A recent article on Asherman’s syndrome (AS) appeared in the UK Daily mirror. It was about Sophie Blake, a TV presenter in the UK, who acquired Asherman’s syndrome as a result of two D&Cs to remove retained placenta after giving birth. It is unfortunate that her situation was not handled differently, as postpartum D&C has been reported to result in Asherman’s syndrome in 25% of cases (1). There are usually alternatives, and in some countries such as Israel, post partum D&C is no longer performed because of AS risks (2).
Toaff and Ballas, 1978
“Puerperal curettage….was discontinued in Israel after publication of Asherman’s observations*”.
*1948!!
Publicity about Asherman’s syndrome is important, and it always helps to have a public figure bring awareness to an overlooked condition. However, according to the article, the moral of the story is to seek early treatment when there is actually no evidence that fertility is more likely to be restored if treatment is sought early. Studies have shown that fertility outcomes are correlated with severity of adhesions (3), however there have been no studies on the effect of length of the condition on fertility. Sometimes damage is too great to be corrected and the uterus will rescar at every attempt to surgically remove adhesions and hormonally stimulate endometrial growth, even when early treatment was commenced. Other times, adhesions are not so severe and treatment after years will result in a live birth. Although treatment by an experienced AS specialist should always be sought, fertility outcome will be dependent most of all on the severity of initial injury (ie. D&C, intrauterine surgery with or without endometritis) which led to the scarring. When too many endometrial cells are removed to allow the endometrium to regenerate, this leads to recurrent adhesions and/or widespread fibrosis. In many cases even some of the underlying myometrium is removed. It is simple, without further progress in treatment strategies, there is nothing that can be done to replenish regenerative tissue that has been removed during curettage or other uterine surgery.
Early treatment does not guarantee success-just as late treatment does not guarantee failure
“Ideally corrective surgery should be performed within six months of the adhesions forming before they get too large”
This suggests that intrauterine adhesions continue to get worse over time, which is not true. Injury results in scarring anywhere in the body, and scarring is not progressive after a certain time point. Adhesions occur when scarring occurs internally and tissues are in direct contact with each other during the healing process. IUA formation is a normal physiological response to trauma-albeit trauma that is usually iatrogenic and should not have occurred in the first place. The consequences of this normal response are pathological because adhesions can lead to infertility, miscarriage and/or obstetric complications when they occur in the uterus. In actuality, IUA formation begins immediately after injury or corrective surgery and is complete by around 6-8 weeks according to Asherman’s syndrome specialists (unfortunately I am unable to find a reference for this, however studies where hysteroscopic followups are performed after D&C mention waiting 6-8 weeks at least). This is even supported in the article:
“I was devastated the scarring had come back so quickly,”
After 8 weeks, IUA do not continue to form/progress. Therefore, someone with stage I AS diagnosed 3 months after surgery will not go on to have stage IV 3 years later, because their adhesions have already fully formed by 8 weeks. There is one study which asserts that women who had early followup compared to late follow up hysteroscopy following adhesiolysis had less severe adhesions, and that early treatment would give a better outcome (4). However, early followup was 2-4 weeks after the initial surgery while late followup was 8-16 months. Thus adhesions may appear to be less ‘severe’ in the early followup group simply because they had not fully formed. The main advantage of early treatment (ie. before 6-8 weeks) is that it makes it easier for the doctor to dissect adhesions and not cause new ones inadvertently. However, in practical terms, it is highly unlikely that women will be diagnosed with AS within 6-8 weeks after a surgery (let alone treated), therefore it is usually applied as a treatment strategy after adhesiolysis instead of a uterine stent (5).
“It makes me seethe because if Asherman’s is caught early it’s totally treatable.”
“It’s treatable in the early stages, but it took two years for me to get a diagnosis.”
It is suggested that had she had surgery sooner, she would have possibly reversed the damage and regained her fertility. This is unlikely. Very severe adhesions tend to recur (3) inspite of surgery or hormone therapy. Early intervention will not make much of a difference because the extent of the initial damage is such that too many regenerative endometrial cells have been removed during the initial trauma.
It has been hypothesized (but not been proven) that the adhesive process can be progressive because adhesions limit uterine muscular activity thereby reducing perfusion of sex steroids to the endometrium which atrophy as the consequence (6). However, endometrial atrophy, which would lead to thin endometrium or fibrosis, is different to IUA. Most current classification systems only take adhesion type and extent into consideration, not fibrosis.
