Unfortunately, I can now talk from experience about how miscarriages can be dealt with post Asherman’s syndrome (AS), and what to expect. I lost my pregnancy at 14 weeks due to a trisomy 21 detected by karyotype analysis and QF-PCR of chorionic villi sampling. The first inkling that something was wrong was at the 12 week scan. Actually, the blood serum levels of PAPP-A and bHCG I’d had during the 11th week already showed a problem, but it wasn’t until my ultrasound that I learned of this. The ultrasound only confirmed that things were not right. Only two weeks earlier I’d had another ultrasound and all seemed fine- the heart beat, the CRL, etc. Now the nuchal fold measured 7mm and there was hydrops- an accumulation of fluid around the fetus. I was told there was a high probability that the pregnancy would end spontaneously.
Fast forward to week 14 and there was no longer a heartbeat.
I’d always talked about misoprostol and ironically now I would have to use it myself. There was no way on earth I’d undergo another D&C (suction curettage or whatever you want to called this blind invasive procedure)- the procedure which caused Asherman’s syndrome when I had it 3 years earlier for a blighted ovum. I could not risk exacerbating the condition. If only my initial ObGyn had agreed to treat me with misoprostol I could have avoided all the surgery and heart ache that followed. I’m quite sure I’d have a child by now.
Since I was relatively far into the pregnancy and the fetus had developed to 14 weeks before dying spontaneously, I booked in the hospital for the misoprostol induction. I don’t know which hospitals/ObGyns use misoprostol regularly, however, in the interest of informing women, my procedure was performed at the Royal Hospital for Women in Randwick (Sydney). I’m sure there are other hospitals (and doctors) that are familiar with misoprostol use, and yes, it is completely legal even if it has not been approved by the TGA (Australia's equivalent of the FDA) for gynecological indications for dubious reasons. By the way, the doctor who refused to give me misoprostol works at St George Hospital. I’d be interested to know if that hospital carries out medical management of miscarriage- please drop me a line or comment below if you know.
In total, I was given a dose of 1 mg (milligram) of misoprostol over the course of a day. Initially, one pill ie. 200 mcg (vaginal) was given to test for any adverse reactions, allergies etc. I began cramping but there was no bleeding. About 5 hours later cervical dilation was checked (closed) and I was given 400 mcg (2 pills). The cramping intensified, but again, there was no bleeding. Shortly after my third and final dose, about 5 hours after the last dose, I began having strong contractions. It was quite painful so I’d definitely recommend panadeine forte. Strangely, there was still no bleeding unlike with my first miscarriage which began like a period. About 40 minutes after my final dose, the waters broke and amniotic fluid spilled out soaking the bed. After this point the pain stopped although I was still feeling crampy for at least a week afterwards. Roughly half an hour after the waters broke, I delivered the tiny baby. The umbilical cord was thin and weak and broke off from the placenta. It is at this point that I began bleeding. I continued bleeding heavily throughout the night and the next day. I also bled strongly for about a week afterwards and on and off during the following week. The placenta should have come out soon afterwards but it was not until 3.5 hours passed that it did. Luckily I’d discussed the possibility of retained placenta previously with my ObGyn and we agreed to wait it out (normally most doctors would jump at the opportunity to do a D&C in this situation) while the nurses and midwives monitored me closely for signs of infection and hemorrhage. As it’s difficult to know if the placenta is complete on visual inspection, and women with a history of Asherman’s syndrome- even after surgical correction- are at an increased risk of placental conditions such as placenta accreta, percreta, increta, and previa, I knew retained placenta was a possibility.
Before the placenta delivered my temperature reached 40 C and the midwife was somewhat concerned, however misoprostol itself can cause fever. The morning after, my blood pressure was 90 on 60 (normally it is around 110-115/65-70) and I was told this could be due to blood loss.
The next morning I underwent an ultrasound to check for retained placental fragments. Around 32 mls of material was found in the uterus but it was impossible to tell whether this was simply blood and blood clots, or if there were retained products of conception (RPOC). Doppler flow analysis suggested that there were retained placental fragments in the posterior of the uterus- the same area where the placenta had implanted in this pregnancy. I had another ultrasound a week after the first. The second ultrasound showed that the fluid in the uterus had roughly halved, but it was still not possible to tell for sure via ultrasound whether there were retained products.
In the following week I bled little despite having around 18 mls of content in my uterus so I became concerned that perhaps there were retained fragments. This would not be a surprise given my pregnancy reached second trimester and my previous history of Asherman’s syndrome. I contacted my trusted Asherman’s syndrome specialist for a hysteroscopic procedure to remove any retained fragments of placenta. This procedure was done 3 weeks after the misoprostol treatment. It turns out I did have many retained fragments which were gently scraped off using the hysteroscope itself. Luckily I did not have any clinical infection from the retained tissue (perhaps just 'subclinical' ;) ?). There were no adhesions. I was given prophylactic antibiotics to prevent infection after the surgery.
I should also mention that to prevent any possible adhesions, I was prescribed 2mg/day progynova (a synthetic estrogen) for 28 days by an Asherman’s syndrome specialist. The other option was Premarin (0.625 mg). These help the endometrium grow and thereby prevent uterine walls from adhering in the case of scarring.
I’m now awaiting my next period after which I’ll have a mid cycle scan to measure endometrial thickness at ovulation, and either an in--office hysteroscopy or an HSG to check for adhesions. Hopefully the removal of RPOCs did not cause any scarring.
Note that the dose of misoprostol I was given was decided according to my pregnancy stage (14 weeks) and status (fetal demise). Doses vary and guidelines should be adhered to.
Here is a summary of my suggestions (as a non MD) if you find yourself in this situation:
1. Don’t have a D&C for a miscarriage as it can cause further damage especially if you have had AS previously. Also, your endometrium may get thinner each time you have a D&C.
2. Misoprostol helps clear out most of the uterine contents. It is more painful than a D&C but worth it in the long run- unless you are not interested in preserving your fertility. NOTE: If you have had a previous Cesarean section or uterine perforation or severe AS, discuss with your ObGyn to see if misoprostol is safe for you (or you may need to take a lower dose than what I was given).
3. You should have estrogen therapy to prevent adhesions from forming. I'm not sure if this is 100% necessary but Asherman's specialists recommend it. Some women didn't use it because of adverse reactions to estrogen (blood clots etc.) and they did not develop adhesions.
4. You will probably have retained tissue and require a hysteroscopy (not a blind D&C!!) to remove it. In most cases if you have had a missed miscarriage you will need to either use misoprostol or, alternatively, wait to miscarry before hysteroscopy can be effective, otherwise there is just too much tissue and blood to work with.
5. Have a mid cycle scan to measure endometrial thickness after your first post-treatment period and always check that your uterine cavity is free of adhesions before you attempt to conceive again just in case. An in-office hysteroscopy is best but failing that, an HSG can be done.
There are also some implications that can be speculated:
1. It may take a few hours for the placenta to deliver when using misoprostol post AS if you are beyond the first trimester.
2. It is likely that if you have had AS, you will have retained products after every future miscarriage. Hysteroscopic removal of tissue allows the doctor to view your uterus as he/she clears it. Note: Hysteroscopy itself can cause complications if undertaken by an unexperienced or unskilled doctor. Please see only a highly experienced specialist.
3. You should anticipate that you may have placenta accreta in a future pregnancy particularly if the placenta does not deliver when expected or you have had confirmed RPOC. Obviously, any woman with past AS should be monitored throughout their pregnancy by a high-risk Obstetrician.
I will try to write about the known pregnancy complications in women with a history of AS in the near future.
There are two more interesting points: Initially I believed that I may not get RPOC because the placenta had implanted in a region which was never affected by intrauterine adhesions. The fact that it is possible to get RPOC in a new, previously unaffected area suggests that perhaps the placenta implants deeply because the endometrium is slightly thinner than it should be ideally. Or maybe blood flow to the uterus is somehow affected and in order for the pregnancy to establish the placenta needs to invade the endometrium more deeply.
Secondly, I have to question once again whether there is any truth at all to the unfounded claim by certain doctors that Asherman’s syndrome can occur ‘spontaneously’ after miscarriage. I would have to have actual evidence to believe this. In my own case I had no adhesions 2 weeks after miscarrying using misoprostol-and this is even after having had intrauterine adhesions in the past (from a D&C). In other words they did not reoccur, nor did any new ones develop. I suspect that if I was treated with blind D&C rather than misoprostol, lo and behold I would develop ‘spontaneous’ adhesions in a new region: the posterior region of my uterus (where the RPOC were). It doesn't make sense for such an evolutionarily destructive mechanism to occur in nature (unless extremely rarely).
In retrospect, I have to wonder why my first Obgyn (ie the one who caused me to have AS) so steadfastly rejected my request to use misoprostol instead of a D&C when it can be used even until the third trimester. He made me believe that it could only be used until 8 or 10 weeks. I also wonder why, as a doctor who was aware about Asherman’s syndrome, my strong concern about acquiring it, and knew of the Asherman’s syndrome support group, he did not refer me for a hysteroscopic removal the supposed RPOC I had? What, may I ask, is the purpose of informing gynecologists about Asherman’s syndrome if they will continue to perform damaging D&Cs while refusing to offer other options? ‘Consent’ for D&Cs is hardly possible when other options are not made available. Please, let us not make Obstetricians/gynecolgists believe that treatment is so simple and effective that causing Asherman’s syndrome is just a little glitch with few consequences for the patient.
Finally, my experience has shown once again that prevention of Asherman’s syndrome is best: the condition leads to a cycle of costly and lengthy complications with retained products (not to mention possible obstetric complications in future pregnancies) which could be avoided if medical management (ie. misoprostol) was used in the first instance.
Tuesday, December 15, 2009
Thursday, November 26, 2009
Misprostol for miscarriage management to prevent Asherman's syndrome
Misoprostol (also known as Cytotec produced by Pfizer) is a synthetic prostaglandin E1 analogue which causes uterine contractions that empty the uterus. Initially developed for the treatment of gastric ulcers, misoprostol was found to have numerous gynecological indications including treatment of missed or incomplete miscarriage (or termination), or retained placenta following full term delivery, postpartum hemorrhaging (PPH) and labour induction. The advantage of using misoprostol for miscarriage/retained placenta management is the avoidance of the invasive, costly and potentially damaging D&C procedure (eg. Asherman's syndrome).
Misoprostol is on the WHO essential medicine list for abortion induction (in combination with mifepristone) and labour induction. Earlier this year the ACOG published a committee opinion supporting the worldwide availability of misoprostol for postabortion care (both spontaneous and induced), acknowledging its ability to prevent needless deaths in developing nations (1). It has been approved in more than 85 countries since 1985. Yet in all but 4 countries (France, Brazil, Taiwan and Egypt) it has only been approved for use in gastric ulcers. It seems that the major obstacle to the US’s FDA approval of misoprostol for gynecological indications is the original manufacturer's refusal to permit the drug to be used for pregnancy-related applications for moral rather than medical reasons: misoprostol can also be used for terminations (2). As long as those with other agendas can proclaim that misoprostol is 'not FDA (or TGA in Australia) approved' and is being used ‘off-label’, they can continue to at least imply that the reasons for this are safety-related, creating fear or uncertainty in patients and doctors alike. In fact, misoprostol is one of the most widely studied prostaglandins and has undergone hundreds of clinical trials for over 20 years. In comparison, by today's high safety and medical ethics standards, there is little doubt that the century-old blind, invasive D&C would fail to gain approval for routine use. Off label use of medication is not only legal, it is also safe when backed by years of clinical trials assessing safety. Unbeknownst to many, off label use of other Obstetric drugs is commonplace.
Could there be another underlying conflict in the D&C versus misoprostol/medical management- a hidden competition between doctors who perfom surgery and the pharmaceutical industry which produces the drug over financial gain from miscarriages/terminations? From the publications of some doctors at least it would appear that the pharmaceutical industry bowing to anti-abortion lobbyists (2) is the main obstacle rather than the collective rejection of doctors to use misoprostol. Having said this, some doctors remain ignorant about its use and hesitant to learn more. More needs to be done to educate doctors on the use of misoprostol for medical management of miscarriage, beginning in medical school where they are instead trained to peform D&Cs for just about every gynecological condition encountered.
To date there is one randomized control trial comparing the use of misoprostol to D&C for treatment of miscarriage with regards to intrauterine adhesion outcomes. Not surprisingly, this study suggests misoprostol would reduce the incidence of intrauterine adhesions (3). Although these results seem intuitive, in medicine (and science) studies are always needed as evidence, especially when a ‘standard’ treatment is to be usurped by a newer method which some doctors seem inexplicably reluctant to embrace. More such studies would also be helpful in putting to rest the ‘subclinical’ infection myth or other unsubstantiated hypotheses on the etiology of Asherman’s syndrome which somehow shift blame away from instrumentation to a yet unproven and uncharacterized patient factor (eg. patient constitution or a ‘naturally’ occurring physiological phenomenon in the absence of surgery).
Unfortunately, for a variety of reasons Gynecological/Obstetric practice has been slow to keep up with research with regards to the use of medical management for miscarriage. Although there are thankfully some doctors who have incorporated misoprostol management of miscarriage into their arsenal of treatments, my experience is that they are far too few and far between at least in some countries. This is inexcusable given the risks of infertility and future obstetric complications in women who have undergone D&C, still regarded as the 'standard care' for treating missed or incomplete miscarriages. Not only is misoprostol effective, it can be used in both first and second trimester pregnancy losses.
The misoprostol.org website provides a useful table summarizing guidelines for using misoprostol for different obstetric indications and at different stages of pregnancy. Like any drug, it must be used according to guidelines and under medical supervision.
I also came across a very helpful website where women shared their experiences with using misoprostol for miscarriage.
I am adding the site to the links to the right of this blog in the hope that it will help enlighten women to the existence of medical management and what to expect. It is a longer process to use misoprostol (and more painful particularly if used for second trimester losses), however these disadvantages pale significantly against the potential complications of D&C. The more women who become aware about Asherman's syndrome and future high risk pregnancies, the more will request misoprostol treatment, hopefully forcing changes in practice and policies of standard treatment for miscarriage.
REFERENCES
1. ACOG. ACOG Committee Opinion No. 427: Misoprostol for postabortion care.
Obstet Gynecol 2009;113(2 Pt 1):465-8.
