For many women who have had Asherman's syndrome, the journey to having a baby is not over with the removal of adhesions. While many doctors will use this to support their theory that they had other underlying fertility problems to begin with, it is equally possible that in some cases, Asherman's syndrome has lasting effects on fertility. Sometimes these are obvious such as inaccessible ostia (adhesions are sometimes too risky to remove) or thin endometrium. Most doctors agree that a lining of at least 8 mm at the time of ovulation is ideal for implantation. There could be other defects that persist after surgical correction such as reduced blood flow to the uterus. There is some disagreement as to whether procedures which reduce blood flow to the uterus, such as uterine artery embolization (UAE) can reduce fertility by affecting ovarian reserve. There is another intriguing link between blood flow and egg quality: it is known that endometriosis reduces egg quality although the mechanism is unknown. This makes me wonder whether I have endometriosis (I've never had a laparoscopy). There is something incongruent about having so many eggs of such poor quality. Unfortunately there is little research and few artifical reproductive techniques which focus on the quality of the endometrium. These few studies will be the topic of a future blog. There is also little research on improving egg quality as most fertility specialists are skeptical that this is possible due to currently accepted dogma on egg development.
Many women with a history of AS end up undergoing fertility treatments. Personally, I experienced infertility for 1.5 years even after AS correction (surgery and estrogen therapy) when I had had no problems conceiving to begin with. Then I went from being infertile to now conceiving once every two months but miscarrying. I have had 5 miscarriages in one year. All of my pregnancies have been naturally conceived. The last 3 have been very early miscarriages. Of course my first thought was that I might have some recurrence adhesions from my last hysteroscopic removal of RPOC in March. An in-office diagnostic hysteroscopy ruled out this possibility. I had molecular karyotyping (MLPA) of my last miscarriage which revealed trisomy 9, 20 and triallelic markers on the X chromosome. This indicates problems with egg quality. The first pregnancy after AS occurred a few months after 2 cycles of unsuccessful IVF. I wonder whether the effect of IVF hormones had a beneficial effect on my endometrium and egg development. My plan is to now find a fertility specialist who is willing to work with me on a protocol that does not include egg retrieval and in vitro fertilization (since I conceive very easily without it), but rather one that concentrates on improving the uterine environment. My idea is to use low dose aspirin (to improve blood flow to the uterus) and low doses of FSH to stimulate about 2 follicles (to double my chances of a healthy embryo) , undergo 'in vivo' fertilization and start taking progesterone pessaries after ovulation (for luteal phase support). FSH stimulates follicles to grow which in turn secrete estrogen to thicken the endometrial lining. Some women with past AS find that their endometrium responds more favourably to this ovarian stimulation than to estrogen pills. I'm also considering the use of DHEA, a controversial hormone which is alleged to improve ovarian reserve and quality, resulting in fewer miscarriages (and presumably aneuploidies).
Unfortunately, a few of the fertility specialists I have seen in the past have been very unflexible and biased in their thinking. Many have their own 'pet' theories about what works and what doesn't without the backup of proper studies. While they are happy to point out that my suggestions have no rigorous evidence of efficacy, they seem oblivious to the fact that their own suggestions also lack robust data and in addition, are often expensive, time consuming, painful and with possible adverse effects on health. When I once pointed this out, a well respected specialist told me to stop thinking like a scientist! He also told me that if I 'really' wanted a baby I would be willing to try risky treatments! There are still many unknowns in the area of infertility and fertility doctors don't know everything (even if some of them think they do!). For instance, this specialist convinced me that my inability to conceive was due to my low AMH levels (an indicator of poor ovarian reserve in my case due to being over 40) and in his words, I would never conceive without IVF, although he couldn't explain how IVF would improve ovarian reserve or egg quality. As an aside, I have very low FSH levels (3 when I was 42) which are meant to indicate excellent ovarian reserve. I didn't know it at the time he said this, but I was already pregnant. I went on to have 4 more pregnancies afterwards. Unfortunately my problem now is recurrent miscarriage, but his statement is still untrue. No one has been able to give me a reasonable explanation as to why I have gone from being unable to conceive for 1.5 years despite treatment for IUA, to conceiving every 2 months.
Below is a link to a chart detailing which tests and treatments are scientifically supported and which are not. Most have not been proven to be useful, although it is possible that in future there will be evidence to support them. It is up to the individual to decide, after considering risks and benefits, whether to proceed with them.
Infertility Tests and Therapies Questioned (Bupa)
More information on the validity of tests and therapies for infertility/recurrent miscarriage:
Cochrane Reviews: Immunotherapy for recurrent miscarriage (Full article: click here)
Note that this systematic review is comprised of studies where exclusion criteria included women with abnormal immune tests (eg. auto-antibody, cytotoxic antibodies, IgA deficiency etc.). Bascially, this review found that in women with recurrent miscarriage without any demonstrated abnormal immune function, there is no significant evidence that immunotherapy is useful (which one would expect). Still, many fertility specialists are eager to use these therapies on such patients.
RCOG: Implantation and Early Development - study group statement.
Miscarriage, Infertility, Antibodies and the Immune System Dr Licciardi's Infertility Blog
Showing posts with label infertility. Show all posts
Showing posts with label infertility. Show all posts
Thursday, October 21, 2010
Friday, July 2, 2010
FAQs Asherman's syndrome
Please see the new page on frequently asked questions about Asherman's syndrome. You can also click on the relevant tab button in the tab bar at the top of the page to view it.
Friday, February 19, 2010
How AS causes infertility or miscarriages
Asherman’s syndrome (AS) can lead infertility in a number of ways. No two cases are identical and it can manifest as infertility according to how and which parts of the reproductive anatomy is affected. AS is characterized by intrauterine adhesions (IUA) and/or fibrosis (non-functional scar tissue).
Infertility may be caused by adhesions occluding the tubal ostia, uterine cavity, or the cervix, thereby interfering with the migration of sperm or implantation of the embryo (1). The presence of defective endometrium in the fundus and ostia which are partially obliterated by the adhesions may also predispose women to tubal and cervical pregnancies (2,3). Partial obstruction of tubes can lead to pregnancy complications such as ectopic pregnancy because the fertilized egg may be physically impeded from migrating to the uterus for implantation. If ostial obstruction is so extensive that it cannot be corrected through hysteroscopic adhesiolysis, in vitro fertilization is the only possibility for a biological offspring (providing that the rest of the uterus is functional and adhesion free). Cervical pregnancy (another form of ectopic pregnancy) may occur if the embryo implants in the cervix. Adhesions involving the cervix may result in the cervix being closed (outlet obstruction). This obviously prevents the sperm from encountering the egg. It has also been noted that in women with outlet obstruction due to adhesions blocking the lower uterus or cervix, endometrial measures are thinner than in women where adhesions are limited to the upper uterus (4). It is thought that the underlying cause of this is a feedback loop to prevent haematometra from occurring. Haematometra is the formation of a large clot of blood from trapped menstrual debris and it very rarely occurs in the former subgroup of women.