On the other hand, it is possible that someone with moderately severe adhesions which are treatable may develop fibrosis if treatment is not sought for years. Fibrosis would impact on fertility, not by causing IUA, but by limiting blood flow to an area of the uterus.
As one never knows whether their case is severe or not, by all means seek treatment with an AS specialist, but the best prognosis is severity.
Prevalence versus incidence“While the exact number of Asherman’s sufferers is not known, it’s estimated that 5% of D&Cs cause the condition – that’s about 3,000 new cases a year.”
The article confuses the estimated prevalence rate of Asherman’s syndrome (5%) with incidence rate after D&C. The prevalence of AS is 5%, meaning that roughly 1 in 20 women in the general population have AS. This does not however mean that the incidence rate of AS after a D&C is 5%. Incidence is the percentage of women who develop AS from a particular procedure, such as D&C. Studies have reported rates varying between 7.7 and 30% after D&C for miscarriage (7,8,9,10,11), and 25% from D&C for post partum retained placenta 2-4 weeks after delivery (2). The reason the incidence is higher than the prevalence is that not all women will have a miscarriage, and not all women who miscarry will have a missed or incomplete miscarriage or will be treated by D&C. Furthermore, there will be undiagnosed cases of AS (either because the woman does not desire more children or her infertility remains ‘unexplained’), and obviously not every woman in the population will undergo diagnosis for IUA. One should also remember that there are other causes of AS including other intrauterine surgery and genital tuberculosis (12) and these carry different incidence rates too.
It is important to report the correct incidence rate after a procedure such as D&C because this gives women a better idea of risks and helps her to make an informed decision before consenting to the procedure. There are almost always equally effective alternatives to D&C such as drugs or minimally invasive surgery like hysteroscopy which incur no or less damage.
Prevention: more information and accuracy needed
“Doctors are increasingly opting for less-invasive methods including suction or the use of tablets”
It’s unfortunate that the focus of the story was on preventing infertility through early treatment-which is misleading-rather than on promoting alternatives to D&C.
There is one sentence about prevention, and sadly it contains an inaccuracy as well as an omission. Suction D&C has never been proven to prevent AS, let alone reduce the incidence rates of AS:
Chapman and Chapman, 1990: (13)
“It is noteworthy that, of the 11 patients with isthmus stenosis, six of them were attributable to termination of pregnancy, of which all but one had been performed by suction curettage”
Dalton et al, 2006 (14)
“Intrauterine adhesions are a possible complication of office MVA (manual vacuum aspiration), even in the absence of sharp curettage, and should be considered when discussing treatment options for EPF (early pregnancy failure) with patients."
“After 262 office MVAs for first trimester pregnancy losses, we have identified 5 cases of IUAs…”
There is also no guarantee that your doctor will use only suction D&C, as many will use blunt or sharp instruments as well during the same procedure.
The mysterious ‘tablets’ mentioned allude to misoprostol, a prostaglandin E1 analogue which can evacuate the uterus after miscarriage, delivery or during termination, by causing uterine contractions. Referred to as medical management of miscarriage or retained placenta, or medical abortion depending on the situation where it is used, misoprostol is a non-invasive method which has been shown to prevent IUA compared to suction D&C in a clinical trial (7).
Here you can find out more about how misoprostol can prevent AS if you have a miscarriage. It can also prevent recurrence of AS in women who have a miscarriage after having had the condition.
REFERENCES
1. Toaff R, Ballas S (1978). "Traumatic hypomenorrhea-amenorrhea (Asherman's syndrome)". Fertil. Steril. 30 (4): 379–87.
2. Jensen, P.A. and W.B. Stromme, Amenorrhea secondary to puerperal curettage (Asherman's syndrome). Am J Obstet Gynecol, 1972. 113(2): p. 150-7.
3. Valle RF, and Sciarra JJ (1988). "Intrauterine adhesions: Hystreoscopic diagnosis, classification, treatment and reproductive outcome". . Am J Obstet 158 (6Pt1): 1459–1470.
4. Shokeir, T.A., M. Fawzy, and M. Tatongy, The nature of intrauterine adhesions following reproductive hysteroscopic surgery as determined by early and late follow-up hysteroscopy: clinical implications. Arch Gynecol Obstet, 2008. 277(5): p. 423-7.