2. Misoprostol and the debate over off-label drug use (Commentary): BJOG: an International Journal of Obstetrics and Gynaecology
March 2005, Vol. 112, pp. 269–272. Link to full pdf
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.
Misoprostol is on the WHO essential medicine list for abortion induction (in combination with mifepristone) and labour induction. Earlier this year the ACOG published a committee opinion supporting the worldwide availability of misoprostol for postabortion care (both spontaneous and induced), acknowledging its ability to prevent needless deaths in developing nations (1). It has been approved in more than 85 countries since 1985. Yet in all but 4 countries (France, Brazil, Taiwan and Egypt) it has only been approved for use in gastric ulcers. It seems that the major obstacle to the US’s FDA approval of misoprostol for gynecological indications is the original manufacturer's refusal to permit the drug to be used for pregnancy-related applications for moral rather than medical reasons: misoprostol can also be used for terminations (2). As long as those with other agendas can proclaim that misoprostol is 'not FDA (or TGA in Australia) approved' and is being used ‘off-label’, they can continue to at least imply that the reasons for this are safety-related, creating fear or uncertainty in patients and doctors alike. In fact, misoprostol is one of the most widely studied prostaglandins and has undergone hundreds of clinical trials for over 20 years. In comparison, by today's high safety and medical ethics standards, there is little doubt that the century-old blind, invasive D&C would fail to gain approval for routine use. Off label use of medication is not only legal, it is also safe when backed by years of clinical trials assessing safety. Unbeknownst to many, off label use of other Obstetric drugs is commonplace.
Could there be another underlying conflict in the D&C versus misoprostol/medical management- a hidden competition between doctors who perfom surgery and the pharmaceutical industry which produces the drug over financial gain from miscarriages/terminations? From the publications of some doctors at least it would appear that the pharmaceutical industry bowing to anti-abortion lobbyists (2) is the main obstacle rather than the collective rejection of doctors to use misoprostol. Having said this, some doctors remain ignorant about its use and hesitant to learn more. More needs to be done to educate doctors on the use of misoprostol for medical management of miscarriage, beginning in medical school where they are instead trained to peform D&Cs for just about every gynecological condition encountered.
To date there is one randomized control trial comparing the use of misoprostol to D&C for treatment of miscarriage with regards to intrauterine adhesion outcomes. Not surprisingly, this study suggests misoprostol would reduce the incidence of intrauterine adhesions (3). Although these results seem intuitive, in medicine (and science) studies are always needed as evidence, especially when a ‘standard’ treatment is to be usurped by a newer method which some doctors seem inexplicably reluctant to embrace. More such studies would also be helpful in putting to rest the ‘subclinical’ infection myth or other unsubstantiated hypotheses on the etiology of Asherman’s syndrome which somehow shift blame away from instrumentation to a yet unproven and uncharacterized patient factor (eg. patient constitution or a ‘naturally’ occurring physiological phenomenon in the absence of surgery).
Unfortunately, for a variety of reasons Gynecological/Obstetric practice has been slow to keep up with research with regards to the use of medical management for miscarriage. Although there are thankfully some doctors who have incorporated misoprostol management of miscarriage into their arsenal of treatments, my experience is that they are far too few and far between at least in some countries. This is inexcusable given the risks of infertility and future obstetric complications in women who have undergone D&C, still regarded as the 'standard care' for treating missed or incomplete miscarriages. Not only is misoprostol effective, it can be used in both first and second trimester pregnancy losses.
The misoprostol.org website provides a useful table summarizing guidelines for using misoprostol for different obstetric indications and at different stages of pregnancy. Like any drug, it must be used according to guidelines and under medical supervision.
I also came across a very helpful website where women shared their experiences with using misoprostol for miscarriage.
I am adding the site to the links to the right of this blog in the hope that it will help enlighten women to the existence of medical management and what to expect. It is a longer process to use misoprostol (and more painful particularly if used for second trimester losses), however these disadvantages pale significantly against the potential complications of D&C. The more women who become aware about Asherman's syndrome and future high risk pregnancies, the more will request misoprostol treatment, hopefully forcing changes in practice and policies of standard treatment for miscarriage.
REFERENCES
1. ACOG. ACOG Committee Opinion No. 427: Misoprostol for postabortion care.
Obstet Gynecol 2009;113(2 Pt 1):465-8.
2. Misoprostol and the debate over off-label drug use (Commentary): BJOG: an International Journal of Obstetrics and Gynaecology
March 2005, Vol. 112, pp. 269–272. Link to full pdf
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.
Tuesday, November 17, 2009
In Memory
Name: Sema
Sex: female
Gestational age: 14 weeks
Length: 11.5 cm
Weight: 40 g
Date of death: 12/11/09
Cause of death: trisomy 21
"Before you were conceived I wanted you, before you were born I loved you."
Tuesday, September 22, 2009
Future research:How stem cells may one day improve Asherman's syndrome treatment
Currently the gold standard for treatment of Asherman’s syndrome is surgery to remove/cut adhesions (hysteroscopic adhesiolysis or synechiolysis) and hormonal therapy to regenerate any residual endometrium. One of the challenges in treating Asherman’s syndrome is the propensity of intrauterine adhesions to reform again during the healing process. To try to overcome this, some doctors place a saline-filled stent (Foley or Cook) or an IUD in the uterus after surgery in order to keep the walls of the uterus and cervix apart during the healing process. If there is little endometrium regrowth adhesions will continue forming again in the same areas. Hormone therapy (2-4mg/day estrogen for up to 2 months followed by progestin (P) to induce a withdrawal bleed) is also used in addition to surgery to prevent adhesions from reforming by promoting regrowth of endometrium. It is also thought that it generally improves the thickness and quality of endometrium- some patients end up with thin endometrium or fibrosis (scar tissue with no viable endometrium) after instrumental trauma from surgery precipitating Asherman’s syndrome (usually a D&C). Adhesion reformation following corrective surgery correlates with the severity of adhesions. According to one study adhesion reformation occurs in 50% of severe cases and 21.6% of moderate cases (1). Sometimes multiple surgeries are needed to correct uterine architecture.
The problem is that if one does not have enough endometrium because it has been scraped away, either adhesions or fibrosis will continue to be a problem no matter how many surgeries are undertaken or how much hormonal stimulation is given.
As you can see from a previous post, the live birth rates after corrective surgery are not very high for moderate to severe cases. To understand why this treatment is not effective in all patients one needs to understand the physiology of the endometrium and adhesion formation. The outermost layer of the uterus is lined by the endometrium which sits above the muscle layer, the myometrium. The endometrium itself is comprised of two layers. The functional layer is outermost and is shed on a monthly basis during menstruation. The underlying basal layer is necessary to produce the functional layer each month. If permanent damage is incurred to the basal layer, the functional layer will not be able to regenerate. Without the regeneration of endometrium the bare myometrium underlying the endometrium will begin to stick to other areas devoid of endometrium as soon as the injury occurs. Adhesion formation is the normal physiogical response to injury whether this is in the uterus or elsewhere in the abdominal cavity. Adhesion formation begins immediately after scar formation from instrumental injury and will be complete by 8 weeks. Any area where injured tissue can come into contact with other injured tissue, adhesions form. Adhesions are a serious health problem related to surgery, not just in the uterus but also in the abdomen and intestines. However abdominal or intestinal surgery does not have alternatives whereas uterine evacuation does. In other words, D&C is not the only available method for effectively emptying the uterus after miscarriage or delivery, however staggeringly, it remains standard care for the former in many advanced countries.
So the problem comes down to endometrial regeneration (or the lack of it). Some tissue in the body is able to regenerate. For example, cells in the the gut and bone marrow regularly divide to repair damaged or worn out tissue. In other tissues such as the heart and brain, cells are only stimulated to divide under special circumstances. Endometrium is another such tissue. Tissue regeneration is due to the activity of stem cells which have special properties. Initially it was thought that only embryonic stem cells had the capacity to differentiate. More recently the existence of adult stem cells was discovered. Adult stem cells are undifferentiated cells usually found in little islands or "niches" in tissues and organs. They are generally thought to have a more limited ability to differentiate than embryonic stem cells which can develop into any type of cell in the body. Adult stem cells, on the other hand, are already partially committed to certain cell lineages. Adult stem cells are thought to play a role in tissue maintenance and reparation in the tissues they are found.
Recently the existence of endometrial adult stem cells was reported in the scientific literature (2). However, if all of the basal and stem cells have been removed from a large part of the uterus, it is impossible to resolve the problem of recurrent adhesion formation and/or fibrosis. Sadly, current therapy can only remove bands of scar tissue and promote endometrial regeneration in areas where there is some remaining basal cells or even perhaps stem cells. Put simply, current treatment will not be successful if the patient does not have enough residual endometrium to regenerate. In theory, the identification of endometrial stem cells in the junction between the endometrium and myometrium opens the possibility of future therapy for damaged endometrium. Stem cells can be introduced either from a donor, or better yet, from the same patient whose stem cells have proliferated in a culture medium. Once inside the right tissue and with the appropriate stimulation, they will be able to differentiate into basal endometrial cells and fill in any 'bald' patches of endometrium. Adhesion formation or sclerosis should no longer be a problem. The advantage of using the patients own cells is that it will avoid immune rejection. The use of adult stem cells also avoids any obstacles from those citing ethical problems in using embryonic stem cells. Note that I have greatly simplified the process in the scenario above.
Stem cell research, both adult and embryonic, are still in their infancy. Most stem cell researchers are focusing on regeneration of heart tissue or other major organs as an alternative to organ transplantation. The problem is that there is little if any research on endometrial regeneration and in particular for the treatment of Asherman’s syndrome. In the past basic research was carried out to improve endometrial growth in animals where AS was artificially produced. This type of research no longer seems to exist. Instead, there is research on uterus transplantation which is much more complex and difficult to achieve. As long as endometrial research remains stalled there is little hope that treatment will continue to progress much beyond what has been attained today- which leaves much to be desired if treatment is regarded as the primary solution to the problem of Asherman’s syndrome.
REFERENCES
1. Valle RF, Sciarra JJ. Intrauterine adhesions: hysteroscopic diagnosis, classification, treatment, and reproductive outcome. Am J Obstet Gynecol. 1988 Jun;158(6 Pt 1):1459-70.
Abstract
2. Gargett BE, Chan RW. Endometrial stem/progenitor cells and proliferative disorders of the endometrium. Minerva Ginecol. 2006 Dec;58(6):511-26.
Abstract
The problem is that if one does not have enough endometrium because it has been scraped away, either adhesions or fibrosis will continue to be a problem no matter how many surgeries are undertaken or how much hormonal stimulation is given.
As you can see from a previous post, the live birth rates after corrective surgery are not very high for moderate to severe cases. To understand why this treatment is not effective in all patients one needs to understand the physiology of the endometrium and adhesion formation. The outermost layer of the uterus is lined by the endometrium which sits above the muscle layer, the myometrium. The endometrium itself is comprised of two layers. The functional layer is outermost and is shed on a monthly basis during menstruation. The underlying basal layer is necessary to produce the functional layer each month. If permanent damage is incurred to the basal layer, the functional layer will not be able to regenerate. Without the regeneration of endometrium the bare myometrium underlying the endometrium will begin to stick to other areas devoid of endometrium as soon as the injury occurs. Adhesion formation is the normal physiogical response to injury whether this is in the uterus or elsewhere in the abdominal cavity. Adhesion formation begins immediately after scar formation from instrumental injury and will be complete by 8 weeks. Any area where injured tissue can come into contact with other injured tissue, adhesions form. Adhesions are a serious health problem related to surgery, not just in the uterus but also in the abdomen and intestines. However abdominal or intestinal surgery does not have alternatives whereas uterine evacuation does. In other words, D&C is not the only available method for effectively emptying the uterus after miscarriage or delivery, however staggeringly, it remains standard care for the former in many advanced countries.
So the problem comes down to endometrial regeneration (or the lack of it). Some tissue in the body is able to regenerate. For example, cells in the the gut and bone marrow regularly divide to repair damaged or worn out tissue. In other tissues such as the heart and brain, cells are only stimulated to divide under special circumstances. Endometrium is another such tissue. Tissue regeneration is due to the activity of stem cells which have special properties. Initially it was thought that only embryonic stem cells had the capacity to differentiate. More recently the existence of adult stem cells was discovered. Adult stem cells are undifferentiated cells usually found in little islands or "niches" in tissues and organs. They are generally thought to have a more limited ability to differentiate than embryonic stem cells which can develop into any type of cell in the body. Adult stem cells, on the other hand, are already partially committed to certain cell lineages. Adult stem cells are thought to play a role in tissue maintenance and reparation in the tissues they are found.
Recently the existence of endometrial adult stem cells was reported in the scientific literature (2). However, if all of the basal and stem cells have been removed from a large part of the uterus, it is impossible to resolve the problem of recurrent adhesion formation and/or fibrosis. Sadly, current therapy can only remove bands of scar tissue and promote endometrial regeneration in areas where there is some remaining basal cells or even perhaps stem cells. Put simply, current treatment will not be successful if the patient does not have enough residual endometrium to regenerate. In theory, the identification of endometrial stem cells in the junction between the endometrium and myometrium opens the possibility of future therapy for damaged endometrium. Stem cells can be introduced either from a donor, or better yet, from the same patient whose stem cells have proliferated in a culture medium. Once inside the right tissue and with the appropriate stimulation, they will be able to differentiate into basal endometrial cells and fill in any 'bald' patches of endometrium. Adhesion formation or sclerosis should no longer be a problem. The advantage of using the patients own cells is that it will avoid immune rejection. The use of adult stem cells also avoids any obstacles from those citing ethical problems in using embryonic stem cells. Note that I have greatly simplified the process in the scenario above.
Stem cell research, both adult and embryonic, are still in their infancy. Most stem cell researchers are focusing on regeneration of heart tissue or other major organs as an alternative to organ transplantation. The problem is that there is little if any research on endometrial regeneration and in particular for the treatment of Asherman’s syndrome. In the past basic research was carried out to improve endometrial growth in animals where AS was artificially produced. This type of research no longer seems to exist. Instead, there is research on uterus transplantation which is much more complex and difficult to achieve. As long as endometrial research remains stalled there is little hope that treatment will continue to progress much beyond what has been attained today- which leaves much to be desired if treatment is regarded as the primary solution to the problem of Asherman’s syndrome.