Another possible way Asherman’s syndrome can result in infertility is by causing endometriosis. Some authors have noted that women with extensive adhesions either in the uterus or cervix, blocking menstrual flow, later develop endometriosis (5). This was discovered because laparoscopic (keyhole) surgery is sometimes carried out at the same time as hysteroscopy when performing adhesiolysis of IUA. Laparoscopy helps to prevent uterine perforation in severe cases where it may be difficult to judge the limits of the uterine cavity. Endometriosis is the growth of endometrial lining outside of the uterus. It can occur anywhere in the body, though most commonly occurs in the abdomen. Although the cause(s) of endometriosis remain unknown, one of the theories put forth by John A. Sampson is known as the theory of retrograde menstruation. It speculates that a back flow of blood and debris through the fallopian tubes and into the abdomen enables its implantation to the peritoneal surface (the lining of the abdominal cavity) where it can proceed to invade the tissue as endometriosis. (As an aside to those who practice yoga, this is why inverted positions such as headstands are avoided during menstruation). Endometriosis itself can lead to infertility by causing pelvic adhesions (Note: not to be confused with intrauterine adhesions which occur INSIDE the uterus). Pelvic adhesions (or extrauterine adhesions) can twist and distort the fallopian tubes and prevent fertilization or implantation.
Many women who have had Asherman’s syndrome develop a thin endometrium even after surgical correction and hormonal therapy to stimulate endometrial regeneration. An optimal thickness of the endometrium (>8mm) is considered to be one of the prerequisites for successful implantation of the embryo. Thin endometrium can be caused by either too much of the endometrium having been removed during D&C (or other uterine surgery) or cervical obstruction (as described above). A thin endometrium may be unresponsive to hormones (6) and may lead to infertility in the form of implantation failure or early miscarriages known as ‘chemical pregnancies’ due to a lack of blood supply and poor placental perfusion. Thin endometrium can also occur in women who have had D&Cs, even if they did not develop Asherman’s syndrome. In fact, a recent study found that the endometrium of women is thinner for about 6 months after a D&C (7). A recent study suggests that treatment with tocopherol (ie. vitamin E) and pentoxifylline may help to thicken the endometrium (8), improving implantation. Of course IUA must be removed before pregnancy can be attempted.
The exact mechanisms by which IUA predispose to miscarriages are unknown, however, it is suspected that constrictions of the uterine cavity by adhesions, lack of adequate functional endometrium to support implantation and defective vascularisation of the residual endometrial tissue due to fibrosis may account for repeated pregnancy loss (9). If an embryo implants in an adhesion or a fibrotic region, it will not grow successfully because it will not have an adequate blood supply, essential for providing the growing embryo with oxygen and nutrients. This can lead to miscarriage. Interestingly, this is analogous to the situation where women with Mullerian malformations such as septate uterus often undergo miscarriage when the embryo implants in the septum (10). If IUAs obstruct the openings of one or both of the fallopian tubes (known as ostia) this prevents the sperm from fertilizing the egg (which normally happens in the fallopian tubes after ovulation).
There is another potential cause of second trimester miscarriage which has been often reported in women with a past history of Asherman’s syndrome: cervical incompetence, also known and cervical insufficiency, however, I will write about this under a future blog topic, post-Asherman’s syndrome obstetric complications, since these miscarriages are not due to adhesions or fibrosis per se but to previous dilations of the cervix during surgeries.
As a consequence of the above, many women who have untreated Asherman’s syndrome are either unable to conceive, or suffer from repeated miscarriages. However, depending on the location, extent and severity of IUA/fibrosis, patients may conceive and carry a pregnancy without treatment. This is not recommended and is usually a chance finding on ultrasound when an adhesion or synechia is detected. There have been isolated case reports of successful and uncomplicated pregnancies in the presence of IUA (11). In the best case scenario, the adhesions are minimal and thin, stretching with the pregnancy such that it does not impinge on the growth of the fetus or uterus. However, women are strongly advised to use contraception to avoid pregnancy until surgical correction of adhesions to avoid pregnancy complications. In women who conceive without removal of adhesions, the reproductive outcome is usually poor: in one well known study, it was reported that of the 46% of patients with untreated IUA who conceived, 40% of the pregnancies ended in spontaneous miscarriage, 12% of which were ectopic. Of the viable pregnancies, 23% delivered prematurely and 13% had placenta accreta with only 53% delivering viable infants (12). Obviously, the more severe the classification of AS, the more likely complications are to occur if a pregnancy occurs. On the other hand, pregnancy itself is probably less likely to occur in more severe cases. Note that these complications may also occur in women after treatment of Asherman’s syndrome, however not as frequently. This will be covered in a future blog.
The moral of the story is: get treated by a trusted Asherman’s specialist if you have Asherman’s syndrome and make sure the uterine cavity is clear (via a follow up hysteroscopy or HSG) and that adhesions have not recurred before trying to conceive. Even better, avoid getting Asherman’s syndrome by using alternatives to D&C.
References
1.Yu, D, Wong, YM, Cheong, Y, Xia, E, and Li, TC. Asherman syndrome--one century later. Fertil Steril 2008;89(4):759-79.
2. Dicker, D, Feldberg, D, Samuel, N, and Goldman, JA. Etiology of cervical pregnancy. Association with abortion, pelvic pathology, IUDs and Asherman's syndrome. J Reprod Med 1985;30(1):25-7.
3. Forssman, L. Posttraumatic intrauterine synechiae and pregnancy. Obstet Gynecol 1965;26(5):710-3.
4. Lo ST, Ramsay P, Pierson R, Manconi F, Munro MG, Fraser IS. Endometrial thickness measured by ultrasound scan in women with uterine outlet obstruction due to intrauterine or upper cervical adhesions.Hum Reprod. 2008 ;23(2):306-9. Link
5. Palter. SF, High Rates of Endometriosis in Patients With Intrauterine Synechiae (Asherman's Syndrome). Fertility and Sterility 2005; 86 (null):S471-S471. Link
6. Shufaro, Y, Simon, A, Laufer, N, and Fatum, M. Thin unresponsive endometrium--a possible complication of surgical curettage compromising ART outcome. J Assist Reprod Genet 2008;25(8):421-5.
7. Moon KS, Richter KS, Levy MJ, Widra EA. Does dilation and curettage versus expectant management for spontaneous abortion in patients undergoing in vitro fertilization affect subsequent endometrial development? Fertil Steril. 2009;92(5):1776-9. PMID 19560759
8. Acharya S, Yasmin E, Balen AH. The use of a combination of pentoxifylline and tocopherol in women with a thin endometrium undergoing assisted conception therapies--a report of 20 cases. Hum Fertil (Camb). 2009;12(4):198-203. Link
9. Polishuk, WZ and Sadovsky, E. A syndrome of recurrent intrauterine adhesions. Am J Obstet Gynecol 1975;123(2):151-8.
10. Golan, A, Schneider, D, Avrech, O, Raziel, A, Bukovsky, I, and Caspi, E.
Hysteroscopic findings after missed abortion. Fertil Steril 1992;58(3):508-10.