5. Robinson JK, Colimon LM, Isaacson KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril. 2008;90(2):409-14.
6. March CM. (1995). "Intrauterine adhesions". Obstet Gynecol Clin N Am 22: 98–103.
7. Tam WH, Lau WC, Cheung LP, Yuen PM, Chung TK. (2002). "Intrauterine adhesions after conservative and surgical management of spontaneous abortion". J Am Assoc Gynecol Laparosc. 9 (2): 182–185.
8. Adoni A, Palti Z, Milwidsky A, Dolberg M. (1982). "The incidence of intrauterine adhesions following spontaneous abortion". Int J Fertil. 27 (2): 117–118.
9. Golan, A., et al., Hysteroscopic findings after missed abortion. Fertil Steril, 1992. 58(3): p. 508-10.
10. Romer, T European Journal of Obstetrics & Gynecology and Reproductive Biology
Volume 57, Issue 3, December 1994, Pages 171-173
11. Friedler S, Margalioth EJ, Kafka I, Yaffe H. (1993). "Incidence of postabortion intra-uterine adhesions evaluated by hysteroscopy: a prospective study". Hum Reprod 8 (3): 442–444.
12. Kodaman PH, Arici AA. (2007). "Intra-uterine adhesions and fertility outcome: how to optimize success?". Curr Opin Obstet Gynecol 19 (3): 207–214.
13. K Chapman and R Chapman. Asherman's syndrome: a review of the literature, and a husband and wife's 20-year world-wide experience. J R Soc Med. 1990 September; 83(9): 576–580.
14. Dalton VK, Saunders NA, Harris LH, Williams JA, Lebovic DI (2006). "Intrauterine adhesions after manual vacuum aspiration for early pregnancy failure". Fertil. Steril. 85 (6): 1823.e1–3
Showing posts with label treatment of Asherman's syndrome. Show all posts
Showing posts with label treatment of Asherman's syndrome. Show all posts
Monday, May 3, 2010
Wednesday, April 21, 2010
The DO’s and DON’T's (and maybe’s) of Managing Intrauterine Adhesions.
Based on: AAGL: Practice Report: Practice Guidelines for Management of Intrauterine Synechiae, The Journal of Minimally Invasive Gynecology Vol. 17, No.1 2010.
Practice committee members:
Malcolm Munro MD, FRCS(C), FACOG
Rafaele F.Valle,MD
Jason A. Abbott, PhD,FRANZCOG,MRCOG
Angus J.M. Thompson, MRCOG
Keith B. Isaacson, MD
Adolf Gallinat, MD
Volker R. Jacobs, MD, PhD, MBA
Fred M. Howard MD
Andrew I. Sokol, MD
Linda D. Bradley, MD
Recently, the Practice Committee of the AAGL developed guidelines for the management of intrauterine adhesions (IUA), published in the Journal of Minimally Invasive Gynecology (2010). This is a welcome initiative, and long-awaited, with over one century passing since the first description of Asherman’s syndrome in the literature (1). Although these guidelines were based on studies published in peer-reviewed medical journals, there are limitations and room for more specific guidelines, as the authors themselves acknowledge, due to a lack of comparative studies and rigorous medical evidence from randomized controlled trials (RCTs). For example, studies were conducted using different surgical modalities, surgical tools, adjunctive therapies, and hormone therapy protocols. Many studies are also old and/or conducted retrospectively. One of the difficulties of studying IUA is that it is under diagnosed so that many women may not realize they have it. This results in a small sample size for studies, especially when patient treatment is spread between different centers. Additionally, the skills of the surgeon are important in influencing outcome which makes comparisons between different studies difficult. Consequently, drawing meaningful conclusions on treatment is problematic. To circumvent these shortcomings, the authors classified data based on the highest level of evidence found in the data and graded them according to a system outlined by the US Preventive Services Task Force. In most cases the evidence is based primarily on consensus and expert opinion (Level C). Hopefully trials will be forthcoming which meet today’s strict standards of clinical research, and recommendations which are stronger and more specific will result from them.
The goal of IUA management is to restore the volume and architecture of the uterine cavity and its communication with the fallopian tubes and cervical canal by removing IUA, preventing their recurrence and regenerating deficient endometrial growth.
Below is a summary of the recommendations of the article. My additional comments are in blue font.DIAGNOSISHysteroscopy is the most accurate method for diagnosis of IUA and should be chosen over HSG and SHG (although the latter are reasonable alternatives if hysteroscopy is not available).