REFERENCES
1. Valle RF, Sciarra JJ. Intrauterine adhesions: hysteroscopic diagnosis, classification, treatment, and reproductive outcome. Am J Obstet Gynecol. 1988 Jun;158(6 Pt 1):1459-70.
Abstract
2. Gargett BE, Chan RW. Endometrial stem/progenitor cells and proliferative disorders of the endometrium. Minerva Ginecol. 2006 Dec;58(6):511-26.
Abstract
Tuesday, September 15, 2009
‘Victims’ in miscarriage headlines are luckier than they think
Oh no. Not another story about a woman who goes to hospital emergency with an impending miscarriage and gets given painkillers and told to go home (click here for 'story'). Or miscarries in the hospital toilet. I don’t know why, but Sydney newspapers abound with such stories. It started off with the famous Jana Horska story. Yesterday I read in the Sydney Morning Herald that women will now be offered D&Cs straight away. OK, I’ve kept silent long enough. When women think that miscarriage and the pain that goes with it are the worst things than can happen to them, I must enlighten them about Asherman’s syndrome. Especially when their complaints have prompted hospitals to consider carrying out even more D&Cs, the number one cause of Asherman’s syndrome.
One in four pregnancies ends in miscarriage. I too had a miscarriage so I know what I’m talking about. I was around 14 weeks into the pregnancy. Mine was a missed miscarriage detected via ultrasound at 11 weeks. The fetus either died (fetal demise) and was resorbed or stopped developing very early on (anembryonic gestation). I was offered a D&C straight away by my ObGyn. I recalled vaguely hearing about the risks of D&C and future fertility. I was 39 and was not about to take a chance. My ObGyn insisted that Asherman’s syndrome and uterine perforation were ‘extremely rare’ (see what the real incidence rates are. Not rare at all!). Still, if there was a chance I could avoid it altogether by waiting to miscarry naturally, I would take that option. I had no other choice as he flatly refused to give me medication (misoprostol). The ObGyn was visibly irritated and disappointed in my choice to avoid a D&C.
The shock and sadness of losing the pregnancy was soon replaced with impatience to miscarry naturally so I could avoid a D&C, and start trying to conceive again with my fertility intact. My goal was to avoid a D&C at all costs. I was relieved when one Sunday morning about 3 weeks later, I finally began to bleed. At first it was like a normal period. As the day progressed the bleeding got heavier, and so did the cramps. By 11 PM I could no longer contain my cries of pain. My husband shut the windows, worried the neighbours might think he was beating me! Finally around midnight when I could no longer stand the pain I sent my husband to an all night pharmacy to get the strongest painkiller available without prescription. He tried to convince me to go to the hospital instead. “Are you nuts?” I retorted. “They’ll just tell me to have a D&C”. Not only that, but I’d have to stifle my moans and sit upright in uncomfortable clothes, surrounded by strangers and without access to a clean toilet. At home I could make as much noise as I wanted in my loose nighty and stand on all fours if that was the most comfortable position. The toilet was less than a meter from my bed and I wouldn’t have to compete with 50 other patients for it while waiting in emergency. He came back with a box of Panadeine forte containing codeine and that took the edge off the labour-like cramps. At some point after midnight I felt a ‘pop’ and instantaneous relief. Instinctively I knew the gestational sac must have burst and I rushed to the toilet. I continued to bleed heavily but was glad everything was coming out.
Later that day I had an appointment with the ObGyn who seemed rather disappointed that I miscarried by myself. Somewhat wistfully, he said that on ultrasound it appeared that there was no remaining tissue. What a relief that was to hear. But for some reason, he insisted I return a few days later to make sure everything was OK. When I returned later that week his story changed. This time he said it appeared that I had large ‘products of conception’ and that I had no other choice than to have a D&C. What??? I asked about drugs again. He refused again, saying they would be ‘ineffective.’ Reluctantly, I had the D&C, got stage 3 Asherman’s syndrome and the rest is history. (Here’s my story).
I’m convinced that the D&C was needless. I lost my fertility for no reason at all.
I wonder if these women who are sent home without a D&C realize how lucky they are to not go through what I did? Instead of noticing something is wrong with their periods, or are no longer able to conceive or miscarry repeatedly… instead of having to find a doctor who believes them and who is aware about the existence of Asherman’s syndrome and is trained to diagnose it with hysteroscopy… instead of having to undergo hysteroscopic surgery and hormone therapy to remove adhesions and salvage any viable endometrium in the hope that they will be able to have a baby in future… they get to try to conceive again right away with any complications whatsoever! And they’re the ones who are complaining! As a victim of D&C, I guarantee you, a miscarriage is nothing compared to the pain of possible loss of fertility and serious future pregnancy complications from D&C.
I wonder, do these women realize that there is absolutely nothing any hospital or doctor can do to stop the miscarriage from happening? They probably miscarried because the babies were not normal and there is unfortunately nothing that can change that. If they really want to be of help, they should insist that hospitals offer medical management with misoprostol and mifepristone in addition to expectant management, which also evacuates the uterus safely. Instead, I fear their indignant cries have resulted in a policy to systematically use D&C to manage miscarriage and will result in an increase in Asherman’s syndrome cases.
When will the lesson be learned? What is the world coming to when no one says a word about the risks of reproductive mutilation from systematic blind D&C, yet C-sections and male circumcision are made out to be the most dangerous,needless and wicked surgery known to humankind?!
Related link:
Here is a youtube clip I made about miscarriage management
This is another website which aims to raise awareness about the risks of D&C: http://www.dandcnow.info/
One in four pregnancies ends in miscarriage. I too had a miscarriage so I know what I’m talking about. I was around 14 weeks into the pregnancy. Mine was a missed miscarriage detected via ultrasound at 11 weeks. The fetus either died (fetal demise) and was resorbed or stopped developing very early on (anembryonic gestation). I was offered a D&C straight away by my ObGyn. I recalled vaguely hearing about the risks of D&C and future fertility. I was 39 and was not about to take a chance. My ObGyn insisted that Asherman’s syndrome and uterine perforation were ‘extremely rare’ (see what the real incidence rates are. Not rare at all!). Still, if there was a chance I could avoid it altogether by waiting to miscarry naturally, I would take that option. I had no other choice as he flatly refused to give me medication (misoprostol). The ObGyn was visibly irritated and disappointed in my choice to avoid a D&C.
The shock and sadness of losing the pregnancy was soon replaced with impatience to miscarry naturally so I could avoid a D&C, and start trying to conceive again with my fertility intact. My goal was to avoid a D&C at all costs. I was relieved when one Sunday morning about 3 weeks later, I finally began to bleed. At first it was like a normal period. As the day progressed the bleeding got heavier, and so did the cramps. By 11 PM I could no longer contain my cries of pain. My husband shut the windows, worried the neighbours might think he was beating me! Finally around midnight when I could no longer stand the pain I sent my husband to an all night pharmacy to get the strongest painkiller available without prescription. He tried to convince me to go to the hospital instead. “Are you nuts?” I retorted. “They’ll just tell me to have a D&C”. Not only that, but I’d have to stifle my moans and sit upright in uncomfortable clothes, surrounded by strangers and without access to a clean toilet. At home I could make as much noise as I wanted in my loose nighty and stand on all fours if that was the most comfortable position. The toilet was less than a meter from my bed and I wouldn’t have to compete with 50 other patients for it while waiting in emergency. He came back with a box of Panadeine forte containing codeine and that took the edge off the labour-like cramps. At some point after midnight I felt a ‘pop’ and instantaneous relief. Instinctively I knew the gestational sac must have burst and I rushed to the toilet. I continued to bleed heavily but was glad everything was coming out.
Later that day I had an appointment with the ObGyn who seemed rather disappointed that I miscarried by myself. Somewhat wistfully, he said that on ultrasound it appeared that there was no remaining tissue. What a relief that was to hear. But for some reason, he insisted I return a few days later to make sure everything was OK. When I returned later that week his story changed. This time he said it appeared that I had large ‘products of conception’ and that I had no other choice than to have a D&C. What??? I asked about drugs again. He refused again, saying they would be ‘ineffective.’ Reluctantly, I had the D&C, got stage 3 Asherman’s syndrome and the rest is history. (Here’s my story).
I’m convinced that the D&C was needless. I lost my fertility for no reason at all.
I wonder if these women who are sent home without a D&C realize how lucky they are to not go through what I did? Instead of noticing something is wrong with their periods, or are no longer able to conceive or miscarry repeatedly… instead of having to find a doctor who believes them and who is aware about the existence of Asherman’s syndrome and is trained to diagnose it with hysteroscopy… instead of having to undergo hysteroscopic surgery and hormone therapy to remove adhesions and salvage any viable endometrium in the hope that they will be able to have a baby in future… they get to try to conceive again right away with any complications whatsoever! And they’re the ones who are complaining! As a victim of D&C, I guarantee you, a miscarriage is nothing compared to the pain of possible loss of fertility and serious future pregnancy complications from D&C.
I wonder, do these women realize that there is absolutely nothing any hospital or doctor can do to stop the miscarriage from happening? They probably miscarried because the babies were not normal and there is unfortunately nothing that can change that. If they really want to be of help, they should insist that hospitals offer medical management with misoprostol and mifepristone in addition to expectant management, which also evacuates the uterus safely. Instead, I fear their indignant cries have resulted in a policy to systematically use D&C to manage miscarriage and will result in an increase in Asherman’s syndrome cases.
When will the lesson be learned? What is the world coming to when no one says a word about the risks of reproductive mutilation from systematic blind D&C, yet C-sections and male circumcision are made out to be the most dangerous,needless and wicked surgery known to humankind?!
Related link:
Here is a youtube clip I made about miscarriage management
This is another website which aims to raise awareness about the risks of D&C: http://www.dandcnow.info/
Friday, September 11, 2009
The cycle of Asherman's syndrome needs to be broken with prevention
In my next blog I will explain why it is that current treatment (surgery and hormone therapy) can never be a cure for all women who have been diagnosed with Asherman’s syndrome (AS). However I also want to explain why my position on prevention as the best approach is unwavering. I’ve always maintained that I would continue to spread my word about prevention even if I was lucky enough to have a baby after AS treatment. This is because I realize that I would be one of the lucky minority if I did. Just because I may be fortunate enough to have a child after my diagnosis and treatment doesn’t mean I should forget about all of the others who didn’t. It’s not about how ‘hard’ you try or how ‘deserving’ you are- one has to understand that the body has its limits according to the damage that was incurred and other factors. I would realize that my case may not have necessary been as severe or my situation not as dire as others who were inflicted with this condition. It would be unfair to the women who have done all they possibly could to achieve a live birth but didn’t succeed to not acknowledge that each case is different not only in severity but also the circumstances in which it happens. As a PhD scientist (molecular microbiology) I know there are no hidden Asherman’s experts out there: all of the ones who are truly experts have peer reviewed published papers on outcomes in their patients following treatment. That is the nature of these careers. One is judged and recognized according to their publication record. And I have read those papers and know what the outcomes are. I would feel daft to go around telling other women not to worry about getting Asherman's syndrome because it can be treated when a) according to statistics from the best doctors, the majority of women will not have a live birth after AS, and b) it doesn't have to happen in the first place. I know also that personally, I could never forget what happened to me for no justifiable reason. Imagine if someone almost accidentally killed you through a preventable and routine careless act but you were saved by a treatment which has a 50% failure rate at best- would you think it was better to promote the treatment , or would you want to do something to prevent another person from possibly losing their life? If I will ever be fortunate to have a child after Asherman’ s syndrome it doesn’t mean that it is still acceptable to damage women through the systematic use of D&C when alternatives exist. I cannot forget the years of suffering, of fearing I will never have a child, the sleepless nights, the tears, the time lost waiting for treatment as I now had to race against my biological clock, the negative pregnancy tests month after month, the failed IVF, the worries that even if I were to become pregnant post AS pregnancies are high risk, none of that will ever be ‘worth it’. For me, to say something is ‘worth it’, it has to be something challenging that I chose for myself, not what someone (ie a treating Dr) did to me. For example, my PhD- those were some of the most difficult and challenging years of my life, performing experiments until late at night and on weekends, reading hundreds of papers, spending months writing my thesis. But I wanted to do, and it was worth it! Without all that hard work I wouldn't have achieved it. On the other hand, it should not be a struggle to have a child when nothing is wrong with you in the first place. Isn't there enough infertility and heartache in the world without doctors causing Asherman's syndrome?
As women we are expected to be martyrs and put up with all kinds of assaults on our bodies without complaining. It’s supposed to be the very essence of being a caring, nurturing Madonna, to put ourselves last. I prefer to be proactive and warn women about the dangers of D&C, and let doctors know it is not OK to perform D&Cs at the drop of a hat. It’s not acceptable to pretend there are no alternatives and to keep silent when prolife activists prevent drug companies from seeking FDA approval for drugs which can prevent fertility loss and even mortality because they also happen to be used for abortion.
You see, it’s not just about me. Of course I’m angry that it happened to me, especially given the particular circumstances- I was 39 and it was my first pregnancy that ended in miscarriage. Given my age I was extremely concerned about future fertility. I had asked about the risks of D&C and in particular about AS only to be told it was rare, I had asked for alternatives like misoprostol only to be told it was ineffective and refused. I had put up a brave stand to avoid D&C by waiting to miscarry myself (which I did) and after all of that I was told that I had RPOC and had to have a D&C or risked getting AS from an infection (balogna!). The pathology report showed that I only had a blood clot and some tiny fragments and no infection. But it's not that I am a disgruntled, childless older woman: even if I were to have a child, it’s the principle that I find objectionable- that women are continuing to go through this needless suffering because doctors will not give up an archaic surgery even when other safer and cheaper medical options have been developed.
Once again, to be clear, I encourage all women who have been diagnosed with Asherman’s syndrome: please seek help from an expert for treatment if you want to have a chance of having a child. I won’t ever regret having treatment even if I don’t succeed in having a child because I know without it there would be no possibility of it. I gave myself the best odds that I could in a situation which never should have happened to me in the first place. But just because it happened to me it doesn’t mean it should continue happening to others! There is nothing I gain out of pain and suffering of other women. It makes me somewhat angry that other women who have had it before me have done nothing to prevent it from happening to me and others. It makes me somewhat resentful that the information I was after about D&C risks and alternatives for miscarriage management were not readily available to me at the time that I needed it. And I refuse to continue that cycle which is why I am doing everything possible to warn and educate women about the big coverup about Asherman’s syndrome and D&C risks and the existence of cheaper and safer alternatives. Not to mention the exaggeration of treatment success to patients as an excuse to hinder prevention. Of course, anything that promotes further dependence on doctors is encouraged and supported by the medical community while prevention is ignored. It’s time to break the cycle-now.
