system, and the high likelihood that their inheritance to their children will be a life similar to theirs.

It is much too simplistic after decades of neglect and inadequate education – denial and repression are not education – and actively withholding information to state simplistically that “it is the parents’ responsibility.” Parents have failed, but most ‘parents’ do not themselves have the necessary skill sets to deal with this problem. Two wage earner households, high divorce rates, and times of a poor economy have left many parents struggling to cope themselves and too easily tempted to turn their children over to the internet as a poor substitute for distraction, nurturing, attention, and sustenance.

Abstinence-alone efforts have also failed as a widespread approach and are practically meaningless anyway to children at the age at which they are now reaching puberty. There is growing data to support that teaching about contraception is “not associated with increased risk of adolescent sexual activity or STD. Adolescents who received comprehensive sex education had a lower risk of pregnancy than adolescents who received abstinence-only or no sex education (Kohler, et al., J Adolesc Health 2008;42:344-51).” But, all this needs to be presented in a program of ongoing education and practical incentivization. “The most expedient way to strengthen the impact of pregnancy prevention programs on adolescent childbearing is to shift the focus of intervention …to helping young women develop goals that make adolescent childbearing a threat to what they want in life. This means intervening actively enough to ensure that goal setting translates into an internal desire to postpone childbearing beyond adolescence (Sheeder, et al., Matern Child Health J 2008: epub May 16).”

Responsible living, grade-appropriate sex education, nutritional counseling, and physical education need to be a part of every school curriculum starting in early grades. These need to be integrated into programs that address responsibility by teaching not only the consequences of shirking responsibility but also the meaning of the word itself in terms of what is necessary to survive. Group support systems conducted by trained and objective educators may be the way of reducing first-time pregnancies as well as recidivism among adolescents (Key, et al., J Adolesc Health 2008;42:394-400). Perhaps it may even be time to reconsider going back to a system of separate education for girls and boys! These programs are going to require a mandate and funding from the governments at the federal, state, and local levels, but what could be more important than the legacy that could provide. It is a small investment to make. The future not only of our children, but the country as a whole is at stake here...

Labels: teen pregnancy

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