(Grade B)
CLASSIFICATION
Although there are several classification systems, none is considered superior over the other, probably reflecting inadequacies in all current systems. (Grade C)
An accurate and universal classification system for IUA is important for enabling the comparison of studies and providing prognostic indicators of fertility outcome. (Grade B)
TREATMENT
DO's:
Only expert hysteroscopists familiar with IUA treatment should attempt to treat extensive or dense adhesions. (Level C)(Surgeons who are inexperienced may inadvertantly cause further irreparable damage).
Direct visualization of the uterus during hysteroscopic lysis of adhesions using a tool for dissection is the treatment of choice for IUA which underlies infertility, recurrent pregnancy loss, pain or other related symptoms. (Level C).
In some women expectant management may be acceptable. (Level C)
(ie. if adhesions are thin and filmy and/or cover a small surface area treatment benefits may not outweigh treatment risks).
Estrogen therapy with or without progestin may reduce reformation of IUAs. (Level B)(Estrogen therapy dose and length will depend on severity. See also Recommendations for Future Research).
MAYBE's:
Gel barriers such as hyaluronic acid and auto-cross-linked hyaluronic acid gel may reduce IUA recurrence follow surgical correction, however there is not enough data on pregnancy outcomes following their use, so should not be used without more rigorous trials. (Level A)
(Potential problems with gel barriers are that they are difficult to keep in place, become less viscous at body temperature, draining out of the uterus. See also Recommendations for Future Research).
Foley catheter or IUD should not be used routinely after corrective surgery without further data from trials supporting their benefit. This is because they may increase the risk for infection. (Level C)
(There have been reports of IUDs puncturing the uterus. Also, some doctors also believe that intrauterine pressure from balloons can hinder endometrial regeneration. However, both the Foley catheter and the Cook stent-which curiously was not mentioned in the article-have been used successfully (2)).
Supporting or refuting the use of prophylactic antibiotics before, during or after surgical adhesiolysis. (Level C)
(However, antibiotic prophylaxis should be used in the case of barriers, as a foreign object inside the uterus increases the risk of infection. See also Recommendations for Future Research).
Medications to improve blood flow to the endometrium should be used only after being supported by rigorous research. (Level C)(These include low-dose aspirin, Coenzyme Q-10, vitamin E, and Sildenafil citrate.ie. Viagra, and even herbal remedies such as raspberry leaf tea).
Prevention of complications (eg. perforation) or improved outcomes with the use of external imaging techniques or laparoscopy, however these techniques may have advantages in case perforation does occur. (Level B)(Another advantage is that laparoscopy allows the surgeon to view the pelvic cavity where there may be endometriosis (3), especially in the more severe cases where laparoscopy is often used).
DON’T's:
There is no evidence to support blind D&C or blind cervical probing in the treatment of IUA (Level C)(The authors state that D&C should not be used because it does not permit accurate diagnosis and classification. The bigger concern should be that blind curettage may cause further and irreversible damage and is the underlying cause of most IUA (4)).
Copper (inflammatory), progestin-releasing (suppress endometrium) and T-shaped IUDs (small surface area) should not be used after adhesiolysis. (Level C)
Laparotomy should be considered as a last resort (eg. when hysteroscopic surgery fails) (Level C)
Electrosurgery/laser: There is some disagreement over which tools are best suited for adhesiolysis. Some surgeons prefer to use microscissors and stress that thermal energy tools offer no advantage over scissor dissection with regards to either speed or hemostasis (2). Furthermore, these modalities (including resectoscope, Nd:YAG laser, monopolar/bipolar electrode) deliver energy that can cause injury to surrounding tissues and therefore some believe it is prudent to avoid them for the treatment of IUA (2). Indeed, electrosurgical tools are normally used for endometrial ablation which burns away endometrium and intentionally induces Asherman’s syndrome in women with excessive bleeding. However, other doctors claim that in experienced hands these tools are safe. Which ever the case, this is an issue which probably needs to be further examined to refute any safety concerns.POSTOPERATIVE ASSESSMENT:Follow-up evaluation of the uterine cavity is recommended after treatment of IUA. (Level B).(This is an important factor in determining outcome as adhesions may reform and further surgery may be needed. If a pregnancy occurs in a uterus with IUA, there is a higher likelihood of infertility, miscarriage and pregnancy complications (5). Patients should undergo either HSG, SHG, or in-office hysteroscopy (with as narrow cervical dilation as possible) in order to verify the uterine cavity is free of adhesions. A mid-cycle scan should also be used to measure the endometrial thickness at ovulation. Ideally this should measure 7-8 mm for implantation to be successful. Some women with corrected IUA have thin endometrium which may require hormone treatment to thicken. If adhesions blocking the ostium are present, natural conception is not possible and IVF will be recommended).