11. Klatsky PC, Tran ND, Strachowski L. A pregnancy complicated by endometrial scarring. Fertil Steril. 2009;91(6):2707-8.
12. Schenker, JG and Margalioth, EJ. Intrauterine adhesions: an updated appraisal. Fertil Steril 1982;37(5):593-610.
Infertility may be caused by adhesions occluding the tubal ostia, uterine cavity, or the cervix, thereby interfering with the migration of sperm or implantation of the embryo (1). The presence of defective endometrium in the fundus and ostia which are partially obliterated by the adhesions may also predispose women to tubal and cervical pregnancies (2,3). Partial obstruction of tubes can lead to pregnancy complications such as ectopic pregnancy because the fertilized egg may be physically impeded from migrating to the uterus for implantation. If ostial obstruction is so extensive that it cannot be corrected through hysteroscopic adhesiolysis, in vitro fertilization is the only possibility for a biological offspring (providing that the rest of the uterus is functional and adhesion free). Cervical pregnancy (another form of ectopic pregnancy) may occur if the embryo implants in the cervix. Adhesions involving the cervix may result in the cervix being closed (outlet obstruction). This obviously prevents the sperm from encountering the egg. It has also been noted that in women with outlet obstruction due to adhesions blocking the lower uterus or cervix, endometrial measures are thinner than in women where adhesions are limited to the upper uterus (4). It is thought that the underlying cause of this is a feedback loop to prevent haematometra from occurring. Haematometra is the formation of a large clot of blood from trapped menstrual debris and it very rarely occurs in the former subgroup of women.
Another possible way Asherman’s syndrome can result in infertility is by causing endometriosis. Some authors have noted that women with extensive adhesions either in the uterus or cervix, blocking menstrual flow, later develop endometriosis (5). This was discovered because laparoscopic (keyhole) surgery is sometimes carried out at the same time as hysteroscopy when performing adhesiolysis of IUA. Laparoscopy helps to prevent uterine perforation in severe cases where it may be difficult to judge the limits of the uterine cavity. Endometriosis is the growth of endometrial lining outside of the uterus. It can occur anywhere in the body, though most commonly occurs in the abdomen. Although the cause(s) of endometriosis remain unknown, one of the theories put forth by John A. Sampson is known as the theory of retrograde menstruation. It speculates that a back flow of blood and debris through the fallopian tubes and into the abdomen enables its implantation to the peritoneal surface (the lining of the abdominal cavity) where it can proceed to invade the tissue as endometriosis. (As an aside to those who practice yoga, this is why inverted positions such as headstands are avoided during menstruation). Endometriosis itself can lead to infertility by causing pelvic adhesions (Note: not to be confused with intrauterine adhesions which occur INSIDE the uterus). Pelvic adhesions (or extrauterine adhesions) can twist and distort the fallopian tubes and prevent fertilization or implantation.
Many women who have had Asherman’s syndrome develop a thin endometrium even after surgical correction and hormonal therapy to stimulate endometrial regeneration. An optimal thickness of the endometrium (>8mm) is considered to be one of the prerequisites for successful implantation of the embryo. Thin endometrium can be caused by either too much of the endometrium having been removed during D&C (or other uterine surgery) or cervical obstruction (as described above). A thin endometrium may be unresponsive to hormones (6) and may lead to infertility in the form of implantation failure or early miscarriages known as ‘chemical pregnancies’ due to a lack of blood supply and poor placental perfusion. Thin endometrium can also occur in women who have had D&Cs, even if they did not develop Asherman’s syndrome. In fact, a recent study found that the endometrium of women is thinner for about 6 months after a D&C (7). A recent study suggests that treatment with tocopherol (ie. vitamin E) and pentoxifylline may help to thicken the endometrium (8), improving implantation. Of course IUA must be removed before pregnancy can be attempted.
The exact mechanisms by which IUA predispose to miscarriages are unknown, however, it is suspected that constrictions of the uterine cavity by adhesions, lack of adequate functional endometrium to support implantation and defective vascularisation of the residual endometrial tissue due to fibrosis may account for repeated pregnancy loss (9). If an embryo implants in an adhesion or a fibrotic region, it will not grow successfully because it will not have an adequate blood supply, essential for providing the growing embryo with oxygen and nutrients. This can lead to miscarriage. Interestingly, this is analogous to the situation where women with Mullerian malformations such as septate uterus often undergo miscarriage when the embryo implants in the septum (10). If IUAs obstruct the openings of one or both of the fallopian tubes (known as ostia) this prevents the sperm from fertilizing the egg (which normally happens in the fallopian tubes after ovulation).
There is another potential cause of second trimester miscarriage which has been often reported in women with a past history of Asherman’s syndrome: cervical incompetence, also known and cervical insufficiency, however, I will write about this under a future blog topic, post-Asherman’s syndrome obstetric complications, since these miscarriages are not due to adhesions or fibrosis per se but to previous dilations of the cervix during surgeries.
As a consequence of the above, many women who have untreated Asherman’s syndrome are either unable to conceive, or suffer from repeated miscarriages. However, depending on the location, extent and severity of IUA/fibrosis, patients may conceive and carry a pregnancy without treatment. This is not recommended and is usually a chance finding on ultrasound when an adhesion or synechia is detected. There have been isolated case reports of successful and uncomplicated pregnancies in the presence of IUA (11). In the best case scenario, the adhesions are minimal and thin, stretching with the pregnancy such that it does not impinge on the growth of the fetus or uterus. However, women are strongly advised to use contraception to avoid pregnancy until surgical correction of adhesions to avoid pregnancy complications. In women who conceive without removal of adhesions, the reproductive outcome is usually poor: in one well known study, it was reported that of the 46% of patients with untreated IUA who conceived, 40% of the pregnancies ended in spontaneous miscarriage, 12% of which were ectopic. Of the viable pregnancies, 23% delivered prematurely and 13% had placenta accreta with only 53% delivering viable infants (12). Obviously, the more severe the classification of AS, the more likely complications are to occur if a pregnancy occurs. On the other hand, pregnancy itself is probably less likely to occur in more severe cases. Note that these complications may also occur in women after treatment of Asherman’s syndrome, however not as frequently. This will be covered in a future blog.
The moral of the story is: get treated by a trusted Asherman’s specialist if you have Asherman’s syndrome and make sure the uterine cavity is clear (via a follow up hysteroscopy or HSG) and that adhesions have not recurred before trying to conceive. Even better, avoid getting Asherman’s syndrome by using alternatives to D&C.
References
1.Yu, D, Wong, YM, Cheong, Y, Xia, E, and Li, TC. Asherman syndrome--one century later. Fertil Steril 2008;89(4):759-79.