Some women speak of the spiritual journey AS has given them in a way where they almost sound thankful that it happened to them! All I can say it that I don' t understand people who are thankful for unnecessary damage to be inflicted upon themselves. Only someone who didn’t feel they were worthy or seriously deluded would think it was a blessing in disguise. Asherman’s syndrome was never ‘meant to be’. It only happens because many doctors are unwilling to offer alternatives to D&Cs and nothing is being done about it.
In my ‘journey’ I have learned a lot from having Asherman’s syndrome. I have learned that there is an urgent need for women to speak out against the routine use of D&C for miscarriage. I have learned that women should at the very least be given the right to choose which treatment option they prefer. I have learned that women must pressure doctors and the government to approve of all drugs which can help to safely evacuate the uterus and that these should be the first line of therapy for miscarriage and other indications instead of D&C. I have learned that not all doctors act in the best interest of their patients so patient activism is required for change.
As women we are expected to be martyrs and put up with all kinds of assaults on our bodies without complaining. It’s supposed to be the very essence of being a caring, nurturing Madonna, to put ourselves last. I prefer to be proactive and warn women about the dangers of D&C, and let doctors know it is not OK to perform D&Cs at the drop of a hat. It’s not acceptable to pretend there are no alternatives and to keep silent when prolife activists prevent drug companies from seeking FDA approval for drugs which can prevent fertility loss and even mortality because they also happen to be used for abortion.
You see, it’s not just about me. Of course I’m angry that it happened to me, especially given the particular circumstances- I was 39 and it was my first pregnancy that ended in miscarriage. Given my age I was extremely concerned about future fertility. I had asked about the risks of D&C and in particular about AS only to be told it was rare, I had asked for alternatives like misoprostol only to be told it was ineffective and refused. I had put up a brave stand to avoid D&C by waiting to miscarry myself (which I did) and after all of that I was told that I had RPOC and had to have a D&C or risked getting AS from an infection (balogna!). The pathology report showed that I only had a blood clot and some tiny fragments and no infection. But it's not that I am a disgruntled, childless older woman: even if I were to have a child, it’s the principle that I find objectionable- that women are continuing to go through this needless suffering because doctors will not give up an archaic surgery even when other safer and cheaper medical options have been developed.
Once again, to be clear, I encourage all women who have been diagnosed with Asherman’s syndrome: please seek help from an expert for treatment if you want to have a chance of having a child. I won’t ever regret having treatment even if I don’t succeed in having a child because I know without it there would be no possibility of it. I gave myself the best odds that I could in a situation which never should have happened to me in the first place. But just because it happened to me it doesn’t mean it should continue happening to others! There is nothing I gain out of pain and suffering of other women. It makes me somewhat angry that other women who have had it before me have done nothing to prevent it from happening to me and others. It makes me somewhat resentful that the information I was after about D&C risks and alternatives for miscarriage management were not readily available to me at the time that I needed it. And I refuse to continue that cycle which is why I am doing everything possible to warn and educate women about the big coverup about Asherman’s syndrome and D&C risks and the existence of cheaper and safer alternatives. Not to mention the exaggeration of treatment success to patients as an excuse to hinder prevention. Of course, anything that promotes further dependence on doctors is encouraged and supported by the medical community while prevention is ignored. It’s time to break the cycle-now.
Some women speak of the spiritual journey AS has given them in a way where they almost sound thankful that it happened to them! All I can say it that I don' t understand people who are thankful for unnecessary damage to be inflicted upon themselves. Only someone who didn’t feel they were worthy or seriously deluded would think it was a blessing in disguise. Asherman’s syndrome was never ‘meant to be’. It only happens because many doctors are unwilling to offer alternatives to D&Cs and nothing is being done about it.
In my ‘journey’ I have learned a lot from having Asherman’s syndrome. I have learned that there is an urgent need for women to speak out against the routine use of D&C for miscarriage. I have learned that women should at the very least be given the right to choose which treatment option they prefer. I have learned that women must pressure doctors and the government to approve of all drugs which can help to safely evacuate the uterus and that these should be the first line of therapy for miscarriage and other indications instead of D&C. I have learned that not all doctors act in the best interest of their patients so patient activism is required for change.
Tuesday, September 8, 2009
Treatment of Asherman's syndrome is not a panacea, Part III
Continued from Part II
In my last post in this series on treatment of Asherman's syndrome I posted the actual live birth rate outcomes according to studies published peer reviewed medical journals to show why it is not the promising solution that it is often promoted as, and why prevention would be a better approach. The gold standard for treatment of intrauterine adhesions (Asherman’s syndrome) is hysteroscopic adhesiolysis (synechiolysis) and hormonal therapy. Most studies so far focus on fertility outcomes following a particular treatment method.
Yet one needs to be cautious when evaluating outcomes because some studies are presented in ways which may mislead the inexperienced or lay reader into believing that the success rates are higher than they actually are. If you have read some of the original abstracts or papers I cited in the references of my last post, you may notice that some of the results I have given differ from those apparently reported by the authors. This is because I gave live birth rates as total number of births per total number of patients treated, which gives a complete and accurate picture of the outcomes. As I explained before, the reason I did this is to include women who may never have conceived as it is very possible that surgery did not restore their fertility. Below are some other examples of how data presentation can be misleading.
Data Presentation
'Success rates’ after surgery may not be what you had in mind. I think most patients like myself are interested in achieving a live birth. Sometimes the author is referring to menstrual outcome. Yasmin et al (1), report that 95% of women in their study resumed normal menstruation. Unfortunately, this is not closely correlated to live birth rate. Accordingly, only 1 patient out of 20 treated ie.5% went on to have a live birth (although followup was short). Restoration of menses is known to be an unreliable criteria for future fertility. In my view this is partly because it is self-reported.
Even pregnancy or conception rates per patients treated or live birth rates per total pregnancies do not necessarily reflect live birth outcomes realistically because not only do 1 in 4-5 pregnancies end in miscarriage under the best of circumstances, women with a history of Asherman’s syndrome are also prone to second trimester pregnancy loss and preterm delivery (2). Other women with residual scarring may conceive but repeatedly miscarry with no live births.
In one study (3) the abstract says that live birth rate was 86.1%. Not only was this an overall rate in a study group where mild and moderate cases greatly outnumbered severe cases (71 vs 18), it is also calculated per pregnancy (instead of per patients treated). This can be gleaned from Table 3 where a 66.6% live birth rate was given among women with severe condition at presentation. In other words, two thirds of the women with severe Asherman’s who were able to conceive after treatment went on to deliver a live baby. This is good but not that inspiring when you consider that most women in this group were not able to conceive. In fact, only 4 out of 18 (22%) women with severe AS in this study had a live birth. Another example of this occurs in Table 6 of Yu et al, 2008 (4) review where outcomes are given in terms of live births/pregnancies.
Perhaps reporting data in this way is seen as acceptable by some because doctors are all too eager to put down the inability to conceive after treatment to ‘other fertility issues’, particularly in women who have had the cruel misfortune of being inflicted with Asherman’s syndrome before having a child. The ridiculous premise is that unless women have a live birth prior to developing this iatrogenic condition, they cannot 'prove' they were ever fertile (infertile unless proven otherwise). Unless these ‘other causes of infertility’ are clearly described and (depending on the cause) pre-existing, there is no evidence to suggest that these women were infertile to begin with and should be discarded from outcomes. If the studies were conducted according to the highest standards, women with ‘other fertility issues’ would be excluded from studies to begin with and not after the fertility results are known. This brings me to…
Study design
Besides data presentation, it is also important to take into account how the study was conducted because this too has important implications on outcomes. Unfortunately, studies on Asherman’s syndrome have not been conducted to meet most rigorous scientific methodology-RCTs, making it difficult to assess the exact outcomes. I have mentioned the lack of RCTs in an earlier post. It follows that there are currently no systematic reviews or meta-analyses of the studies either since they are not conducted to stringent standards.
RCTs are clinical trials which have to meet certain criteria in order for the results to be considered unbiased, accurate and of statistical significance. In summary, studies must be done prospectively, they must be randomized with respect to treatment strategies depending on the outcome measure(s), there must be blinding of the doctors, investigators with regard to diagnoses/assessment of outcome with regards to treatment, a clear definition of exclusion and inclusion criteria for patients must be set in order to avoid outcome bias, and there must be enough participants in the/each study group(s) such that statistical analyses can be deemed to have significant value.
RCTs can be carried out to test the efficacy of a particular treatment, or to compare the efficacies of two or more different treatments. Most Asherman's studies focus on fertility outcomes following a given treatment protocol. The risk for potential bias comes mainly from unclearly defined patient inclusion/exclusion criteria, retrospective analyses and sample size and composition.
With regards to study design, the most blatant weakness is when studies are done retrospectively. This means that the doctor/investigator chooses the data to present after they already know the outcomes. This approach introduces the possibility of bias in outcomes because they may select, for example, all of the patients who went on to have live births after treatment, but leave out a portion of those who did not regain their fertility from the study without ever mentioning it. This would obviously make the success rate of treatment appear to be higher than in actuality. Most studies are now carried out prospectively.
Even if a study is done prospectively there are ways in which the outcome can be premeditatingly skewed to enhance outcomes. This is why in proper RCTs everything about the study (except for the results and conclusions) is decided in detail in advance and recorded in a repository. This leaves little space for modifications which can incorporate bias.
If exclusion/inclusion criteria are not stringent from the outset, some of the women who did not achieve a pregnancy could still be discounted on account that they had ‘other' fertility problems. Some authors write their study before allowing a reasonable followup time (1,5) and suggest that the success rate is potentially higher because at the time of writing it was too soon for X number of patients to try to conceive. Others may include patients with ongoing pregnancies (4,6,7,8) which may later not eventuate in live birth on complete followup. In one study, (9) live birth rates were reported as 83% a figure that sticks out like a sore thumb compared to other studies. It turns out that the study, which was done on 365 women, only included 186 patients in the live birth rate outcome. The justification for this was the 179 patients who were left out did not desire a pregnancy. Call me skeptical but I find it hard to believe that 179 women would undergo surgery just to get their periods back. If you include all 365 women in the study the live birth rates don’t look quite as remarkable -42.7%- blending in with the rates recorded by other studies.
Another thing to keep in mind is patient composition: how many have mild, moderate and severe disease? Since an increase in disease severity is associated with a poorer prognosis in terms of live births, a study group consisting of proportionally fewer severe cases could artificially bump up the live birth rate. Therefore it is important to either indicate this by giving a breakdown of outcomes according to disease severity, or to carry out studies where there are equal numbers of patients of the different disease classifications. Many studies will report overall birth rates among patients without giving a breakdown according to disease severity at presentation. It is up to the reader to do their own calculations.
I think the above examples show why proper RCTs are needed to not just to compare different methods of treatment, but to give accurate data regarding live birth outcomes. It would also be of help if there was a more standard way of reporting outcomes such as live births per total patients treated.
REFERENCES
1. Yasmin H, Nasir A, Noorani KJ. Hystroscopic management of Asherman’s syndromeJ Pak Med Assoc. 2007 Nov;57(11):553-5.
2. Capella-Allouc, S, Morsad, F, Rongieres-Bertrand, C, Taylor, S, and Fernandez, H. Hysteroscopic treatment of severe Asherman's syndrome and subsequent fertility. Hum Reprod 1999;14(5):1230-3.
3. Roy KK, Baruah J, Sharma JB, Kumar S, Kachawa G, Singh N.Reproductive outcome following hysteroscopic adhesiolysis in patients with infertility due to Asherman's syndrome. Arch Gynecol Obstet. 2009
4. Yu, D, Li, TC, Xia, E, Huang, X, Liu, Y, and Peng, X. Factors affecting reproductive outcome of hysteroscopic adhesiolysis for Asherman's syndrome. Fertil Steril 2008;89(3):715-22.
5. A. Thomson, J. Abbott, A. Kingston, M. Lenart, T. Vancaillie. Fluoroscopically guided synechiolysis for patients with Asherman’s syndrome: menstrual and fertility outcomes. Fertil Steril, 2007; Volume 87(2):405-410
6. Goldenberg, M, Sivan, E, Sharabi, Z, Mashiach, S, Lipitz, S, and Seidman, DS. Reproductive outcome following hysteroscopic management of intrauterine septum and adhesions. Hum Reprod 1995;10(10):2663-5.
7. Robinson, JK, Colimon, LM, and Isaacson, KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril 2008;90(2):409-14.
8. Protopapas, A, Shushan, A, and Magos, A. Myometrial scoring: a new technique for the management of severe Asherman's syndrome. Fertil Steril 1998;69(5):860-4.
9. Feng, Z, Yang, B, Shao, J, and Liu, S. Diagnostic and therapeutic hysteroscopy for traumatic intrauterine adhesions after induced abortions: clinical analysis of 365 cases. Gynaecol Endosc 1999;8(2):95-98.
In my last post in this series on treatment of Asherman's syndrome I posted the actual live birth rate outcomes according to studies published peer reviewed medical journals to show why it is not the promising solution that it is often promoted as, and why prevention would be a better approach. The gold standard for treatment of intrauterine adhesions (Asherman’s syndrome) is hysteroscopic adhesiolysis (synechiolysis) and hormonal therapy. Most studies so far focus on fertility outcomes following a particular treatment method.
Yet one needs to be cautious when evaluating outcomes because some studies are presented in ways which may mislead the inexperienced or lay reader into believing that the success rates are higher than they actually are. If you have read some of the original abstracts or papers I cited in the references of my last post, you may notice that some of the results I have given differ from those apparently reported by the authors. This is because I gave live birth rates as total number of births per total number of patients treated, which gives a complete and accurate picture of the outcomes. As I explained before, the reason I did this is to include women who may never have conceived as it is very possible that surgery did not restore their fertility. Below are some other examples of how data presentation can be misleading.