RECOMMENDATIONS FOR FUTURE RESEARCH:
1. Prospective trials on the effect of intraoperative and postoperative antibiotic prophylaxis on surgical and fertility outcome.(I don’t know of doctors who do not use antibiotics during or after operative hysteroscopy. Also, the article states: “…it has been proposed that infection may be a primary cause of IUAs…” Antibiotic prophylaxis is wise for preventing infections whether or not they lead to IUA. However, at this stage, there is actually no evidence to support that most IUAs result from infection, whether frank or subclinical. In fact, there is limited evidence to the contrary (6,7). Also see The subclinical infection myth).2. Prospective trials of adjunctive hormone therapy efficacy with respect to surgical and fertility outcome.(The optimum dosage of estrogen (E2 with or without progestin, P4) and length of treatment have not been studied. Progynova (Estradiol valerate) a synthetic version of a naturally occurring estrogen or Premarin, a combination of around 11 conjugated equine estrogens extracted from pregnant mare urine, are usually used. These compounds have not been compared to each other in trials).
3. Prospective trials of barrier method (IUD, Foley catheter and gel adhesion barriers) efficacy with respect to surgical and fertility outcome.
(Presumably the Cook stent, which is used by some doctors (2), should also be included in trials. Regarding the use of gel adhesion barriers which are potentially the least invasive and risky type of barrier, one questions why there is not more research on their use to prevent IUA from occurring in the first place. If gel barriers are therapeutic for reducing IUA reformation after hysteroscopic adhesiolysis perhaps their use after D&C and other primary intrauterine surgery would reduce the incidence of IUA. There is so far only one study and results show only 10% of women who received Seprafilm after curettage for miscarriage developed IUA vs 50% amongst controls (8)).
4. Stem cells for future treatment: As discussed in a previous blog, some cases are currently not treatable because the extent of damage to the basal endometrium (sometimes curettage even removes part of the underlying myometrium) from which the functional layer regenerates. This leads to persistently thin endometrium or reformation of IUA after corrective surgery and excludes the possibility of carrying a pregnancy. Surrogacy is the only option in such cases. However Dr Chaitanya Nagori and Dr Sonal Panchal of Nagori Institute of Infertility in India claim to have used stem cell technology to thicken the endometrium in women who underwent excessive ‘cleaning’ up of the uterus (ie. a euphemism for D&C), although they do not mention the presence of IUA. The process involved isolating adult stem cells from the bone marrow of the patient, transplanting the purified stem cells into the patient’s uterine cavity under transvaginal sonographic guidance, and stimulating the production of endometrial angiogenic stem cells by administering estrogen before IVF treatment. Using this technique they reportedly were able to increase ‘negligible’ endometrial growth to 6mm three months after the transfer and estrogen therapy. Although they assert that IVF drugs alone did not increase the patient’s endometrial measurement, it remains to be proven whether this effect is due to the post-transplant estrogen treatment or from the stem cell therapy. Nonetheless, the concept of using stem cells for tissue repair in the uterus is intriguing, and possibly the best hope in future for very severe cases of IUA (uterine transplant is another future possibility). This could be more convincing if recurrent IUA was prevented with stem cells following hysteroscopic adhesiolysis. Definitive proof would be obtained if the stem cells and their progeny were biochemically labeled so as to be identifiable from the original tissue. This could be done in animal studies, for example. The great advantage of stem cells is that they have the capacity to differentiate into a range of cells that are necessary to rebuild a normal uterus, from myometrium and endometrium to the blood vessels which supply them with blood and hormones. Furthermore, as the stem cells are derived from the patient’s own bone marrow ie. autologous adult stem cells, there is no risk of either rejection or ethical controversy (as with embryonic stem cells). Unfortunately at this stage there are no published studies on this treatment.
