A genetic predisposition: from speculation to opinion to 'fact' without any data (Part II)

In my last blog post I presented the ‘evidence’ (or lack thereof) on which the theory of a genetic/constitutional predisposition for Asherman's syndrome was based. To recap the gist of these observations which pass for proof:

a) some women develop a severe form of IUA after undergoing the ‘same’ traumatic procedures as others who do not acquire AS, and 

b) some women respond more ‘favourably’ to treatment than others who suffer from recurrent adhesions. 

Before deconstructing these observations, the most obvious argument against a genetic basis is the lack of familial clustering of the ‘pathology’. Assuming a polygenic mode of inheritance (as opposed to a Mendelian one) it would be expected that those with a first degree relative with Asherman’s syndrome would have a higher risk of  developing AS than those without a close relative who has the condition. I have yet to read a study of identical twins with Asherman’s syndrome, let alone any study showing the sisters or daughters of patients having a higher risk. In over a century since its first report, there is no evidence of familial clustering to lend support to this theory. Nor is there any evidence that women with scarring defects (eg. keloids) or connective tissue disorders (Marfan’s syndrome, Ehlers-Danlos syndrome) are more prone to AS as one might expect. 

How can trauma be quantified when surgery is blind?

As for the ‘evidence’ above, with regards to a), what proof is there that the women who develop severe IUA actually underwent the exact same trauma as those who did not acquire it? This is a an unfounded statement given differences in doctor’s skill, technique and more importantly, the mis- or under-diagnosis of AS and the blind nature of D&Cs- the number one cause of AS. The problem with bind surgery is that one relies on guess work and instinct to not scrape too deeply. ‘Too deeply’ can be one millimeter too much. How is it possible to detect this difference when not even an ultrasound is used during the procedure? Even with visualization it is not possible to tell where the functional endometrium ends and the basal endometrium begins. However, techniques which utilize visualization for intrauterine surgery (i.e. hysteroscopy) are inherently less risky with regards to instrumental injury because they allow the surgeon to only scrape/dissect/remove parts of the endometrium which need to be treated thus sparing underlying and adjacent tissue from potential injury. Furthermore, each woman has a different anatomy, and different location of retained products of conception. Some have retroverted uteri, others have Mullerian malformations, and the shape, widths and lengths of uteri vary enough between women to be a significant factor with regards to acquiring an injury during a blind procedure. A D&C consists of blindly scraping away the top layer of the endometrium (the functional layer) which can vary in thickness between women but is often not thicker than a few millimeters in most parts. It is simply impossible for a clinician or midwife to know whether they have scraped into the basal endometrium, particularly when no visual guidance is used. 

In summary, the above argument is akin to saying that not all smokers develop lung cancer therefore lung cancer is not caused by cigarettes. Why not theorize that those who develop lung cancer have a genetic predisposition instead? (Note: this comment was intended to highlight the absurdity of believing that cigarette smoking does not cause lung cancer, and hence the absurdity of believing that the fact that all women who have D&Cs do not acquire Asherman's syndrome proves that the condition is not caused by D&Cs but is instead genetic. I later learned that the famous statistician RA Fisher actually theorized half a century ago that people who are genetically predisposed to lung cancer are also genetically predisposed to becoming smokers. Of course this theory was refuted by a study of monozygotic twins versus dizygotic twins who were discordant for cigarette smoking, and it turns out,  lung cancer risk. This example points out how easily theories can be taken seriously just because an expert, or in this case, a genius put it forth, and that experts too have biases which affect their views (he smoked and was a consultant for the tobacco industry!). These theories, will not hold up against evidence from well-designed studies, but until these are done, they impede medical progress).

Recurrence depends on initial severity and treatment methods

With respect to the second part of the argument, the fact that some women respond more ‘favourably’ to treatment than others who suffer from recurrent adhesions can be rationally explained in other ways.