Data Presentation
'Success rates’ after surgery may not be what you had in mind. I think most patients like myself are interested in achieving a live birth. Sometimes the author is referring to menstrual outcome. Yasmin et al (1), report that 95% of women in their study resumed normal menstruation. Unfortunately, this is not closely correlated to live birth rate. Accordingly, only 1 patient out of 20 treated ie.5% went on to have a live birth (although followup was short). Restoration of menses is known to be an unreliable criteria for future fertility. In my view this is partly because it is self-reported.
Even pregnancy or conception rates per patients treated or live birth rates per total pregnancies do not necessarily reflect live birth outcomes realistically because not only do 1 in 4-5 pregnancies end in miscarriage under the best of circumstances, women with a history of Asherman’s syndrome are also prone to second trimester pregnancy loss and preterm delivery (2). Other women with residual scarring may conceive but repeatedly miscarry with no live births.
In one study (3) the abstract says that live birth rate was 86.1%. Not only was this an overall rate in a study group where mild and moderate cases greatly outnumbered severe cases (71 vs 18), it is also calculated per pregnancy (instead of per patients treated). This can be gleaned from Table 3 where a 66.6% live birth rate was given among women with severe condition at presentation. In other words, two thirds of the women with severe Asherman’s who were able to conceive after treatment went on to deliver a live baby. This is good but not that inspiring when you consider that most women in this group were not able to conceive. In fact, only 4 out of 18 (22%) women with severe AS in this study had a live birth. Another example of this occurs in Table 6 of Yu et al, 2008 (4) review where outcomes are given in terms of live births/pregnancies.
Perhaps reporting data in this way is seen as acceptable by some because doctors are all too eager to put down the inability to conceive after treatment to ‘other fertility issues’, particularly in women who have had the cruel misfortune of being inflicted with Asherman’s syndrome before having a child. The ridiculous premise is that unless women have a live birth prior to developing this iatrogenic condition, they cannot 'prove' they were ever fertile (infertile unless proven otherwise). Unless these ‘other causes of infertility’ are clearly described and (depending on the cause) pre-existing, there is no evidence to suggest that these women were infertile to begin with and should be discarded from outcomes. If the studies were conducted according to the highest standards, women with ‘other fertility issues’ would be excluded from studies to begin with and not after the fertility results are known. This brings me to…
Study design
Besides data presentation, it is also important to take into account how the study was conducted because this too has important implications on outcomes. Unfortunately, studies on Asherman’s syndrome have not been conducted to meet most rigorous scientific methodology-RCTs, making it difficult to assess the exact outcomes. I have mentioned the lack of RCTs in an earlier post. It follows that there are currently no systematic reviews or meta-analyses of the studies either since they are not conducted to stringent standards.
RCTs are clinical trials which have to meet certain criteria in order for the results to be considered unbiased, accurate and of statistical significance. In summary, studies must be done prospectively, they must be randomized with respect to treatment strategies depending on the outcome measure(s), there must be blinding of the doctors, investigators with regard to diagnoses/assessment of outcome with regards to treatment, a clear definition of exclusion and inclusion criteria for patients must be set in order to avoid outcome bias, and there must be enough participants in the/each study group(s) such that statistical analyses can be deemed to have significant value.
RCTs can be carried out to test the efficacy of a particular treatment, or to compare the efficacies of two or more different treatments. Most Asherman's studies focus on fertility outcomes following a given treatment protocol. The risk for potential bias comes mainly from unclearly defined patient inclusion/exclusion criteria, retrospective analyses and sample size and composition.
With regards to study design, the most blatant weakness is when studies are done retrospectively. This means that the doctor/investigator chooses the data to present after they already know the outcomes. This approach introduces the possibility of bias in outcomes because they may select, for example, all of the patients who went on to have live births after treatment, but leave out a portion of those who did not regain their fertility from the study without ever mentioning it. This would obviously make the success rate of treatment appear to be higher than in actuality. Most studies are now carried out prospectively.
Even if a study is done prospectively there are ways in which the outcome can be premeditatingly skewed to enhance outcomes. This is why in proper RCTs everything about the study (except for the results and conclusions) is decided in detail in advance and recorded in a repository. This leaves little space for modifications which can incorporate bias.
If exclusion/inclusion criteria are not stringent from the outset, some of the women who did not achieve a pregnancy could still be discounted on account that they had ‘other' fertility problems. Some authors write their study before allowing a reasonable followup time (1,5) and suggest that the success rate is potentially higher because at the time of writing it was too soon for X number of patients to try to conceive. Others may include patients with ongoing pregnancies (4,6,7,8) which may later not eventuate in live birth on complete followup. In one study, (9) live birth rates were reported as 83% a figure that sticks out like a sore thumb compared to other studies. It turns out that the study, which was done on 365 women, only included 186 patients in the live birth rate outcome. The justification for this was the 179 patients who were left out did not desire a pregnancy. Call me skeptical but I find it hard to believe that 179 women would undergo surgery just to get their periods back. If you include all 365 women in the study the live birth rates don’t look quite as remarkable -42.7%- blending in with the rates recorded by other studies.
Another thing to keep in mind is patient composition: how many have mild, moderate and severe disease? Since an increase in disease severity is associated with a poorer prognosis in terms of live births, a study group consisting of proportionally fewer severe cases could artificially bump up the live birth rate. Therefore it is important to either indicate this by giving a breakdown of outcomes according to disease severity, or to carry out studies where there are equal numbers of patients of the different disease classifications. Many studies will report overall birth rates among patients without giving a breakdown according to disease severity at presentation. It is up to the reader to do their own calculations.
I think the above examples show why proper RCTs are needed to not just to compare different methods of treatment, but to give accurate data regarding live birth outcomes. It would also be of help if there was a more standard way of reporting outcomes such as live births per total patients treated.
REFERENCES
1. Yasmin H, Nasir A, Noorani KJ. Hystroscopic management of Asherman’s syndromeJ Pak Med Assoc. 2007 Nov;57(11):553-5.
2. Capella-Allouc, S, Morsad, F, Rongieres-Bertrand, C, Taylor, S, and Fernandez, H. Hysteroscopic treatment of severe Asherman's syndrome and subsequent fertility. Hum Reprod 1999;14(5):1230-3.
3. Roy KK, Baruah J, Sharma JB, Kumar S, Kachawa G, Singh N.Reproductive outcome following hysteroscopic adhesiolysis in patients with infertility due to Asherman's syndrome. Arch Gynecol Obstet. 2009
4. Yu, D, Li, TC, Xia, E, Huang, X, Liu, Y, and Peng, X. Factors affecting reproductive outcome of hysteroscopic adhesiolysis for Asherman's syndrome. Fertil Steril 2008;89(3):715-22.
5. A. Thomson, J. Abbott, A. Kingston, M. Lenart, T. Vancaillie. Fluoroscopically guided synechiolysis for patients with Asherman’s syndrome: menstrual and fertility outcomes. Fertil Steril, 2007; Volume 87(2):405-410
6. Goldenberg, M, Sivan, E, Sharabi, Z, Mashiach, S, Lipitz, S, and Seidman, DS. Reproductive outcome following hysteroscopic management of intrauterine septum and adhesions. Hum Reprod 1995;10(10):2663-5.
7. Robinson, JK, Colimon, LM, and Isaacson, KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril 2008;90(2):409-14.
8. Protopapas, A, Shushan, A, and Magos, A. Myometrial scoring: a new technique for the management of severe Asherman's syndrome. Fertil Steril 1998;69(5):860-4.
9. Feng, Z, Yang, B, Shao, J, and Liu, S. Diagnostic and therapeutic hysteroscopy for traumatic intrauterine adhesions after induced abortions: clinical analysis of 365 cases. Gynaecol Endosc 1999;8(2):95-98.
Friday, August 28, 2009
Treatment of Asherman's syndrome is not a panacea, Part II
Continued from Part I
One century after its first description, treatment of Asherman’s syndrome (1) has not progressed enough to ensure that a high percentage of patients will regain fertility. I hope that one day it will be 100% treatable but it seems that this is a long way off and not a top priority for researchers or funding bodies. As important as treatment is for the women who have been diagnosed with Asherman’s syndrome, it is still difficult to justify why so little is being done to prevent it in the first place. Not all cases are preventable depending on the cause, but most are. Most cases (over 90% according to one study) (2) are caused by D&C and yet there are alternatives to D&C for every indication for which it is used. When D&C continues to be standard care for miscarriage management most cases of Asherman’s syndrome will continue to occur in women who have miscarried.
Asherman’s syndrome was first described in 1894 (1) and later further characterized in 1948(3). In those days there were no other options to D&C so naturally treatment (or more selective use of D&C) was the only solution to the problem. The situation today is very different with the discovery of drugs and hysteroscopy to replace D&C. These approaches would undoubtedly reduce the incidence of Asherman’s syndrome.
Unfortunately treatment is not a panacea. The outcomes of studies speak for themselves (see below). They range from 27% to 43% and include women of different classification severities (so presumably this rate is even less inspiring for women with more severe presentation). Note that all of these studies are recent. The most accurate way to present these results is to report number of live births per total patients treated because some women will either never conceive or give birth after treatment. Reporting live births per pregnancy is deceptive because the women who never got pregnant are discounted from the outcomes. It is very possible that some women never conceived because the endometrial damage they sustained and which led to Asherman’s syndrome was permanent and not able to be repaired by treatment enough to allow for successful implantation. Absence of adhesions does not imply that the endometrium is functioning properly- there could be fibrosis or very thin unresponsive endometrium. Unfortunately, to this date, there is no test which can ensure that the entire endometrium is functional. In the next part of this discussion about treatment (Part III), I will discuss in further detail the results from studies and difficulties in conducting studies on Asherman's syndrome.
Studies of modern success rates (#live births/#patients treated) after treatment of Asherman’s syndrome:
* the paper itself quotes a 47% live birth rate but excludes 10 women ie. one third of the patient sample size from the calculation on the basis that they were not trying for pregnancy.
**the paper quotes a 46% (7/15) live birth rate, however 3 of those pregnancies were still ongoing at the time of publication.
The real outcomes, including the results of treatment by the best doctors in the field according to the Asherman's Syndrome International Support Group don’t look as inspirational in statistics as they do when presented as personal success stories.
Are these live birth rates high enough to justify treatment as the best solution to the problem of iatrogenic Asherman’s syndrome? Or that D&C should continue to be used routinely or as ‘standard care’?
I will not get into the serious obstetric complications sometimes encountered in future pregnancies (should patients be fortunate enough to be able to conceive and carry a pregnancy). I have saved this for another post as it is a whole other area that needs to be discussed in detail.
There is another very important reason for women to told the true success rates of treatment (and about future obstetric complications): awareness will undoubtedly create a push among patients and and more importantly women, in general, for prevention by using alternatives to D&C…
Continued in Part III
REFERENCES
1. Fritsch, H. Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung Zentralbl Gynaekol 1894;18:1337-1342.
2. Schenker, JG and Margalioth, EJ. Intrauterine adhesions: an updated appraisal. Fertil Steril 1982;37(5):593-610.
3. Asherman, JG. Amenorrhea traumatica (atretica). J Obstet Gynaec Brit Emp 1948;55(23).
4. Zikopoulos, KA, Kolibianakis, EM, Platteau, P, de Munck, L, Tournaye, H, Devroey, P et al. Live delivery rates in subfertile women with Asherman's syndrome after hysteroscopic adhesiolysis using the resectoscope or the Versapoint system. Reprod Biomed Online 2004;8(6):720-5. Abstract
5. Fernandez, H, Al-Najjar, F, Chauveaud-Lambling, A, Frydman, R, and Gervaise, A. Fertility after treatment of Asherman's syndrome stage 3 and 4. J Minim Invasive Gynecol 2006;13(5):398-402. Abstract
6. Thomson Angus J M; Abbott Jason A; Kingston Ashley; Lenart Meegan; Vancaillie Thierry G. Fluoroscopically guided synechiolysis for patients with Asherman's syndrome: menstrual and fertility outcomes. Fertility and sterility 2007;87(2):405-10. Abstract
7. Robinson, JK, Colimon, LM, and Isaacson, KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril 2008;90(2):409-14. Abstract
8. Yu, D, Li, TC, Xia, E, Huang, X, Liu, Y, and Peng, X. Factors affecting reproductive outcome of hysteroscopic adhesiolysis for Asherman's syndrome. Fertil Steril 2008;89(3):715-22. Abstract
9. Pabuccu Recai; Onalan Gogsen; Kaya Cemil; Selam Belgin; Ceyhan Temel; Ornek Turkan; Kuzudisli Ebru. Efficiency and pregnancy outcome of serial intrauterine device-guided hysteroscopic adhesiolysis of intrauterine synechiae. Fertility and sterility 2008;90(5):1973-7.
Abstract
One century after its first description, treatment of Asherman’s syndrome (1) has not progressed enough to ensure that a high percentage of patients will regain fertility. I hope that one day it will be 100% treatable but it seems that this is a long way off and not a top priority for researchers or funding bodies. As important as treatment is for the women who have been diagnosed with Asherman’s syndrome, it is still difficult to justify why so little is being done to prevent it in the first place. Not all cases are preventable depending on the cause, but most are. Most cases (over 90% according to one study) (2) are caused by D&C and yet there are alternatives to D&C for every indication for which it is used. When D&C continues to be standard care for miscarriage management most cases of Asherman’s syndrome will continue to occur in women who have miscarried.
Asherman’s syndrome was first described in 1894 (1) and later further characterized in 1948(3). In those days there were no other options to D&C so naturally treatment (or more selective use of D&C) was the only solution to the problem. The situation today is very different with the discovery of drugs and hysteroscopy to replace D&C. These approaches would undoubtedly reduce the incidence of Asherman’s syndrome.
Unfortunately treatment is not a panacea. The outcomes of studies speak for themselves (see below). They range from 27% to 43% and include women of different classification severities (so presumably this rate is even less inspiring for women with more severe presentation). Note that all of these studies are recent. The most accurate way to present these results is to report number of live births per total patients treated because some women will either never conceive or give birth after treatment. Reporting live births per pregnancy is deceptive because the women who never got pregnant are discounted from the outcomes. It is very possible that some women never conceived because the endometrial damage they sustained and which led to Asherman’s syndrome was permanent and not able to be repaired by treatment enough to allow for successful implantation. Absence of adhesions does not imply that the endometrium is functioning properly- there could be fibrosis or very thin unresponsive endometrium. Unfortunately, to this date, there is no test which can ensure that the entire endometrium is functional. In the next part of this discussion about treatment (Part III), I will discuss in further detail the results from studies and difficulties in conducting studies on Asherman's syndrome.