REFERENCES
1. Fritsch H, Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung. Zentralbl Gynaekol 1894; 18:1337-1342.
2. March, CM; Miller, CE. Hysteroscopic lysis of intrauterine adhesions. Ob.Gyn. News 2006; 41(23):36-37. Abstract
3. Palter. SF, High Rates of Endometriosis in Patients With Intrauterine Synechiae (Asherman's Syndrome). Fertility and Sterility 2005; 86 (null):S471-S471. Link
4. Palter S, Spyrou P. Asherman’s syndrome: Etiologic factors, patterns of pregnancy loss, and treatment results. Results from an international registry. Fertility and Sterility 2003; 80(3):36-7. Link
5. March CM. Intrauterine adhesions. Obstet Gynecol Clin N Am 1995;22(3):491-505. Abstract
6. Jensen, P.A. and Stromme, W.B. Amenorrhea secondary to puerperal curettage (Asherman's syndrome). Am J Obstet Gynecol 1972; 113: 150–4.
7. Polishuk, SO Anteby and D Weinstein, Puerperal endometritis and intrauterine adhesions, Int Surg 1975;60:418–420. Abstract
8. Tsapanos VS, Stathopoulou LP, Papathanassopoulou VS, Tzingounis VA. The role of Seprafilm bioresorbable membrane in the prevention and therapy of endometrial synechiae. Biomed Material Res. 2002;63:10-14. Abstract
Related Links:Good news: Grow endometrium by stem cells. (Times of India)
Recommendation Grading:
Level A: Recommendations are based on good and consistent scientific evidence.
Level B: Recommendations are based on limited or incomsistent scientific evidence.
Level C: Recommendations are based primarily on consensus and expert opinion.
Practice committee members:
Malcolm Munro MD, FRCS(C), FACOG
Rafaele F.Valle,MD
Jason A. Abbott, PhD,FRANZCOG,MRCOG
Angus J.M. Thompson, MRCOG
Keith B. Isaacson, MD
Adolf Gallinat, MD
Volker R. Jacobs, MD, PhD, MBA
Fred M. Howard MD
Andrew I. Sokol, MD
Linda D. Bradley, MD
Recently, the Practice Committee of the AAGL developed guidelines for the management of intrauterine adhesions (IUA), published in the Journal of Minimally Invasive Gynecology (2010). This is a welcome initiative, and long-awaited, with over one century passing since the first description of Asherman’s syndrome in the literature (1). Although these guidelines were based on studies published in peer-reviewed medical journals, there are limitations and room for more specific guidelines, as the authors themselves acknowledge, due to a lack of comparative studies and rigorous medical evidence from randomized controlled trials (RCTs). For example, studies were conducted using different surgical modalities, surgical tools, adjunctive therapies, and hormone therapy protocols. Many studies are also old and/or conducted retrospectively. One of the difficulties of studying IUA is that it is under diagnosed so that many women may not realize they have it. This results in a small sample size for studies, especially when patient treatment is spread between different centers. Additionally, the skills of the surgeon are important in influencing outcome which makes comparisons between different studies difficult. Consequently, drawing meaningful conclusions on treatment is problematic. To circumvent these shortcomings, the authors classified data based on the highest level of evidence found in the data and graded them according to a system outlined by the US Preventive Services Task Force. In most cases the evidence is based primarily on consensus and expert opinion (Level C). Hopefully trials will be forthcoming which meet today’s strict standards of clinical research, and recommendations which are stronger and more specific will result from them.
The goal of IUA management is to restore the volume and architecture of the uterine cavity and its communication with the fallopian tubes and cervical canal by removing IUA, preventing their recurrence and regenerating deficient endometrial growth.
Below is a summary of the recommendations of the article. My additional comments are in blue font.DIAGNOSISHysteroscopy is the most accurate method for diagnosis of IUA and should be chosen over HSG and SHG (although the latter are reasonable alternatives if hysteroscopy is not available).
(Grade B)
CLASSIFICATION
Although there are several classification systems, none is considered superior over the other, probably reflecting inadequacies in all current systems. (Grade C)
An accurate and universal classification system for IUA is important for enabling the comparison of studies and providing prognostic indicators of fertility outcome. (Grade B)
TREATMENT
DO's:
Only expert hysteroscopists familiar with IUA treatment should attempt to treat extensive or dense adhesions. (Level C)(Surgeons who are inexperienced may inadvertantly cause further irreparable damage).
Direct visualization of the uterus during hysteroscopic lysis of adhesions using a tool for dissection is the treatment of choice for IUA which underlies infertility, recurrent pregnancy loss, pain or other related symptoms. (Level C).
In some women expectant management may be acceptable. (Level C)
(ie. if adhesions are thin and filmy and/or cover a small surface area treatment benefits may not outweigh treatment risks).
Estrogen therapy with or without progestin may reduce reformation of IUAs. (Level B)(Estrogen therapy dose and length will depend on severity. See also Recommendations for Future Research).