2. Dicker, D, Feldberg, D, Samuel, N, and Goldman, JA. Etiology of cervical pregnancy. Association with abortion, pelvic pathology, IUDs and Asherman's syndrome. J Reprod Med 1985;30(1):25-7.
3. Forssman, L. Posttraumatic intrauterine synechiae and pregnancy. Obstet Gynecol 1965;26(5):710-3.
4. Lo ST, Ramsay P, Pierson R, Manconi F, Munro MG, Fraser IS. Endometrial thickness measured by ultrasound scan in women with uterine outlet obstruction due to intrauterine or upper cervical adhesions.Hum Reprod. 2008 ;23(2):306-9. Link
5. Palter. SF, High Rates of Endometriosis in Patients With Intrauterine Synechiae (Asherman's Syndrome). Fertility and Sterility 2005; 86 (null):S471-S471. Link
6. Shufaro, Y, Simon, A, Laufer, N, and Fatum, M. Thin unresponsive endometrium--a possible complication of surgical curettage compromising ART outcome. J Assist Reprod Genet 2008;25(8):421-5.
7. Moon KS, Richter KS, Levy MJ, Widra EA. Does dilation and curettage versus expectant management for spontaneous abortion in patients undergoing in vitro fertilization affect subsequent endometrial development? Fertil Steril. 2009;92(5):1776-9. PMID 19560759
8. Acharya S, Yasmin E, Balen AH. The use of a combination of pentoxifylline and tocopherol in women with a thin endometrium undergoing assisted conception therapies--a report of 20 cases. Hum Fertil (Camb). 2009;12(4):198-203. Link
9. Polishuk, WZ and Sadovsky, E. A syndrome of recurrent intrauterine adhesions. Am J Obstet Gynecol 1975;123(2):151-8.
10. Golan, A, Schneider, D, Avrech, O, Raziel, A, Bukovsky, I, and Caspi, E.
Hysteroscopic findings after missed abortion. Fertil Steril 1992;58(3):508-10.
11. Klatsky PC, Tran ND, Strachowski L. A pregnancy complicated by endometrial scarring. Fertil Steril. 2009;91(6):2707-8.
12. Schenker, JG and Margalioth, EJ. Intrauterine adhesions: an updated appraisal. Fertil Steril 1982;37(5):593-610.
Saturday, January 30, 2010
A hidden cause of ‘unexplained’ infertility and miscarriages: ignorance about AS
Asherman’s syndrome remains a cause of infertility –ie. the inability to conceive or carry a pregnancy- the latter sometimes resulting in repeat miscarriages- which is often overlooked. This is because both doctors and women alike are often unaware of this ‘syndrome’ which rarely gets a mention outside of infrequent gynecological journal articles or anti-abortion propaganda (which ignores the fact that a D&C for any reason or intrauterine surgery can cause the condition). Furthermore, it may be difficult to make a link between a surgery and problems or complications which may occur years later. Another reason is that it is incorrectly thought of as being a rare condition, despite reports of up to 30% of women developing intrauterine adhesions (IUA) after D&C for missed miscarriage and 25% if D&C is performed following delivery (1,2).
Ironically, perhaps another reason it remains so hidden is due to its very symptoms: infertility and miscarriages. Unfortunately, even among highly educated medical professionals, there remains a tendency to consider women who exhibit these as having other fertility flaws rather than to contemplate that problems could be the result of a routine procedure they or a colleague carried out. I was dismayed to have read so many peer-reviewed medical articles where this view is expressed. In fact, Dr. Joseph Asherman, the doctor who described the condition in detail in 1948 and whose name the condition was coined after, quite strangely believed that "adhesions are certainly not to blame for the incapacity to conceive" (3). Of course, this view is certainly refuted today. I will write about this and other errors Dr Asherman (and others) made in a future blog. With all due respect, one should keep in mind that his speculations were based on what he could extrapolate from the imaging techniques and medical and scientific knowledge available in the 1940s and 1950s. Today we are in a much better position to analyze medical conditions. However many study authors continue to suggest that any failure to achieve pregnancy or live birth after 'successful' treatment of IUA as ‘evidence’ of other additional underlying fertility issues even though there could be endometrial dysfunction due to fibrosis for which there are currently no accurate tests. Current live birth outcomes are around 40% at best. This means that they attribute at least 60% of post AS infertility to hypothetical additional infertility factors. Therefore, secondary infertility is often incorrectly labeled as primary infertility.
It is of no surprise that Asherman's syndrome was first noted in a woman who developed amenorrhea after a postpartum curettage (6). If she had not 'proven' her fertility by giving birth her infertility would surely be ascribed to some other undefined cause. Thus, if a childless woman who has a D&C to treat a miscarriage and develops AS, many doctors are less likely to investigate it and put down her future infertility (and prior miscarriage) to other 'unknown' fertility problems. It does not help that the older a woman, the more likely she is to have a miscarriage and therefore undergo a D&C- and develop AS. Age-related infertility can then be the excuse, and if you are a woman aged 40 or over and have ever been to see a fertility specialist as I have, you will have this drummed into you like a mantra. (On a personal note, this is why it especially sucks to get AS after the miscarriage of a first pregnancy when you are an older woman!!!). Most D&Cs are carried out for miscarriage, and proportionally more miscarriages occur in older women at the same time as their natural fertility is declining.
Also unfortunate is that the indirect association between women who do have other fertility problems and AS is often thought to be a direct association. The correlation is due to the fact that women with fertility problems are more likely to miscarry, and therefore have D&Cs-the cause of AS- however unfortunately some doctors will only look at the simplest assocation. There is a review article (4) which misleadingly describes Mullerian defects (eg. septate uterus) as a cause of AS due to 'stagnation of menstrual debris or old blood inside the uterine cavity'. This assertion has no basis whatsoever, nor have I read any similar claim in any other peer-reviewed medical article. (Note: incidentally, that article which is ironically titled 'Ashermans syndrome (IUA): Has there been any progress over the last 20 years?' is undoubtedly the most unconventional review on Asherman's syndrome I have ever come across. Perhaps I can go into the details of this in a blog of its own). In fact it has already been noted that women with Mullerian defects often have had several miscarriages and D&Cs, and it is the latter which increases their risk of developing AS (5). Furthermore, it doesn't take a rocket scientist to realize that blindly scraping in any uterus, let alone an unusually shaped uterus with a wall in the middle, is likely to result in injury leading to IUA. In reality, the only female population that is ‘predisposed’ to AS is anyone who is likely to undergo D&C or intrauterine surgery more frequently than the 'normal' population, whatever the reason might be. No wonder there is so little sympathy or admission of responsibility by the medical community when it is in their interest to blame the patient’s age or other undefined fertility issues for infertility instead of standard medical care.
Even when menstrual disturbances -which are hallmarks of AS- are reported by patients they are either brushed aside as imaginary, explained as normal for one’s age or following miscarriage, or put down to other ‘proof’ of other fertility problems.