Studies of modern success rates (#live births/#patients treated) after treatment of Asherman’s syndrome:
| STUDY | REF | BIRTHS/PATIENTS | BIRTH RATE |
|---|---|---|---|
| 1. Zikopoulos et al, 2004 | (4) | 20/46 | 43.5% |
| 2. Fernandez et al, 2006 | (5) | 21/64 | 32.8% |
| 3. Thomson et al, 2007 | (6) | 8/27 | 29.6%* |
| 4. Yu et al, 2008 | (7) | 25/85 | 29% |
5. Robinson et al, 2008 | (8) | 4/15 | 27% ** |
| 6. Pabuccu et al, 2008 | (9) | 22/71 | 31% |
* the paper itself quotes a 47% live birth rate but excludes 10 women ie. one third of the patient sample size from the calculation on the basis that they were not trying for pregnancy.
**the paper quotes a 46% (7/15) live birth rate, however 3 of those pregnancies were still ongoing at the time of publication.
The real outcomes, including the results of treatment by the best doctors in the field according to the Asherman's Syndrome International Support Group don’t look as inspirational in statistics as they do when presented as personal success stories.
Are these live birth rates high enough to justify treatment as the best solution to the problem of iatrogenic Asherman’s syndrome? Or that D&C should continue to be used routinely or as ‘standard care’?
I will not get into the serious obstetric complications sometimes encountered in future pregnancies (should patients be fortunate enough to be able to conceive and carry a pregnancy). I have saved this for another post as it is a whole other area that needs to be discussed in detail.
There is another very important reason for women to told the true success rates of treatment (and about future obstetric complications): awareness will undoubtedly create a push among patients and and more importantly women, in general, for prevention by using alternatives to D&C…
Continued in Part III
REFERENCES
1. Fritsch, H. Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung Zentralbl Gynaekol 1894;18:1337-1342.
2. Schenker, JG and Margalioth, EJ. Intrauterine adhesions: an updated appraisal. Fertil Steril 1982;37(5):593-610.
3. Asherman, JG. Amenorrhea traumatica (atretica). J Obstet Gynaec Brit Emp 1948;55(23).
4. Zikopoulos, KA, Kolibianakis, EM, Platteau, P, de Munck, L, Tournaye, H, Devroey, P et al. Live delivery rates in subfertile women with Asherman's syndrome after hysteroscopic adhesiolysis using the resectoscope or the Versapoint system. Reprod Biomed Online 2004;8(6):720-5. Abstract
5. Fernandez, H, Al-Najjar, F, Chauveaud-Lambling, A, Frydman, R, and Gervaise, A. Fertility after treatment of Asherman's syndrome stage 3 and 4. J Minim Invasive Gynecol 2006;13(5):398-402. Abstract
6. Thomson Angus J M; Abbott Jason A; Kingston Ashley; Lenart Meegan; Vancaillie Thierry G. Fluoroscopically guided synechiolysis for patients with Asherman's syndrome: menstrual and fertility outcomes. Fertility and sterility 2007;87(2):405-10. Abstract
7. Robinson, JK, Colimon, LM, and Isaacson, KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril 2008;90(2):409-14. Abstract
8. Yu, D, Li, TC, Xia, E, Huang, X, Liu, Y, and Peng, X. Factors affecting reproductive outcome of hysteroscopic adhesiolysis for Asherman's syndrome. Fertil Steril 2008;89(3):715-22. Abstract
9. Pabuccu Recai; Onalan Gogsen; Kaya Cemil; Selam Belgin; Ceyhan Temel; Ornek Turkan; Kuzudisli Ebru. Efficiency and pregnancy outcome of serial intrauterine device-guided hysteroscopic adhesiolysis of intrauterine synechiae. Fertility and sterility 2008;90(5):1973-7.
Abstract
Friday, August 14, 2009
Treatment of Asherman's syndrome is not a panacea (Part I)
Not all that long ago Asherman’s syndrome patients may have been told to forget about ever having a(nother) child. Treatment has come a long way with the advent of hysteroscopy, hormonal treatment, stents and adhesive barriers. It’s not surprising that before these were available, success rates were very low and often more damage was incurred from ‘treatment’ resulting in worse outcomes. One of the reasons for this is that some doctors used to treat Asherman’s syndrome by performing a blind D&C to break apart intrauterine adhesions they couldn’t even see. It’s hard to imagine why anyone would think that performing the same procedure as the one which usually causes the condition could fix things, but lots of doctors did- and some continue to do so with disastrous consequences.
Some doctors might still have the attitude that anyone whom they cannot treat successfully should give up hope, even if they are not highly skilled or experienced in the treatment of intrauterine adhesions. However, a new and equally detrimental view is being encouraged among sufferers: that treatment has come so far that anyone who is diagnosed stands a very good chance of conceiving and delivering a healthy baby (provided they go to the right doctors). While it’s true that some doctors have much more training, experience and expertise in the treatment of Asherman’s syndrome, the harsh reality is that the overall success rate is not above 50% (and lower for the moderate to severe cases)- even with the best doctors. If anyone tells you that there are doctors who have higher success rates with moderate to severe cases than 50%, they are either not being truthful or simply don’t know (or prefer not to accept) the reality.
It’s a bitter pill to swallow, but women need to be made aware of this fact. Not to crush any optimism, but to give realistic expectations, and perhaps to avoid the costs and heartbreak of ‘unexplained infertility’ following ‘successful’ treatment. There is a very fine line between giving encouragement and creating false hope. You may read of success stories, you may hear of women overcoming seemingly astonishing odds, and photos of women beaming with their babies, praising their ‘miracle’ doctors, but make no mistake: these are the faces and stories of less than 50% of women who are diagnosed with IUA and get treatment by the best doctors. But they do not reflect the reality for more than half of women diagnosed with Asherman’s syndrome. The latter are the women who fade into the background, the ones doctors and patients alike would like to forget about, or blame the lack of success on other reasons. Let us not underestimate the significance of the initial trauma underlying the Asherman’s syndrome. Some of us got a worse deal than the others. Worst of all, there is no clear way of predicting whether treatment will be successful or even knowing if it was successful. The only way to know is to try to conceive. If you do have a baby, your treatment was successful. If you don’t, your treatment may not have fully restored your fertility (or you have other causes of unexplained infertility). But let’s not exaggerate the likelihood of the latter- why would someone who was previously capable of getting pregnant suddenly have ‘unexplained infertility’ after having had Asherman’s syndrome? Fibrosis from Asherman’s syndrome can affect blood flow to the endometrium and reduce the chance of implantation or maintaining a pregnancy. I’m not saying one should not seek treatment. By all means, please do whatever is necessary to improve your chances of regaining your fertility! But don’t be too surprised if you don’t end up with a success story.
The attitude of the medical community is also to blame for encouraging the view that treatment is the best answer to the problem. For reasons which evade me, they seem to think it is more logical to subject all women to blind surgery causing Asherman's syndrome in a non-negligible proportion of them, and then to attempt surgical correction and hormonal therapy on those who do develop IUA in the hope that at most 50% of them will have a child (30-40% with moderate to severe IUA, 80% with mild IUA). Not to mention that these future pregnancies are at risk of serious complications, like placenta accreta, preterm delivery, intrauterine growth restriction, cervical incompetence etc. How logical is this? What is the advantage or logic in performing two (or more) expensive, difficult and potentially risky uterine surgeries- one which can cause damage, and one (or more) to repair the damage of the first surgery? Why not nip it at the bud and not cause damage to begin with?
Why not simply use drugs or hysteroscopy to empty the uterus, preventing scarring in the first place? When you consider that there are ways of emptying the uterus without blind surgery (either by using drugs like misoprostol or mifepristone, or visually guided hysteroscopy) the surgical approach makes no sense whatsoever. Is the approach of D&C followed by corrective surgery in the best interest of patients? Absolutely not.
In my next post I will include modern studies on outcomes of treatment as evidence.
Continued in Part II
Some doctors might still have the attitude that anyone whom they cannot treat successfully should give up hope, even if they are not highly skilled or experienced in the treatment of intrauterine adhesions. However, a new and equally detrimental view is being encouraged among sufferers: that treatment has come so far that anyone who is diagnosed stands a very good chance of conceiving and delivering a healthy baby (provided they go to the right doctors). While it’s true that some doctors have much more training, experience and expertise in the treatment of Asherman’s syndrome, the harsh reality is that the overall success rate is not above 50% (and lower for the moderate to severe cases)- even with the best doctors. If anyone tells you that there are doctors who have higher success rates with moderate to severe cases than 50%, they are either not being truthful or simply don’t know (or prefer not to accept) the reality.
It’s a bitter pill to swallow, but women need to be made aware of this fact. Not to crush any optimism, but to give realistic expectations, and perhaps to avoid the costs and heartbreak of ‘unexplained infertility’ following ‘successful’ treatment. There is a very fine line between giving encouragement and creating false hope. You may read of success stories, you may hear of women overcoming seemingly astonishing odds, and photos of women beaming with their babies, praising their ‘miracle’ doctors, but make no mistake: these are the faces and stories of less than 50% of women who are diagnosed with IUA and get treatment by the best doctors. But they do not reflect the reality for more than half of women diagnosed with Asherman’s syndrome. The latter are the women who fade into the background, the ones doctors and patients alike would like to forget about, or blame the lack of success on other reasons. Let us not underestimate the significance of the initial trauma underlying the Asherman’s syndrome. Some of us got a worse deal than the others. Worst of all, there is no clear way of predicting whether treatment will be successful or even knowing if it was successful. The only way to know is to try to conceive. If you do have a baby, your treatment was successful. If you don’t, your treatment may not have fully restored your fertility (or you have other causes of unexplained infertility). But let’s not exaggerate the likelihood of the latter- why would someone who was previously capable of getting pregnant suddenly have ‘unexplained infertility’ after having had Asherman’s syndrome? Fibrosis from Asherman’s syndrome can affect blood flow to the endometrium and reduce the chance of implantation or maintaining a pregnancy. I’m not saying one should not seek treatment. By all means, please do whatever is necessary to improve your chances of regaining your fertility! But don’t be too surprised if you don’t end up with a success story.
The attitude of the medical community is also to blame for encouraging the view that treatment is the best answer to the problem. For reasons which evade me, they seem to think it is more logical to subject all women to blind surgery causing Asherman's syndrome in a non-negligible proportion of them, and then to attempt surgical correction and hormonal therapy on those who do develop IUA in the hope that at most 50% of them will have a child (30-40% with moderate to severe IUA, 80% with mild IUA). Not to mention that these future pregnancies are at risk of serious complications, like placenta accreta, preterm delivery, intrauterine growth restriction, cervical incompetence etc. How logical is this? What is the advantage or logic in performing two (or more) expensive, difficult and potentially risky uterine surgeries- one which can cause damage, and one (or more) to repair the damage of the first surgery? Why not nip it at the bud and not cause damage to begin with?
Why not simply use drugs or hysteroscopy to empty the uterus, preventing scarring in the first place? When you consider that there are ways of emptying the uterus without blind surgery (either by using drugs like misoprostol or mifepristone, or visually guided hysteroscopy) the surgical approach makes no sense whatsoever. Is the approach of D&C followed by corrective surgery in the best interest of patients? Absolutely not.
In my next post I will include modern studies on outcomes of treatment as evidence.
Continued in Part II
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.
Tuesday, July 28, 2009
Update on latest articles (29/7/09)
I just did my regular NCBI Pubmed search using the keywords Asherman's syndrome and intrauterine adhesions and was glad to see 2 new articles:
1. Faivre E, Deffieux X, Mrazguia C, Gervaise A, Chauveaud-Lambling A, Frydman R, Fernandez H. Hysteroscopic management of residual trophoblastic tissue and reproductive outcome: a pilot study. J Minim Invasive Gynecol. 2009 Jul-Aug;16(4):487-90.
Click here to read abstract. This one is an observational study.
2. Thomson AJ, Abbott JA, Deans R, Kingston A, Vancaillie TG. The management of intrauterine synechiae. Curr Opin Obstet Gynecol. 2009 Aug;21(4):335-41.
Click here to read abstract. This one is a review on treatment and outcomes.
I haven't read them yet but will do so as soon as I get them, and will pass on any relevant information/comments. I am particularly happy to see that the first article proposes the use of hysteroscopic guidance instead of blind surgical curettage (ie. D&C) to remove retained products of conception (trophoblastic tissue). This would certainly be a step in the right direction. Prof. Herve Fernandez has notably another publication on hysteroscopic outcomes in patients with severe Asherman's syndrome.
The group leader of the second article, A/Prof Thierry Vancaillie, practices in Sydney, Australia, where I live and is one of a handful of 'A list' Asherman's specialists from around the world who who was recommended to me by the Asherman's International Support Group. He officially diagnosed my intrauterine adhesions.
1. Faivre E, Deffieux X, Mrazguia C, Gervaise A, Chauveaud-Lambling A, Frydman R, Fernandez H. Hysteroscopic management of residual trophoblastic tissue and reproductive outcome: a pilot study. J Minim Invasive Gynecol. 2009 Jul-Aug;16(4):487-90.
Click here to read abstract. This one is an observational study.
2. Thomson AJ, Abbott JA, Deans R, Kingston A, Vancaillie TG. The management of intrauterine synechiae. Curr Opin Obstet Gynecol. 2009 Aug;21(4):335-41.
Click here to read abstract. This one is a review on treatment and outcomes.
I haven't read them yet but will do so as soon as I get them, and will pass on any relevant information/comments. I am particularly happy to see that the first article proposes the use of hysteroscopic guidance instead of blind surgical curettage (ie. D&C) to remove retained products of conception (trophoblastic tissue). This would certainly be a step in the right direction. Prof. Herve Fernandez has notably another publication on hysteroscopic outcomes in patients with severe Asherman's syndrome.
The group leader of the second article, A/Prof Thierry Vancaillie, practices in Sydney, Australia, where I live and is one of a handful of 'A list' Asherman's specialists from around the world who who was recommended to me by the Asherman's International Support Group. He officially diagnosed my intrauterine adhesions.
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…
Thursday, July 9, 2009
(Opinion) Asherman's syndrome and abortion: A convenient misconception?