MAYBE's:
Gel barriers such as hyaluronic acid and auto-cross-linked hyaluronic acid gel may reduce IUA recurrence follow surgical correction, however there is not enough data on pregnancy outcomes following their use, so should not be used without more rigorous trials. (Level A)
(Potential problems with gel barriers are that they are difficult to keep in place, become less viscous at body temperature, draining out of the uterus. See also Recommendations for Future Research).
Foley catheter or IUD should not be used routinely after corrective surgery without further data from trials supporting their benefit. This is because they may increase the risk for infection. (Level C)
(There have been reports of IUDs puncturing the uterus. Also, some doctors also believe that intrauterine pressure from balloons can hinder endometrial regeneration. However, both the Foley catheter and the Cook stent-which curiously was not mentioned in the article-have been used successfully (2)).
Supporting or refuting the use of prophylactic antibiotics before, during or after surgical adhesiolysis. (Level C)
(However, antibiotic prophylaxis should be used in the case of barriers, as a foreign object inside the uterus increases the risk of infection. See also Recommendations for Future Research).
Medications to improve blood flow to the endometrium should be used only after being supported by rigorous research. (Level C)(These include low-dose aspirin, Coenzyme Q-10, vitamin E, and Sildenafil citrate.ie. Viagra, and even herbal remedies such as raspberry leaf tea).
Prevention of complications (eg. perforation) or improved outcomes with the use of external imaging techniques or laparoscopy, however these techniques may have advantages in case perforation does occur. (Level B)(Another advantage is that laparoscopy allows the surgeon to view the pelvic cavity where there may be endometriosis (3), especially in the more severe cases where laparoscopy is often used).
DON’T's:
There is no evidence to support blind D&C or blind cervical probing in the treatment of IUA (Level C)(The authors state that D&C should not be used because it does not permit accurate diagnosis and classification. The bigger concern should be that blind curettage may cause further and irreversible damage and is the underlying cause of most IUA (4)).
Copper (inflammatory), progestin-releasing (suppress endometrium) and T-shaped IUDs (small surface area) should not be used after adhesiolysis. (Level C)
Laparotomy should be considered as a last resort (eg. when hysteroscopic surgery fails) (Level C)
Electrosurgery/laser: There is some disagreement over which tools are best suited for adhesiolysis. Some surgeons prefer to use microscissors and stress that thermal energy tools offer no advantage over scissor dissection with regards to either speed or hemostasis (2). Furthermore, these modalities (including resectoscope, Nd:YAG laser, monopolar/bipolar electrode) deliver energy that can cause injury to surrounding tissues and therefore some believe it is prudent to avoid them for the treatment of IUA (2). Indeed, electrosurgical tools are normally used for endometrial ablation which burns away endometrium and intentionally induces Asherman’s syndrome in women with excessive bleeding. However, other doctors claim that in experienced hands these tools are safe. Which ever the case, this is an issue which probably needs to be further examined to refute any safety concerns.POSTOPERATIVE ASSESSMENT:Follow-up evaluation of the uterine cavity is recommended after treatment of IUA. (Level B).(This is an important factor in determining outcome as adhesions may reform and further surgery may be needed. If a pregnancy occurs in a uterus with IUA, there is a higher likelihood of infertility, miscarriage and pregnancy complications (5). Patients should undergo either HSG, SHG, or in-office hysteroscopy (with as narrow cervical dilation as possible) in order to verify the uterine cavity is free of adhesions. A mid-cycle scan should also be used to measure the endometrial thickness at ovulation. Ideally this should measure 7-8 mm for implantation to be successful. Some women with corrected IUA have thin endometrium which may require hormone treatment to thicken. If adhesions blocking the ostium are present, natural conception is not possible and IVF will be recommended).
RECOMMENDATIONS FOR FUTURE RESEARCH:
1. Prospective trials on the effect of intraoperative and postoperative antibiotic prophylaxis on surgical and fertility outcome.(I don’t know of doctors who do not use antibiotics during or after operative hysteroscopy. Also, the article states: “…it has been proposed that infection may be a primary cause of IUAs…” Antibiotic prophylaxis is wise for preventing infections whether or not they lead to IUA. However, at this stage, there is actually no evidence to support that most IUAs result from infection, whether frank or subclinical. In fact, there is limited evidence to the contrary (6,7). Also see The subclinical infection myth).2. Prospective trials of adjunctive hormone therapy efficacy with respect to surgical and fertility outcome.(The optimum dosage of estrogen (E2 with or without progestin, P4) and length of treatment have not been studied. Progynova (Estradiol valerate) a synthetic version of a naturally occurring estrogen or Premarin, a combination of around 11 conjugated equine estrogens extracted from pregnant mare urine, are usually used. These compounds have not been compared to each other in trials).