The sayings:
“Science progresses best when observations force us to alter our preconceptions.” (Vera Rubin)
“Those who have excess faith in their theories or in their ideas are not only poorly disposed to make discoveries, but they also make very poor observations.” (Claude Bernard)
come to mind.
The bad news is that if Gyns/ObGyns are missing (intentionally or not) the link between cause and effect (ie. D&C and infertility/miscarriages) and making biased and incorrect assumptions about other causes of infertility to ‘explain’ reproductive outcome failure, this gives less incentive for doctors to replace the current standard of care for miscarriage with drugs such as misoprostol or hysteroscopic removal of retained tissue instead. Instead, these attitudes help to maintain the status quo and enables D&Cs to continue to be used widely and indiscrimminately, ignoring the risks.
The most accurate method for diagnosis of IUA is hysteroscopy because it allows a direct view of the inside of the uterus however it is not routinely carried out during infertility workups. Couples considering artificial reproductive technology (ART) are referred for other diagnostic procedures such as ultrasound and HSG however these may not accurately detect the presence of IUA. Also, there is currently no test available for endometrial function which is essential to proper embryo implantation and successful pregnancy. Unfortunately there are few gynecologists who are trained to perform hysteroscopy. Only 15% of US doctors perform office hysteroscopy (7). In comparison, 100% of urologists use office cytoscopy to evaluate bladder pathology. I find it disconcerting that hysteroscopy is such an underutilized technique and question if this would be the case if those likely to benefit from it were men (similarly, would D&C continue to be used if it caused male infertility?). Perhaps our own inaction and passivity as women are in part to blame. Undergoing IVF in the presence of AS is a very expensive waste of time and once again, it is the patient (and broader community if fertility treatment is government subsidized, as in some countries) who suffers most from it, not the fertility specialists! (on the contrary...) IVF is bound to fail if the cavity is not suited for embryo implantation/growth. Even if a patient has other fertility problems such as blocked tubes or her husband has poor sperm quality, the patient must first correct IUA, if present, to enable her to conceive and carry a pregnancy through IVF.
Prospective studies in women with infertility and/or recurrent miscarriages who underwent diagnostic hysteroscopy revealed AS rates of 19-23.6% (8)(9)(10)(11). In other words, 1 in 4 to 1 in 5 women who are infertile or suffer repeat miscarriages have been shown to have IUA. For this reason, diagnostic hysteroscopy should be considered by any woman with unexplained infertility especially if she has ever had a D&C or intrauterine surgery for ANY reason. It especially makes sense to investigate the cavity further if she is either considering IVF or has had unsuccessful IVF treatments. The recommendation to use hysteroscopy in infertility workups appears to be controversial. Interestingly, diagnostic D&Cs are far more commonly used in gynecology even though they carry more risks and provide zero information about the presence of IUA. In the following
Quoting from the presentation:
“It is no more acceptable for a gynecologist to insert a sharp curette into a uterine cavity blindly to discover and remove suspected pathology than it is for an orthopedist to insert a curette into a knee joint blindly.”
REFERENCES
1. Adoni, A, Palti, Z, Milwidsky, A, and Dolberg, M. The incidence of intrauterine
adhesions following spontaneous abortion. Int J Fertil 1982;27(2):117-8.
2. Eriksen, J and Kaestel, C. The incidence of uterine atresia after post-partum
curettage. A follow-up examination of 141 patients. Dan Med Bull 1960;7:50-1.
3. Asherman J. Traumatic intrauterine adhesions and their effect on fertility. Int J Fertil 2:49, 1957.
4. Panayotidis C, Weyers S, Bosteels J, van Herendael B.5. Intrauterine adhesions (IUA): has there been progress in understanding and treatment over the last 20 years? (2009) Gynecol Surg 6(3):197-211.
Hysteroscopic findings after missed abortion. Fertil Steril 1992;58(3):508-10.
6. Fritsch, H. Ein Fall von volligem Schwaund der Gebormutterhohle nach
Auskratzung Zentralbl Gynaekol 1894;18:1337-1342.
7. Isaacson, K. Office hysteroscopy: a valuable but under-utilized technique. Curr
Opin Obstet Gynecol 2002;14(4):381-5.
8. Raziel, A, Arieli, S, Bukovsky, I, Caspi, E, and Golan, A. Investigation of the
uterine cavity in recurrent aborters. Fertil Steril 1994;62(5):1080-2.
9. Preutthipan, S and Linasmita, V. Reproductive outcome following hysteroscopic
lysis of intrauterine adhesions: a result of 65 cases at Ramathibodi Hospital. J Med
Assoc Thai 2000;83(1):42-6.
10. Ventolini, G, Zhang, M, and Gruber, J. Hysteroscopy in the evaluation of patients
with recurrent pregnancy loss:
11. Dendrinos, S, Grigoriou, O, Sakkas, EG, Makrakis, E, and Creatsas, G.
Hysteroscopy in the evaluation of habitual abortions. Eur J Contracept Reprod
Health Care 2008;13(2):198-200.
Tuesday, August 4, 2009
Asherman's syndrome after curettage is not rare
Asherman's syndrome is ‘uncommon’. How many times have I come across that sentence or a variation of it (Asherman’s syndrome is ‘rare’ or even ‘extremely rare’ etc.). They were my ObGyn’s famous last words too. Oh, how I wish they were true. A simple google search of Asherman’s syndrome will show that many links contain this inaccuracy. Even the reputable ncbi/nih writes:
"Asherman syndrome is a rare condition. In most cases, it occurs in women who have had several dilatation and curettage (D&C) procedures."
No true!!! It often happens after a single D&C procedure. How often? Well, according to various studies published in peer-reviewed medical journals, the actual incidence of intrauterine adhesions (IUA) after D&C for miscarriage ranges between 7.7% and 30%, and after a repeat procecure, up to 40%. To be clear, some of these studies are not new. However, there is no reason to suspect that incidence rates would change as the techniques used are for the most part the same. The main cause of IUA is blind instrumentation in a uterus softened by the presence of hormones (as in pregnancy). Even the more recent manual vacuum aspiration has been associated with IUA (Dalton et al, 2006). Furthermore, sharp/blunt/suction D&C are often all used in the same procedure. Anyone who is familiar with the literature on Asherman’s syndrome will know that the references below are cited as references in recent review papers (see Yu et al,2008; Kodaman and Arici, 2007). [Obviously an institutional (or personal) subscription is needed to view the entire article]. Another potential criticism about these studies is that they are not RCTs. (One is an RCT but it does not meet the criteria for inclusion in the Cochrane Collaboration 's library (click here for more details). For non-scientists/doctors, I will describe what RCTs and the Cochrane library are in further detail in a later blog. For now, suffice to say that RCTs meet the most rigorous standards of scientific methodology.) Unfortunately, to date there are NO RCTs on Asherman’s syndrome (including etiology and treatment) in the Cochrane database.
Nevertheless, according to the available studies on the topic, the following incidence rates have been reported:
1. Adoni et al (1982) found the incidence of IUA to be 30.9% after D&C for a ‘late’ miscarriage. This is taken to mean a missed miscarriage where the products of conception have not been expelled despite the pregnancy’s failure. IUA were detected via hysterography.