In my last post I brought up the issue of abortion because usually the topic of Asherman's syndrome only gets mentioned by the public in the context of abortion which is very misleading. I just want to remind you that the intention of this blog is not about abortion, but about Asherman's syndrome, D&C safety, medical ethics and alternatives to D&C.
As I mentioned in my last post, one reason for the misconception linking Asherman's syndrome only to abortion is that doctors rarely address the point by clarifying that:
-There are ways to perform abortions without the use of surgery (D&C), therefore safely, so the point is irrelevant, and
-The same surgery as that used for abortions (D&C) is used commonly in gynecology and obstetrics.
In this youtube clip Dr Paul Indman, who is experienced in the treatment of Asherman's syndrome, states that the condition is more often seen in women after a D&C for miscarriage or retained placenta, especially when repeated, than in women who have had a D&C for abortion.
Despite this medically known fact, this and many other myths about Asherman's syndrome continue to linger. Please watch my youtube clip.
Many women who have had Asherman’s syndrome from a D&C, myself included, feel strongly that D&Cs should not be performed, whether they are for miscarriages, diagnostic purposes or for abortion. Yet many doctors-even some Asherman's syndrome experts- are adamant that D&Cs can never be replaced, something which I as a PhD scientist and student of Public Health and Evidence Based Medicine know for a fact is untrue after having read several clinical trials on misoprostol use for miscarriage management (1)(2)(3)(4)(5). In some parts of Europe misoprostol has gained acceptance as a valid alternative to D&C. Perhaps the absence of anti-abortion activists and strong religious influences accounts for the widespread availability of misoprostol and mifepristone in Switzerland and some parts of Europe.
Therefore doctors continue to perform D&C even though it is known that complications can occur, and that there are some good alternatives including drugs for uterine evacuation (eg. miscarriage, retained placenta, abortion) and hysteroscopy for uterine surgery (eg. fibroids, polyps) and in selected cases for miscarriage management (6). Only about 15% of US Gynecologists are trained in office hysteroscopy. The drug misoprostol, for example, is very cheap and there are no surgery related costs including anesthesia or operating room costs. Yet women in developed countries continue to have their reproductive organ-their endometrium-mutilated by the continued use of D&Cs.
Could it be that many doctors see it's in their best interest to stick to D&Cs which are more financially rewarding than prescribing drugs and less skill intensive than hysteroscopy? It may even be convenient that this whole D&C safety issue can be covered up by the abortion debate. There's nothing like a moral controversy to hide inconvenient truths. It is also a good way to deny responsibility for what is really an iatrogenic condition, avoiding law suits. In fact, doctors refrain from using the word 'iatrogenic' when describing Asherman's syndrome, yet it is more often than not the case. Their attitude towards abortion is different though. Abortion is a woman's choice, and they reason that if she chooses to have an abortion and her uterus ends up scarred by the D&C, it was the result of her own choice (not really because anyone should be given informed consent, but that is how some people might see it). They may feel it is more important to warn women about the risks of abortions- which she could (and perhaps in their mind 'should') choose not to have- than a miscarriage, which a woman has no control over. Or they may reason that women who abort should be given drugs instead of surgery to reduce the risk of infertility resulting from her own decision. I saw this inconsistent line of thinking in a paper and felt it was offensive. The medical community is doing a big disservice to women when it does not point out that these complications happen to women who never chose to miscarry, or have D&Cs imposed on them for other reasons. It is equally unacceptable for women to develop fertility and/or obstetric complications from a D&C for treating a miscarriage or for other reasons that were not of her own choice. All women need to be protected equally from potential harm.
Whether the present situation is due to ignorance, moral confusion or denial on the part of many doctors about possible complications from D&C and alternative treatments, something needs to be done to change current mentality and awareness of the problem. Already over a century has passed since the link between Asherman's syndrome and D&C was first made (7). In some countries at least, blind surgery continues...and worst of all, possibly due to a warped argument of 'morality'.
References
(Please note that in medical terminology, 'abortion' is often used s a synonym for 'miscarriage' and does not refer to elective termination...which probably fuels myths among people who don't understand this.)
1. Moodliar, S, Bagratee, JS, and Moodley, J. Medical vs. surgical evacuation of first-trimester spontaneous abortion. Int J Gynaecol Obstet 2005;91(1):21-6.
2. Bique, C, Usta, M, Debora, B, Chong, E, Westheimer, E, and Winikoff, B. Comparison of misoprostol and manual vacuum aspiration for the treatment of incomplete abortion. Int J Gynaecol Obstet 2007;98(3):222-6.
3. Weeks, A, Alia, G, Blum, J, Winikoff, B, Ekwaru, P, Durocher, J et al. A randomized trial of misoprostol compared with manual vacuum aspiration for incomplete abortion. Obstet Gynecol 2005;106(3):540-7.
4. Shwekerela, B, Kalumuna, R, Kipingili, R, Mashaka, N, Westheimer, E, Clark, W et al. Misoprostol for treatment of incomplete abortion at the regional hospital level: results from Tanzania. Bjog 2007;114(11):1363-7.
5. Dao, B, Blum, J, Thieba, B, Raghavan, S, Ouedraego, M, Lankoande, J et al. Is misoprostol a safe, effective and acceptable alternative to manual vacuum aspiration for postabortion care? Results from a randomised trial in Burkina Faso, West Africa. Bjog 2007;114(11):1368-75.
6. Goldenberg, M., Schiff, E.' Achiron, R.' Lipitz, S.' Mashiach, S. Managing residual trophoblastic tissue. Hysteroscopy for directing curettage. J Reprod Med. 42(1)26-8.
7.Fritsch, H. Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung Zentralbl Gynaekol 1894;18:1337-1342.
As I mentioned in my last post, one reason for the misconception linking Asherman's syndrome only to abortion is that doctors rarely address the point by clarifying that:
-There are ways to perform abortions without the use of surgery (D&C), therefore safely, so the point is irrelevant, and
-The same surgery as that used for abortions (D&C) is used commonly in gynecology and obstetrics.
In this youtube clip Dr Paul Indman, who is experienced in the treatment of Asherman's syndrome, states that the condition is more often seen in women after a D&C for miscarriage or retained placenta, especially when repeated, than in women who have had a D&C for abortion.
Despite this medically known fact, this and many other myths about Asherman's syndrome continue to linger. Please watch my youtube clip.
Many women who have had Asherman’s syndrome from a D&C, myself included, feel strongly that D&Cs should not be performed, whether they are for miscarriages, diagnostic purposes or for abortion. Yet many doctors-even some Asherman's syndrome experts- are adamant that D&Cs can never be replaced, something which I as a PhD scientist and student of Public Health and Evidence Based Medicine know for a fact is untrue after having read several clinical trials on misoprostol use for miscarriage management (1)(2)(3)(4)(5). In some parts of Europe misoprostol has gained acceptance as a valid alternative to D&C. Perhaps the absence of anti-abortion activists and strong religious influences accounts for the widespread availability of misoprostol and mifepristone in Switzerland and some parts of Europe.
Therefore doctors continue to perform D&C even though it is known that complications can occur, and that there are some good alternatives including drugs for uterine evacuation (eg. miscarriage, retained placenta, abortion) and hysteroscopy for uterine surgery (eg. fibroids, polyps) and in selected cases for miscarriage management (6). Only about 15% of US Gynecologists are trained in office hysteroscopy. The drug misoprostol, for example, is very cheap and there are no surgery related costs including anesthesia or operating room costs. Yet women in developed countries continue to have their reproductive organ-their endometrium-mutilated by the continued use of D&Cs.
Could it be that many doctors see it's in their best interest to stick to D&Cs which are more financially rewarding than prescribing drugs and less skill intensive than hysteroscopy? It may even be convenient that this whole D&C safety issue can be covered up by the abortion debate. There's nothing like a moral controversy to hide inconvenient truths. It is also a good way to deny responsibility for what is really an iatrogenic condition, avoiding law suits. In fact, doctors refrain from using the word 'iatrogenic' when describing Asherman's syndrome, yet it is more often than not the case. Their attitude towards abortion is different though. Abortion is a woman's choice, and they reason that if she chooses to have an abortion and her uterus ends up scarred by the D&C, it was the result of her own choice (not really because anyone should be given informed consent, but that is how some people might see it). They may feel it is more important to warn women about the risks of abortions- which she could (and perhaps in their mind 'should') choose not to have- than a miscarriage, which a woman has no control over. Or they may reason that women who abort should be given drugs instead of surgery to reduce the risk of infertility resulting from her own decision. I saw this inconsistent line of thinking in a paper and felt it was offensive. The medical community is doing a big disservice to women when it does not point out that these complications happen to women who never chose to miscarry, or have D&Cs imposed on them for other reasons. It is equally unacceptable for women to develop fertility and/or obstetric complications from a D&C for treating a miscarriage or for other reasons that were not of her own choice. All women need to be protected equally from potential harm.
Whether the present situation is due to ignorance, moral confusion or denial on the part of many doctors about possible complications from D&C and alternative treatments, something needs to be done to change current mentality and awareness of the problem. Already over a century has passed since the link between Asherman's syndrome and D&C was first made (7). In some countries at least, blind surgery continues...and worst of all, possibly due to a warped argument of 'morality'.
References
(Please note that in medical terminology, 'abortion' is often used s a synonym for 'miscarriage' and does not refer to elective termination...which probably fuels myths among people who don't understand this.)
1. Moodliar, S, Bagratee, JS, and Moodley, J. Medical vs. surgical evacuation of first-trimester spontaneous abortion. Int J Gynaecol Obstet 2005;91(1):21-6.
2. Bique, C, Usta, M, Debora, B, Chong, E, Westheimer, E, and Winikoff, B. Comparison of misoprostol and manual vacuum aspiration for the treatment of incomplete abortion. Int J Gynaecol Obstet 2007;98(3):222-6.
3. Weeks, A, Alia, G, Blum, J, Winikoff, B, Ekwaru, P, Durocher, J et al. A randomized trial of misoprostol compared with manual vacuum aspiration for incomplete abortion. Obstet Gynecol 2005;106(3):540-7.
4. Shwekerela, B, Kalumuna, R, Kipingili, R, Mashaka, N, Westheimer, E, Clark, W et al. Misoprostol for treatment of incomplete abortion at the regional hospital level: results from Tanzania. Bjog 2007;114(11):1363-7.
5. Dao, B, Blum, J, Thieba, B, Raghavan, S, Ouedraego, M, Lankoande, J et al. Is misoprostol a safe, effective and acceptable alternative to manual vacuum aspiration for postabortion care? Results from a randomised trial in Burkina Faso, West Africa. Bjog 2007;114(11):1368-75.
6. Goldenberg, M., Schiff, E.' Achiron, R.' Lipitz, S.' Mashiach, S. Managing residual trophoblastic tissue. Hysteroscopy for directing curettage. J Reprod Med. 42(1)26-8.
7.Fritsch, H. Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung Zentralbl Gynaekol 1894;18:1337-1342.
Sunday, July 5, 2009
Opinion: Abortion debate masks real issues on D&C safety
Unfortunately, I have become all too aware of the distortion of medical facts and findings since being diagnosed with Asherman' syndrome in 2007 following a D&C for incomplete miscarriage (I have never had an abortion). High on the list of misinformation about Asherman's syndrome, a complication of D&C, is that it is caused only by abortion. One can never repeat enough that Asherman's syndrome as well as other complications result from D&C, NOT 'abortion' per se. Abortion is just a 'reason' for performing the D&C, the same way a miscarriage, or retained placenta for example, are. As I explained in the introductory blog, D&C is (unfortunately) used commonly in gynecology and obstetrics to treat everything from fibroids and polyps to miscarriage and postpartum hemorrhage. There is sufficient evidence in the medical literature (and I will provide this in a future post) that the incidences of Asherman's syndrome are roughly the same or even lower following D&C performed for termination, than those following miscarriage and delivery.
It is well known that women who undergo repeated dilation and curettage (or even a single dilation of over 12 mm) are at a high risk of cervical incompetence (cervical insufficiency) which is thought to account for second trimester pregnancy loss in women with a history of Asherman's syndrome (1). This particular complication is not caused by the endometrial damage itself (ie. adhesions or fibrosis of Asherman's syndrome) but as a by-product of the stretching or dilating (as in 'dilation and curettage of D&C) of the cervix during D&C (which caused the Asherman's syndrome) and also during corrective surgery to remove adhesions (hysteroscopic adhesiolysis).
Prolife proponents will often twist medical research findings to benefit their own anti-abortion agenda. Whenever a study shows increased obstetric or fertility complications following D&C, the message blaring from these lobbyists will be that abortion (not the medical technique of dilation and curettage) is the cause. As such, they completely ignore these risks apply equally to women who have a D&C for other causes, such as miscarriage, retained post partum placenta or other indications. By associating the procedure with such a highly contentious topic, all reasonable debate about the medical safety of the medical procedure is overtaken by an emotional moral debate about people's personal opinions regarding a woman's right to choose versus an embryos right to life.
For example, an oral presentation given at the recent 25th annual meeting of ESHRE (European Society of Human Reproduction and Embryology) in Amsterdam (28 June-1 July 2009. Click here to read the original press release on the oral presentation) "Complications early in pregnancy or in previous pregnancies adversely affect existing or subsequent pregnancies" summarized that:
"The researchers found that a history of one or more miscarriages nearly doubled the risk in an ongoing pregnancy of preterm premature rupture of the membrane that surrounds the baby in the womb, and increased the risk of premature or very premature delivery."
and
"Recurrent miscarriages (three or more miscarriages) increased the risk in a subsequent pregnancy of all of these conditions; in addition, it increased the risk of placenta praevia (where the placenta partially or completely blocks the cervix) six-fold and congenital malformations nearly two-fold."
Then there is the logical mention of abortion since the two are linked to D&C:
"If a previous pregnancy had to be terminated for any reason, this increased the risk of premature rupture of the membrane, premature and very premature delivery in subsequent pregnancies."
It seems obvious that the reason for these complications is that D&Cs are often used to treat miscarriages AND for terminations. Hence, women who have been exposed to D&Cs for either miscarriages or abortion would both be at a risk for D&C-related complications.
Yet prolife proponents insist on interpreting medical data as above with a moral view instead of a scientifically rigorous one. This is demonstrated by the scientifically illogical reasoning of Josephine Quintavalle, of the campaign group Comment On Reproductive Ethics, in response to the above findings:
"There's a logic. The body is protecting a healthy baby. By producing an abortion, you destroy that protection and make the cervix - the neck of the womb - more vulnerable.