Firstly, it is not surprising that some women need more than one hysteroscopic adhesiolysis surgeries than others, depending on severity. This has been known for many years and reported in the literature. The more damage incurred on the endometrium, the higher the rate of IUA recurrence, and the more surgeries needed for correction, although at some point, damage is too great to allow for endometrial regeneration resulting in recurrent adhesions or fibrotic endometrium.

Another important point to consider is that hysteroscopy was not used for diagnosis or treatment when the observation about treatment outcomes was made. Asherman’s syndrome was still ‘treated’ with blind D&C, the same procedure which is responsible for most cases of AS. This would understandably result in inconsistent outcomes. The absence of accurate diagnosis (and hence classification) in those days also distorted the correlation between severity and outcome. A patient with seemingly severe AS presenting with total amenorrhea may ‘inexplicably’ have had a better outcome after surgery than someone with supposedly less severe AS who had some menstrual flow. We now know that amenorrhea is not always due to severe and widespread adhesions. It can be due to cervical adhesions alone. As the rest of the uterus may be intact in such cases, the reproductive prognosis is better than a patient who has deep adhesions in part of her uterus but no outflow obstruction (and thus has menstrual bleeding, albeit reduced flow). 

With regards to treatment, estrogen therapy was not carried out as part of post surgical therapy in the past. It is generally accepted that estrogen supplementation plays an important role in the prevention of adhesion recurrence following surgery/adhesioloysis by stimulating endometrial regeneration. Thus in the absence of hysteroscopic adhesiolysis, uterine stents and estrogen therapy, more severe cases were less treatable than they are today. 

It is well known that the functional endometrium is regenerated from the underlying basal endometrial layer. As a simple analogy, imagine the lining of the uterus as a lawn. The grass seeds would be the stem cells from which the grass grew with the addition of water (i.e. estrogen). The functional layer would be the grass, and the roots would be the basal endometrium. If someone came along to trim the lawn (i.e. D&C) and accidentally dug out the roots of the grass, the grass would regrow after watering only in the areas where there were either some residual roots, or seeds. Imagining that the seeds are in a slightly deeper layer of soil (for the purpose of this analogy), if the gardener dug very deeply so that even the seeds were removed, no amount of watering would regrow the grass. This could happen in a patch of grass or the whole lawn. In this simple analogy the bald patches would be endometrial sclerosis (unstuck Asherman’s), but adhesions would result if two bald patches came into contact with eachother in the uterus.

More recently, the presence of endometrial stem cells at the myometrial junction was reported. These should be able to transform into endometrial stem cells with the right stimulation. The discovery of the existence of endometrial stem cells could explain why in some cases an apparently denuded endometrium (ie.no visible endometrium) will regenerate while in other cases it will not. Or why some women have recurring adhesions while others do not. This would explain why estrogen therapy after hysteroscopic adhesiolysis can in some cases stimulate the regerenation of endometrium while other cases of IUA are recurrent no matter the dose of estrogen therapy and the length of uterine barrier therapy. Endometrium is what keeps the myometrial layer of the uterus from adhering to opposing walls of the uterus. Once again, it is imposible to observe with the naked eye whether stem cells have been removed by curettage or not which would give rise to ‘paradoxical’ outcomes between patients with the ‘same’ severity of injury. In addition, differences in methods for dissecting adhesions can account for differing outcomes. Mechanical methods for adhesion dissection may also be preferable to methods which utilize thermal energy as the latter may damage adjacent tissue.

A modern perspective on an old problem

Authors need to re-evaluate the validity of assumptions, speculations and theories made in publications written when conditions and standards differed greatly to those of today, taking into consideration medical progress.   Although older papers are still important and interesting to read, they need to be interpreted carefully and in the context of limitations in medical technology and critical thinking, lower standards needed for proof and gaps in scientific understanding at the time they were written. Blind repetition of theories cited from papers that were published decades ago without any questioning is simply archaic, unrigorous and unscientific. If there is a case for a genetic or constitutional basis for AS, data from well designed studies would be more persuasive than citing theories which lack any experimental support of any kind. In what seems to be a recurring theme in AS, absence of evidence may not be evidence of absence, but by today’s standards in medicine only presence of evidence is evidence of presence.