2. Golan et al.(1992) did a prospective analysis of 60 women and found that 16.7% of women undergoing D&C for missed miscarriage had IUA detected by hysteroscopy (gold standard method of diagnosis).
3. Friedler et al (1993) also did a prospective study on women with missed miscarriages who underwent D&C and found that 16 of the 98 patients, or 16.3%, had IUA detected by hysteroscopy.
4. Romer et al’s (1994) prospective study diagnosed IUA in 30.2% of women who had D&C for either missed or incomplete miscarriage. This was diagnosed hysteroscopically.
5. Westendorp et al (1998) prospectively examined wome who had repeat D&C for incomplete miscarriage or retained POC (after either miscarriage or delivery) and found that on hysteroscopy, a whopping 40% of them had IUA. 30% were severe.
6. Tam et al (2002) performed a prospective study on IUA incidence after D&C for missed or incomplete miscarriage and compared it to women treated expectantly or using misoprostol. They found that 7.7% of women in the D&C group developed IUA while none developed it in the misoprostol group or expectant group. Again, hysteroscopy, was used for detection.
7. Eriksen and Kaestel (1960) reported in their retrospective analysis that approximately 25% of women undergoing post partum curettage developed IUA.
I don’t know about you, but I find all this unsettling. Why didn’t anyone tell me this before I had a D&C?!
Asherman’s syndrome is thought to affect 5% of the population. I don’t recall if there is a particular reference for this, but I know I’ve heard a few Asherman’s syndrome specialists say it. Of course it is difficult to know the exact prevalence as many cases are not diagnosed. Also, some women may have it but not desire a further pregnancy so they never find out if they are infertile or have pregnancy complications associated with Asherman’s syndrome.
What is striking is that this incidence (5%), is not very different from the rate of conditions such as PCOS, another cause of infertility (which, by the way, is not iatrogenic...) Yet, when do you ever hear people say: PCOS is a rare condition?! You will read everywhere that PCOS is ‘common’ or ‘exceedingly common’. There are entire sections of gynecology journals devoted to this condition and hundreds of studies. Asherman’s syndrome, in contrast, is largely ignored by the medical community. Are doctors repeating the supposed ‘rarity’ of Asherman’ syndrome to make women feel that D&Cs are safer than they really are?
Perhaps this misconception once served a purpose- to prevent doctors from hesitating to perform D&Cs in situations where uterine evacuation was necessary and in a time when there was no other option, and to prevent patients from fearing a necessary treatment. Today this myth no longer serves a purpose. D&C is no longer a ‘necessary evil’ as there are other methods such as hysteroscopic guidance or uterus-evacuating drugs to obtain the same result- minus the serious complications.
The first step towards change would be to accept that Asherman’s syndrome is NOT rare.
References (in order of appearance in text)
Dalton VK, Saunders NA,Harris LH, Williams JA, Lebovic DI. Intrauterine adhesions after manual vacuum aspiration for early pregnancy failure. Fertil Steril 2006;85(6):1823 e1-3.
Kodaman, PH and Arici, A. Intra-uterine adhesions and fertility outcome: how to optimize success? Curr Opin Obstet Gynecol 2007;19(3):207-14.
Yu, D, Wong, YM, Cheong, Y, Xia, E, and Li, TC. Asherman syndrome--one century later. Fertil Steril 2008;89(4):759-79.
Adoni, A, Palti, Z, Milwidsky, A, and Dolberg, M. The incidence of intrauterine adhesions following spontaneous abortion. Int J Fertil 1982;27(2):117-8.
Golan, A, Schneider, D, Avrech, O, Raziel, A, Bukovsky, I, and Caspi, E. Hysteroscopic findings after missed abortion. Fertil Steril 1992;58(3):508-10.
Friedler, S, Margalioth, EJ, Kafka, I, and Yaffe, H. Incidence of post-abortion intra-uterine adhesions evaluated by hysteroscopy--a prospective study. Hum Reprod 1993;8(3):442-4.
Romer, T. Post-abortion-hysteroscopy--a method for early diagnosis of congenital and acquired intrauterine causes of abortions. Eur J Obstet Gynecol Reprod Biol 1994;57(3):171-3.
Tam, WH, Lau, WC, Cheung, LP, Yuen, PM, and Chung, TK. Intrauterine adhesions after conservative and surgical management of spontaneous abortion. J Am Assoc Gynecol Laparosc 2002;9(2):182-5.
Westendorp, IC, Ankum, WM, Mol, BW, and Vonk, J. Prevalence of Asherman's syndrome after secondary removal of placental remnants or a repeat curettage for incomplete abortion. Hum Reprod 1998;13(12):3347-50.
Eriksen J, Kaestel C. The incidence of uterine atresia after post-partum curettage. A follow-up examination of 141 patients. Dan Med Bull 1960; 7:50-1.
"Asherman syndrome is a rare condition. In most cases, it occurs in women who have had several dilatation and curettage (D&C) procedures."
No true!!! It often happens after a single D&C procedure. How often? Well, according to various studies published in peer-reviewed medical journals, the actual incidence of intrauterine adhesions (IUA) after D&C for miscarriage ranges between 7.7% and 30%, and after a repeat procecure, up to 40%. To be clear, some of these studies are not new. However, there is no reason to suspect that incidence rates would change as the techniques used are for the most part the same. The main cause of IUA is blind instrumentation in a uterus softened by the presence of hormones (as in pregnancy). Even the more recent manual vacuum aspiration has been associated with IUA (Dalton et al, 2006). Furthermore, sharp/blunt/suction D&C are often all used in the same procedure. Anyone who is familiar with the literature on Asherman’s syndrome will know that the references below are cited as references in recent review papers (see Yu et al,2008; Kodaman and Arici, 2007). [Obviously an institutional (or personal) subscription is needed to view the entire article]. Another potential criticism about these studies is that they are not RCTs. (One is an RCT but it does not meet the criteria for inclusion in the Cochrane Collaboration 's library (click here for more details). For non-scientists/doctors, I will describe what RCTs and the Cochrane library are in further detail in a later blog. For now, suffice to say that RCTs meet the most rigorous standards of scientific methodology.) Unfortunately, to date there are NO RCTs on Asherman’s syndrome (including etiology and treatment) in the Cochrane database.
Nevertheless, according to the available studies on the topic, the following incidence rates have been reported:
1. Adoni et al (1982) found the incidence of IUA to be 30.9% after D&C for a ‘late’ miscarriage. This is taken to mean a missed miscarriage where the products of conception have not been expelled despite the pregnancy’s failure. IUA were detected via hysterography.
2. Golan et al.(1992) did a prospective analysis of 60 women and found that 16.7% of women undergoing D&C for missed miscarriage had IUA detected by hysteroscopy (gold standard method of diagnosis).