And if you make the cervix more vulnerable, you are more at risk of a premature baby."
The problem with that explanation is that the cervix is weakened whether or not there is a 'baby' (healthy or not) in the womb because cervical dilation (D&C stands dilation and curettage) stretches the cervix open so that instruments can access the uterus. If the cervix had some sort of 'moral' sensor as Ms Quintavalle seems to believe, D&Cs and dilations for reasons other than abortion should not lead to cervical insufficiency or preterm births. The medical fact however is that the same complications occur after an abortion as after repeated dilation even if there is a dead baby inside (ie. a miscarriage) or the remains of a miscarriage, or polyps, or for any reason a D&C is used, or a cervix is mechanically stretched.
What has been happening for decades is that complications of D&C are being hijacked by those on the prolife side of the abortion debate as 'arguments' against abortion. They also hope it can be used to scare women from terminating pregnancies. This simplistic argument overlooks the fact that there are ways to abort without surgery: mifepristone (RU486) and misoprostol (Cytotec), to name the most popular drugs which can be used instead of D&C. (Note: Not surprisingly, the prolifers in the know about this also disseminate false information about the risks of these drugs to scare women). They are also behind the movement banning these drugs from being carried by most pharmacies or prescribed by private doctors. Unfortunately, this fixation on the rights of embryonic life is at the expense of the thousands, if not millions, of women who are only given the option of D&C for other indications. It seems that to these prolifers, it is more important to prevent abortion than to prevent all women, even those who miscarry or have delivery complications, from being subjected to the risks and complications of D&C including future infertility and/or life-threatening obstetric complications such as placenta accreta. In other words, they consider an embryo to have have more of a right to life than an adult woman. The biggest irony, however, is that these drugs which can replace D&C are often only available in abortion clinics but not to women who miscarry! As a society, we should be asking ourselves why this is so.
Meanwhile, I frequently hear from those on the prochoice side of the abortion debate, denials about the risks associated with abortion probably because they do not want to have this 'inconvenient truth' tarnish women's 'freedom of choice'. Presumably they are also unaware that drugs can replace D&C so the argument is invalid to begin with. What they also fail to realize is that D&Cs are hardly a 'feminist'option. Consider what the procedure is: a doctor inserts sharp and/or an extremely powerful suctioning instrument into a sexual reproductive organ which contains fragile tissue (the endometrium) necessary for implantation and a normal pregnancy and then scrapes at it without even being able to see what they are doing! On top of this, the doctor usually doesn't tell them that complications are not uncommon and that if he makes a mistake and renders them infertile, chances are he will get away with it ($1,000 richer). In my opinion, a woman's right includes the right to be accurately informed about the true risks of a procedure and the right to be given other available options regarding what is done to her body.
So the real issue here-that is, the health and fertility risks of blind surgery (D&C)- is being clouded by the abortion debate. Who benefits from this? Certainly NOT women.
As someone who developed Asherman's syndrome after a D&C for incomplete miscarriage, I feel that the myth that only abortion causes complications should be actively dispelled. Firstly, it stigmatizes all women who have Asherman's syndrome by associating their condition with the highly controversial issue of abortion. It suggests that any woman with Asherman's syndrome is 'responsible' for her situation when in truth she may have done nothing of her choosing to cause it. It may also be one of the reasons that women with Asherman's syndrome often prefer to stay anonymous about it. The second reason it must be dispelled is because it is a distraction from the real issue-the risks of D&C. It hides the fact that in the 21st century, women are being subjected to blind surgery of the reproductive organs, which causes injury (possibly impairing fertility) in up to 31% of cases (2) DESPITE THE EXISTENCE OF SAFE, NON-INVASIVE, EFFECTIVE ALTERNATIVES. The uninformed view that only abortion causes complications will come as a rude shock to women who get these complications from D&Cs (or uterine surgery) for other reasons. But it is too late for them. The third and most important reason it must be debunked in particular is that the misinformation about risks is the reason why D&Cs continue to be performed for all types of reasons and why complications from them continue to occur. Prevention is not being practiced even though use of drugs could significantly reduce the number of D&Cs and subsequent complications.
There is undoubtedly much ignorance in the public arena concerning gynecological procedures and what they are used for unless people have undergone it themselves or have a medical or paramedical background. This explains in part why these false ideas continue to flourish. What is less clear is why the medical community does not step forward to dismiss these so-called arguments. Could this possibly be because D&Cs are one of the most common procedures on women of reproductive age and that admitting that all D&Cs carry a risk would mean this veritable 'industry' of blind surgery (and associated income)? Little experience is needed to perform D&Cs, unlike hysteroscopy, and if drugs such as misoprostol can replace D&Cs, the money will go to the pharmaceutical companies that produce it, instead of the ObGyn, Hospital and Anesthesiologist. Also, could an uneasiness with performing terminations be the reason why medical management is used for abortions but not for miscarriages? In other words, do doctors themselves, or medical bodies feel it is 'unethical' to perform abortions and so prefer to gain as little from it as possible or play a less active role in the procedure than with a D&C?
Surgery- and complications from that surgery-do not discrimminate between what is morally 'right' or 'wrong'- people do. Science cannot answer whether it is ethical to terminate a pregnancy but it can frame the debate by showing that complications from D&C exist, regardless of the moral context in which it is used. For the informed person, the issue should not be 'should abortions must be banned because of possible complications?' but 'should the medical community continue to perform D&Cs on women-for any reason- when these complications exist and alternatives are available?'
References:
(1) Capella-Allouc S, Morsad F, Rongieres-Bertrand C, et al. (1999). "Hysteroscopic treatment of severe Asherman's syndrome and subsequent fertility". Hum Reprod 14 (5): 1230–1233. PMID 10325268
(2) Adoni A, Palti Z, Milwidsky A, Dolberg M. (1982). "The incidence of intrauterine adhesions following spontaneous abortion". Int J Fertil. 27 (2): 117–118.
It is well known that women who undergo repeated dilation and curettage (or even a single dilation of over 12 mm) are at a high risk of cervical incompetence (cervical insufficiency) which is thought to account for second trimester pregnancy loss in women with a history of Asherman's syndrome (1). This particular complication is not caused by the endometrial damage itself (ie. adhesions or fibrosis of Asherman's syndrome) but as a by-product of the stretching or dilating (as in 'dilation and curettage of D&C) of the cervix during D&C (which caused the Asherman's syndrome) and also during corrective surgery to remove adhesions (hysteroscopic adhesiolysis).
Prolife proponents will often twist medical research findings to benefit their own anti-abortion agenda. Whenever a study shows increased obstetric or fertility complications following D&C, the message blaring from these lobbyists will be that abortion (not the medical technique of dilation and curettage) is the cause. As such, they completely ignore these risks apply equally to women who have a D&C for other causes, such as miscarriage, retained post partum placenta or other indications. By associating the procedure with such a highly contentious topic, all reasonable debate about the medical safety of the medical procedure is overtaken by an emotional moral debate about people's personal opinions regarding a woman's right to choose versus an embryos right to life.
For example, an oral presentation given at the recent 25th annual meeting of ESHRE (European Society of Human Reproduction and Embryology) in Amsterdam (28 June-1 July 2009. Click here to read the original press release on the oral presentation) "Complications early in pregnancy or in previous pregnancies adversely affect existing or subsequent pregnancies" summarized that:
"The researchers found that a history of one or more miscarriages nearly doubled the risk in an ongoing pregnancy of preterm premature rupture of the membrane that surrounds the baby in the womb, and increased the risk of premature or very premature delivery."
and
"Recurrent miscarriages (three or more miscarriages) increased the risk in a subsequent pregnancy of all of these conditions; in addition, it increased the risk of placenta praevia (where the placenta partially or completely blocks the cervix) six-fold and congenital malformations nearly two-fold."
Then there is the logical mention of abortion since the two are linked to D&C:
"If a previous pregnancy had to be terminated for any reason, this increased the risk of premature rupture of the membrane, premature and very premature delivery in subsequent pregnancies."
It seems obvious that the reason for these complications is that D&Cs are often used to treat miscarriages AND for terminations. Hence, women who have been exposed to D&Cs for either miscarriages or abortion would both be at a risk for D&C-related complications.
Yet prolife proponents insist on interpreting medical data as above with a moral view instead of a scientifically rigorous one. This is demonstrated by the scientifically illogical reasoning of Josephine Quintavalle, of the campaign group Comment On Reproductive Ethics, in response to the above findings:
"There's a logic. The body is protecting a healthy baby. By producing an abortion, you destroy that protection and make the cervix - the neck of the womb - more vulnerable.
And if you make the cervix more vulnerable, you are more at risk of a premature baby."
The problem with that explanation is that the cervix is weakened whether or not there is a 'baby' (healthy or not) in the womb because cervical dilation (D&C stands dilation and curettage) stretches the cervix open so that instruments can access the uterus. If the cervix had some sort of 'moral' sensor as Ms Quintavalle seems to believe, D&Cs and dilations for reasons other than abortion should not lead to cervical insufficiency or preterm births. The medical fact however is that the same complications occur after an abortion as after repeated dilation even if there is a dead baby inside (ie. a miscarriage) or the remains of a miscarriage, or polyps, or for any reason a D&C is used, or a cervix is mechanically stretched.
What has been happening for decades is that complications of D&C are being hijacked by those on the prolife side of the abortion debate as 'arguments' against abortion. They also hope it can be used to scare women from terminating pregnancies. This simplistic argument overlooks the fact that there are ways to abort without surgery: mifepristone (RU486) and misoprostol (Cytotec), to name the most popular drugs which can be used instead of D&C. (Note: Not surprisingly, the prolifers in the know about this also disseminate false information about the risks of these drugs to scare women). They are also behind the movement banning these drugs from being carried by most pharmacies or prescribed by private doctors. Unfortunately, this fixation on the rights of embryonic life is at the expense of the thousands, if not millions, of women who are only given the option of D&C for other indications. It seems that to these prolifers, it is more important to prevent abortion than to prevent all women, even those who miscarry or have delivery complications, from being subjected to the risks and complications of D&C including future infertility and/or life-threatening obstetric complications such as placenta accreta. In other words, they consider an embryo to have have more of a right to life than an adult woman. The biggest irony, however, is that these drugs which can replace D&C are often only available in abortion clinics but not to women who miscarry! As a society, we should be asking ourselves why this is so.
Meanwhile, I frequently hear from those on the prochoice side of the abortion debate, denials about the risks associated with abortion probably because they do not want to have this 'inconvenient truth' tarnish women's 'freedom of choice'. Presumably they are also unaware that drugs can replace D&C so the argument is invalid to begin with. What they also fail to realize is that D&Cs are hardly a 'feminist'option. Consider what the procedure is: a doctor inserts sharp and/or an extremely powerful suctioning instrument into a sexual reproductive organ which contains fragile tissue (the endometrium) necessary for implantation and a normal pregnancy and then scrapes at it without even being able to see what they are doing! On top of this, the doctor usually doesn't tell them that complications are not uncommon and that if he makes a mistake and renders them infertile, chances are he will get away with it ($1,000 richer). In my opinion, a woman's right includes the right to be accurately informed about the true risks of a procedure and the right to be given other available options regarding what is done to her body.
So the real issue here-that is, the health and fertility risks of blind surgery (D&C)- is being clouded by the abortion debate. Who benefits from this? Certainly NOT women.
As someone who developed Asherman's syndrome after a D&C for incomplete miscarriage, I feel that the myth that only abortion causes complications should be actively dispelled. Firstly, it stigmatizes all women who have Asherman's syndrome by associating their condition with the highly controversial issue of abortion. It suggests that any woman with Asherman's syndrome is 'responsible' for her situation when in truth she may have done nothing of her choosing to cause it. It may also be one of the reasons that women with Asherman's syndrome often prefer to stay anonymous about it. The second reason it must be dispelled is because it is a distraction from the real issue-the risks of D&C. It hides the fact that in the 21st century, women are being subjected to blind surgery of the reproductive organs, which causes injury (possibly impairing fertility) in up to 31% of cases (2) DESPITE THE EXISTENCE OF SAFE, NON-INVASIVE, EFFECTIVE ALTERNATIVES. The uninformed view that only abortion causes complications will come as a rude shock to women who get these complications from D&Cs (or uterine surgery) for other reasons. But it is too late for them. The third and most important reason it must be debunked in particular is that the misinformation about risks is the reason why D&Cs continue to be performed for all types of reasons and why complications from them continue to occur. Prevention is not being practiced even though use of drugs could significantly reduce the number of D&Cs and subsequent complications.
There is undoubtedly much ignorance in the public arena concerning gynecological procedures and what they are used for unless people have undergone it themselves or have a medical or paramedical background. This explains in part why these false ideas continue to flourish. What is less clear is why the medical community does not step forward to dismiss these so-called arguments. Could this possibly be because D&Cs are one of the most common procedures on women of reproductive age and that admitting that all D&Cs carry a risk would mean this veritable 'industry' of blind surgery (and associated income)? Little experience is needed to perform D&Cs, unlike hysteroscopy, and if drugs such as misoprostol can replace D&Cs, the money will go to the pharmaceutical companies that produce it, instead of the ObGyn, Hospital and Anesthesiologist. Also, could an uneasiness with performing terminations be the reason why medical management is used for abortions but not for miscarriages? In other words, do doctors themselves, or medical bodies feel it is 'unethical' to perform abortions and so prefer to gain as little from it as possible or play a less active role in the procedure than with a D&C?
Surgery- and complications from that surgery-do not discrimminate between what is morally 'right' or 'wrong'- people do. Science cannot answer whether it is ethical to terminate a pregnancy but it can frame the debate by showing that complications from D&C exist, regardless of the moral context in which it is used. For the informed person, the issue should not be 'should abortions must be banned because of possible complications?' but 'should the medical community continue to perform D&Cs on women-for any reason- when these complications exist and alternatives are available?'
References:
(1) Capella-Allouc S, Morsad F, Rongieres-Bertrand C, et al. (1999). "Hysteroscopic treatment of severe Asherman's syndrome and subsequent fertility". Hum Reprod 14 (5): 1230–1233. PMID 10325268
(2) Adoni A, Palti Z, Milwidsky A, Dolberg M. (1982). "The incidence of intrauterine adhesions following spontaneous abortion". Int J Fertil. 27 (2): 117–118.
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