A genetic predisposition: from speculation to opinion to 'fact' without any data (Part I)

The theory that Asherman’s syndrome has a ‘constitutional’ or ‘genetic’ basis has been making rounds for a while. It is time to critical appraise this idea with a view of our understanding of modern medicine.

From where did this theory originate and is there any evidence to support it? From my own thorough research of the literature on Asherman’s syndrome, having read most of the peer reviewed publications dating back to the early 60s, the first mention of the possibility of a hypothetical constitutional factor comes from a publication by Foix et al in 1966 (1). They write: (page 1028): "Besides the above-mentioned presidposing factors, there appears sometimes to be a constitutional element, for some of our patients treated for adhesions after each of several induced abortions, always developed new ones.” Thus they give no supporting references or evidence other than their own subjective observations.

Most reviews or studies mentioning this theory cite a review paper by Schenker and Margoliath in 1982 (2). In it they elaborate on the same ideas, citing a case series by Polishuk and Sadovsky in 1973 (3) as ‘support’. Schenker and Margoliath’s rationale was that:

a) some women develop a severe form of IUA after undergoing the ‘same’ traumatic procedures as others who do not acquire AS, and

b) some women respond more ‘favourably’ to treatment than others who suffer from recurrent adhesions.

They go further and conjecture that 28 women plucked from studies they compiled from the literature ‘may have possessed this predisposing factor, which might have been the reason for the development of IUA after normal delivery or following abortion without subsequent curettage, or even when lacking any attributable trauma.” This is a very bold, if not preposterous assertion to make about patients they have never examined or treated. Needless to say, diagnosis from a distance by third party observers is not a credible source of evidence.

The Polishuk and Sadovsky paper also fails to provide any proof. In fact, Polishuk and Sadovsky themselves never mentioned the idea of a genetic predisposition in their paper or set out to prove such a theory. Instead, they present a case series of 11 patients who have recurrent adhesions, one of three types of adhesions, they explain. Adhesions recurred in all cases after curettage for removal of adhesions or following abortion in a new pregnancy. They suggest that the patients in their study may have had extensive endometrial ‘repair’ i.e. fibrosis, where the endometrium is replaced by connective tissue, which they attempted to treat by removing it. Their understanding of cellular physiology, like their contemporaries, is incorrect but excusable given what was known at the the time it was written. They conclude that their treatment was not encouraging. It should not be surprising to doctors today that blind lysis using curettage is not a successful treatment for IUA or that the removal of fibrotic tissue does not result in endometrial regeneration. I will explain later...(Part II)

Since the speculation by Foix et al and later Schenker and Margoliath, numerous authors have subsequenty made it a habit to include this under etiology of AS, apparently without much thought. The theory also seems to have gained credibility with authors stating it as a fact rather than a hypothesis without any further ‘evidence’. The quality of referencing in many articles about Asherman’s syndrome is lacking. Some authors even cite other reviews which never made the speculation. Clearly, many authors simply copy references from other papers without ever reading the original article to confirm or verify what was actually written.

Back in 1948 Asherman himself seemed to have understood that the underlying cause of IUA are usually trauma from instrumentation (although severe infection, especially endometrial tuberculosis can also cause physical injury to the lining) when he named the condition ‘traumatic amenorrhea’ (4). Unfortunately, the medical community has since been trying to attribute other causes or factors necessary for its development (another example of this is ‘subclinical infection’) perhaps to redeem their dependence on blind curettage as a standard procedure, and also to compensate for their lack of understanding about cellular physiology and insight into the condition. The condition has also been renamed (or misnomered) ‘Asherman’s syndrome’ which distances it from an iatrogenic cause. The word ‘traumatic’ made some doctors feel uncomfortable (5):

(See Discussion Dr John Morton LA California): “The nomenclature also is objectionable. The “traumatic” part of the phrase indicates an iatrogenic lesion, which may not always be justified. (my edit: This is true, but many if not most cases are actually iatrogenic since surgery is involved).