3. Friedler et al (1993) also did a prospective study on women with missed miscarriages who underwent D&C and found that 16 of the 98 patients, or 16.3%, had IUA detected by hysteroscopy.
4. Romer et al’s (1994) prospective study diagnosed IUA in 30.2% of women who had D&C for either missed or incomplete miscarriage. This was diagnosed hysteroscopically.
5. Westendorp et al (1998) prospectively examined wome who had repeat D&C for incomplete miscarriage or retained POC (after either miscarriage or delivery) and found that on hysteroscopy, a whopping 40% of them had IUA. 30% were severe.
6. Tam et al (2002) performed a prospective study on IUA incidence after D&C for missed or incomplete miscarriage and compared it to women treated expectantly or using misoprostol. They found that 7.7% of women in the D&C group developed IUA while none developed it in the misoprostol group or expectant group. Again, hysteroscopy, was used for detection.
7. Eriksen and Kaestel (1960) reported in their retrospective analysis that approximately 25% of women undergoing post partum curettage developed IUA.
I don’t know about you, but I find all this unsettling. Why didn’t anyone tell me this before I had a D&C?!
Asherman’s syndrome is thought to affect 5% of the population. I don’t recall if there is a particular reference for this, but I know I’ve heard a few Asherman’s syndrome specialists say it. Of course it is difficult to know the exact prevalence as many cases are not diagnosed. Also, some women may have it but not desire a further pregnancy so they never find out if they are infertile or have pregnancy complications associated with Asherman’s syndrome.
What is striking is that this incidence (5%), is not very different from the rate of conditions such as PCOS, another cause of infertility (which, by the way, is not iatrogenic...) Yet, when do you ever hear people say: PCOS is a rare condition?! You will read everywhere that PCOS is ‘common’ or ‘exceedingly common’. There are entire sections of gynecology journals devoted to this condition and hundreds of studies. Asherman’s syndrome, in contrast, is largely ignored by the medical community. Are doctors repeating the supposed ‘rarity’ of Asherman’ syndrome to make women feel that D&Cs are safer than they really are?
Perhaps this misconception once served a purpose- to prevent doctors from hesitating to perform D&Cs in situations where uterine evacuation was necessary and in a time when there was no other option, and to prevent patients from fearing a necessary treatment. Today this myth no longer serves a purpose. D&C is no longer a ‘necessary evil’ as there are other methods such as hysteroscopic guidance or uterus-evacuating drugs to obtain the same result- minus the serious complications.
The first step towards change would be to accept that Asherman’s syndrome is NOT rare.
References (in order of appearance in text)
Dalton VK, Saunders NA,Harris LH, Williams JA, Lebovic DI. Intrauterine adhesions after manual vacuum aspiration for early pregnancy failure. Fertil Steril 2006;85(6):1823 e1-3.
Kodaman, PH and Arici, A. Intra-uterine adhesions and fertility outcome: how to optimize success? Curr Opin Obstet Gynecol 2007;19(3):207-14.
Yu, D, Wong, YM, Cheong, Y, Xia, E, and Li, TC. Asherman syndrome--one century later. Fertil Steril 2008;89(4):759-79.
Adoni, A, Palti, Z, Milwidsky, A, and Dolberg, M. The incidence of intrauterine adhesions following spontaneous abortion. Int J Fertil 1982;27(2):117-8.
Golan, A, Schneider, D, Avrech, O, Raziel, A, Bukovsky, I, and Caspi, E. Hysteroscopic findings after missed abortion. Fertil Steril 1992;58(3):508-10.
Friedler, S, Margalioth, EJ, Kafka, I, and Yaffe, H. Incidence of post-abortion intra-uterine adhesions evaluated by hysteroscopy--a prospective study. Hum Reprod 1993;8(3):442-4.
Romer, T. Post-abortion-hysteroscopy--a method for early diagnosis of congenital and acquired intrauterine causes of abortions. Eur J Obstet Gynecol Reprod Biol 1994;57(3):171-3.
Tam, WH, Lau, WC, Cheung, LP, Yuen, PM, and Chung, TK. Intrauterine adhesions after conservative and surgical management of spontaneous abortion. J Am Assoc Gynecol Laparosc 2002;9(2):182-5.
Westendorp, IC, Ankum, WM, Mol, BW, and Vonk, J. Prevalence of Asherman's syndrome after secondary removal of placental remnants or a repeat curettage for incomplete abortion. Hum Reprod 1998;13(12):3347-50.
Eriksen J, Kaestel C. The incidence of uterine atresia after post-partum curettage. A follow-up examination of 141 patients. Dan Med Bull 1960; 7:50-1.
Thursday, July 23, 2009
Law suits and Asherman's syndrome: another failure for victims
You would think that if a ObGyn that performed a 'straightforward, routine' D&C which resulted in intrauterine adhesions and infertility (ie. Asheman's syndrome) you would have legal recourse. Think again. The vast majority of these cases end up with the patient not winning any damages. Incredible but, sadly, true. This is why I am so gung-ho on replacing D&Cs with drug alternatives which currently exist. It's simple madness to go through with a D&C which can decimate your fertility while the doctor gets away with it scot free. No wonder D&C continues to be such a popular surgery- there is no incentive to stop or at least be a little more discrimminating in its use when doctors are not held accountable for the outcomes. So simple too, even an intern can do it and no one will find out if it was a disaster until the damage is already done!
I would love for there to be an open list of doctors who caused Asherman's syndrome from D&Cs that were deemed to be simple and straighforward, not in any life-threatening emergency situation, for example (I'm more sympathetic to doctors who faced emergencies). This list would at least warn other women to avoid those doctors and have well-deserved repercussions on their wallets. It is afterall, their duty to care for their patients and not cause them harm and if they caused Asherman's syndrome from such a 'straightforward' procedure, they clearly breached their contract as a medical professional.
OK, I contend that it is difficult, maybe impossible, to not cause any damage from a D&C when you are poking objects into a small, soft, and fragile organ you cannot even see. But this is my point: if doctors want to continue pretending that it's acceptable to do D&Cs and stubbornly refuse to offer cheaper and less invasive drugs or a visually guided method like hysteroscopy, they should be held responsible for the consequences. As the situation stands, they continue to have their cake and eat it too. D&Cs, unlike hysteroscopy, do not require much skill (it’s hard to judge the outcome when the organ is concealed), and unlike misoprostol, it is financially rewarding to hospitals, Gyns/ObGyns, and anesthesiologists. Why would they want to work harder than they already do or earn less?
So why do these legal suits lose? One obvious reason is that medical malpractice suits have always been difficult to win because doctors are very well protected. Doctors are extremely supportive of each other and it is difficult to find a doctor who is willing to give expert medical advice in a case implicating a peer. This probably stems from reciprocity: "I'll scratch your back, if you scratch mine." Who knows if said medical expert will not face a malpractice suit (justified or not) some time in their career...
What perplexes me is that a lawyer can take on a medical case without having a medical or scientific degree or understanding basic health issues. Come to think of it, it is also somewhat disturbing that doctors don't need to be taught how to think objectively and critically to practice medicine, but I digress...