(…)

Dr Jones (closing):It is true that the term “traumatic” is not wholly satisfactory, but it is the term most frequently used in current literature to describe the abnormality under discussion. H W Jones Jr has suggested that the term “postcurettage atresia of the endometrial cavity” is more descriptive, and this may avoid the iatrogenic connotation of the word “traumatic”.

(…)

Thus, there must be an inflammatory factor in the etiology of intrauterine adhesions (my edit: Trauma to the tissue causes inflammation-not to be confused with infection). Parenthetically this too underlines Dr Morton’s objection to the term ‘traumatic’.”

I won’t go into why the above reasoning is incorrect here, my point was to display the obvious discomfort doctors felt in acknowledging an iatrogenic etiology, which probably contributed to its eventual name change as well as the reason why the medical community is so willing to accommodate other unproven causes of Asherman’s syndrome. It’s as if the mentality with regards to Asherman’s syndrome is caught in a time warp where principles of modern medicine such as using modern techniques, well designed studies, objectivie interpretation of data and the requirement of evidence have been temporarily waived.

Although it is natural to consider the possibility that any condition may have a genetic basis, a current understanding of adhesions, the advent of hysteroscopy and techniques to view inside the uterus, a century of observations and plain common sense suggest that such an explanation is not only based on speculation and flawed thinking, and cannot obscure the lack of even the weakest level of research evidence (eg. a case study) exists to support it. Next time I will explain exactly why.

We know now that adhesions (whether intra unterine or intra abdominal) are not a pathological response: they are a normal physiological response to injury adjacent mucosa. Adhesions are only pathological in the sense that they can lead to pathologies such as infertility, bowel obstruction and pain, depending on their location. They are the end result of normal wound healing, of which inflammation (not to be confused with infection) is an inherent process. They occur very commonly in intraabdominal surgery because there is no regenerative layer unlike the uterus which is lined with a regenerative endometrium. Yet no intraabdominal surgeon has attempted to label the condition as ‘genetic’ or ‘constitutional. However, not surprisingly, the endometrium will not regenerate if it is entirely removed, which should not occur during curettage, but which may happen unintentionally due to the blind nature of the procedure. The situation in the uterus then becomes analogous to that in the peritoneum, and adhesion formation ensues.

Lastly, with regards to Polishuk and Sadovsky’s paper, if anything, these cases should highlight the dangers of blind curettage as a method of treating Asherman’s syndrome and miscarriage, the latter particularly in women who have had Asherman’s syndrome. It would appear that endometrial damage leading to AS predisposes to further adhesions probably by facilitating injury, even after previous treatment to restore an open cavity. This is consistent with the observation that even after corrective surgery, women who have a history of Asherman’s syndrome are at an increased risk of specific obstetric complications. It is therefore of no surprise that the common underlying characteristic of these complications is a defective utero-placental interface.

REFERENCES

1.  Foix A, Bruno RO, Davison T, Baltasar L. The pathology of postcurettage intrauterine adhesions. Am J Obst & Gynec.1966; 96(7):1027-33.
2. Schenker JG, Margoliath EJ. Intrauterine adhesions: an updated appraisal. 1982; 37(5):593-610.
3. Polishuk WZ, Sadovsky E. A syndrome of recurrent intrauterine adhesions. Am J Obstet Gynecol 1975 151-8.
4. Asherman J, Amenorrhoea traumatic (Atretica). J Obstet Gynecol 1948; Br Emp 55:23.
5. Jones W. Traumatic Intrauterine adhesion; a report of 8 cases with emphasis on therapy. Am J Obstet & Gynec 1964; 89(3):304-13.

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.

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…

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.