Defense lawyers and doctors will come up with all sorts of excuses to dismiss a valid medical case against them. This is where the Asherman's syndrome myths come in so handy. They are ‘facts’ which continue to be accepted without real evidence, often hypothesized decades ago at a time when well respected doctors in the field could formulate opinions without any scientific basis or need for clinical trials (no wonder some of them developed a ‘God complex’) and their peers believed them and even today continue to cite their published theories in the guise of ‘evidence’ in peer-reviewed medical journal articles. These opinions, in particular about Asherman’s syndrome, have over the years transformed into ‘dogma’ which medical school students are indoctrinated with. Somehow no one ever asks “Why are we blindly accepting what this doctor 50 years ago suggested when they didn’t have the advances in knowledge, diagnostic/surgical tools and understanding of evidence based medicine that we have today? ” Which leads me to wonder, as medicine is becoming more and more scientific in nature (evidence-based medicine), will this change the expected outcomes of some cases? I think it will inevitably do so. But there is still a long way to go.
I also wanted to mention a legal perspective which has always riled me in relation to Asherman's syndrome (I would think it also applies to other medical injuries affecting fertility): in a court of law where the nature of injury and of suffering are apparently graded, it makes no difference whether you had 10 children or none before the injury leading to infertility. Now, I know from the Asherman's International Support Group that such an attitude is promoted to keep the peace and encourage bonding (“we’re all in the same boat”), but to think that the law makes no distinction between someone who has been prevented from ever reproducing (a basic human right according to the United Nations charter) and someone who has done so is just plain cruel. There is no 'scientifically correct' answer to this, but one would think that the logical and instinctive answer is that the condition has more consequences for those who never had children before the injury than those who have.
It is difficult to find information about Asherman’s syndrome law suits on the internet, and judging by the number of visits this particular entry gets, it would appear to be an area that many women would like to learn more about. I have downloaded the few articles on lawsuits I have been able to find and will write another blog entry (one day) about what I find out from them. From a quick scan though, what I can say is that it appears that most of the successful lawsuits do not stem from injury of the D&C per se which caused Asherman’s syndrome, but from ‘negligence’ of a doctor to correctly identify and remove retained products of conception/placenta. It would appear that the law considers D&Cs an inherent risk, although curiously, women who give their ‘informed consent’ are rarely told of the specific risks of Asherman’s syndrome or the correct incidence rates.
The failure of justice for Asherman’s syndrome sufferers who underwent routine D&Cs for standard care is yet another argument in favour of Asherman’s syndrome prevention by replacing D&Cs with medical management or hysteroscopy…
I would love for there to be an open list of doctors who caused Asherman's syndrome from D&Cs that were deemed to be simple and straighforward, not in any life-threatening emergency situation, for example (I'm more sympathetic to doctors who faced emergencies). This list would at least warn other women to avoid those doctors and have well-deserved repercussions on their wallets. It is afterall, their duty to care for their patients and not cause them harm and if they caused Asherman's syndrome from such a 'straightforward' procedure, they clearly breached their contract as a medical professional.
OK, I contend that it is difficult, maybe impossible, to not cause any damage from a D&C when you are poking objects into a small, soft, and fragile organ you cannot even see. But this is my point: if doctors want to continue pretending that it's acceptable to do D&Cs and stubbornly refuse to offer cheaper and less invasive drugs or a visually guided method like hysteroscopy, they should be held responsible for the consequences. As the situation stands, they continue to have their cake and eat it too. D&Cs, unlike hysteroscopy, do not require much skill (it’s hard to judge the outcome when the organ is concealed), and unlike misoprostol, it is financially rewarding to hospitals, Gyns/ObGyns, and anesthesiologists. Why would they want to work harder than they already do or earn less?
So why do these legal suits lose? One obvious reason is that medical malpractice suits have always been difficult to win because doctors are very well protected. Doctors are extremely supportive of each other and it is difficult to find a doctor who is willing to give expert medical advice in a case implicating a peer. This probably stems from reciprocity: "I'll scratch your back, if you scratch mine." Who knows if said medical expert will not face a malpractice suit (justified or not) some time in their career...
What perplexes me is that a lawyer can take on a medical case without having a medical or scientific degree or understanding basic health issues. Come to think of it, it is also somewhat disturbing that doctors don't need to be taught how to think objectively and critically to practice medicine, but I digress...
Defense lawyers and doctors will come up with all sorts of excuses to dismiss a valid medical case against them. This is where the Asherman's syndrome myths come in so handy. They are ‘facts’ which continue to be accepted without real evidence, often hypothesized decades ago at a time when well respected doctors in the field could formulate opinions without any scientific basis or need for clinical trials (no wonder some of them developed a ‘God complex’) and their peers believed them and even today continue to cite their published theories in the guise of ‘evidence’ in peer-reviewed medical journal articles. These opinions, in particular about Asherman’s syndrome, have over the years transformed into ‘dogma’ which medical school students are indoctrinated with. Somehow no one ever asks “Why are we blindly accepting what this doctor 50 years ago suggested when they didn’t have the advances in knowledge, diagnostic/surgical tools and understanding of evidence based medicine that we have today? ” Which leads me to wonder, as medicine is becoming more and more scientific in nature (evidence-based medicine), will this change the expected outcomes of some cases? I think it will inevitably do so. But there is still a long way to go.
I also wanted to mention a legal perspective which has always riled me in relation to Asherman's syndrome (I would think it also applies to other medical injuries affecting fertility): in a court of law where the nature of injury and of suffering are apparently graded, it makes no difference whether you had 10 children or none before the injury leading to infertility. Now, I know from the Asherman's International Support Group that such an attitude is promoted to keep the peace and encourage bonding (“we’re all in the same boat”), but to think that the law makes no distinction between someone who has been prevented from ever reproducing (a basic human right according to the United Nations charter) and someone who has done so is just plain cruel. There is no 'scientifically correct' answer to this, but one would think that the logical and instinctive answer is that the condition has more consequences for those who never had children before the injury than those who have.
It is difficult to find information about Asherman’s syndrome law suits on the internet, and judging by the number of visits this particular entry gets, it would appear to be an area that many women would like to learn more about. I have downloaded the few articles on lawsuits I have been able to find and will write another blog entry (one day) about what I find out from them. From a quick scan though, what I can say is that it appears that most of the successful lawsuits do not stem from injury of the D&C per se which caused Asherman’s syndrome, but from ‘negligence’ of a doctor to correctly identify and remove retained products of conception/placenta. It would appear that the law considers D&Cs an inherent risk, although curiously, women who give their ‘informed consent’ are rarely told of the specific risks of Asherman’s syndrome or the correct incidence rates.
The failure of justice for Asherman’s syndrome sufferers who underwent routine D&Cs for standard care is yet another argument in favour of Asherman’s syndrome prevention by replacing D&Cs with medical management or hysteroscopy…
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