3. Prospective trials of barrier method (IUD, Foley catheter and gel adhesion barriers) efficacy with respect to surgical and fertility outcome.
(Presumably the Cook stent, which is used by some doctors (2), should also be included in trials. Regarding the use of gel adhesion barriers which are potentially the least invasive and risky type of barrier, one questions why there is not more research on their use to prevent IUA from occurring in the first place. If gel barriers are therapeutic for reducing IUA reformation after hysteroscopic adhesiolysis perhaps their use after D&C and other primary intrauterine surgery would reduce the incidence of IUA. There is so far only one study and results show only 10% of women who received Seprafilm after curettage for miscarriage developed IUA vs 50% amongst controls (8)).
4. Stem cells for future treatment: As discussed in a previous blog, some cases are currently not treatable because the extent of damage to the basal endometrium (sometimes curettage even removes part of the underlying myometrium) from which the functional layer regenerates. This leads to persistently thin endometrium or reformation of IUA after corrective surgery and excludes the possibility of carrying a pregnancy. Surrogacy is the only option in such cases. However Dr Chaitanya Nagori and Dr Sonal Panchal of Nagori Institute of Infertility in India claim to have used stem cell technology to thicken the endometrium in women who underwent excessive ‘cleaning’ up of the uterus (ie. a euphemism for D&C), although they do not mention the presence of IUA. The process involved isolating adult stem cells from the bone marrow of the patient, transplanting the purified stem cells into the patient’s uterine cavity under transvaginal sonographic guidance, and stimulating the production of endometrial angiogenic stem cells by administering estrogen before IVF treatment. Using this technique they reportedly were able to increase ‘negligible’ endometrial growth to 6mm three months after the transfer and estrogen therapy. Although they assert that IVF drugs alone did not increase the patient’s endometrial measurement, it remains to be proven whether this effect is due to the post-transplant estrogen treatment or from the stem cell therapy. Nonetheless, the concept of using stem cells for tissue repair in the uterus is intriguing, and possibly the best hope in future for very severe cases of IUA (uterine transplant is another future possibility). This could be more convincing if recurrent IUA was prevented with stem cells following hysteroscopic adhesiolysis. Definitive proof would be obtained if the stem cells and their progeny were biochemically labeled so as to be identifiable from the original tissue. This could be done in animal studies, for example. The great advantage of stem cells is that they have the capacity to differentiate into a range of cells that are necessary to rebuild a normal uterus, from myometrium and endometrium to the blood vessels which supply them with blood and hormones. Furthermore, as the stem cells are derived from the patient’s own bone marrow ie. autologous adult stem cells, there is no risk of either rejection or ethical controversy (as with embryonic stem cells). Unfortunately at this stage there are no published studies on this treatment.
REFERENCES
1. Fritsch H, Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung. Zentralbl Gynaekol 1894; 18:1337-1342.
2. March, CM; Miller, CE. Hysteroscopic lysis of intrauterine adhesions. Ob.Gyn. News 2006; 41(23):36-37. Abstract
3. Palter. SF, High Rates of Endometriosis in Patients With Intrauterine Synechiae (Asherman's Syndrome). Fertility and Sterility 2005; 86 (null):S471-S471. Link
4. Palter S, Spyrou P. Asherman’s syndrome: Etiologic factors, patterns of pregnancy loss, and treatment results. Results from an international registry. Fertility and Sterility 2003; 80(3):36-7. Link
5. March CM. Intrauterine adhesions. Obstet Gynecol Clin N Am 1995;22(3):491-505. Abstract
6. Jensen, P.A. and Stromme, W.B. Amenorrhea secondary to puerperal curettage (Asherman's syndrome). Am J Obstet Gynecol 1972; 113: 150–4.
7. Polishuk, SO Anteby and D Weinstein, Puerperal endometritis and intrauterine adhesions, Int Surg 1975;60:418–420. Abstract
8. Tsapanos VS, Stathopoulou LP, Papathanassopoulou VS, Tzingounis VA. The role of Seprafilm bioresorbable membrane in the prevention and therapy of endometrial synechiae. Biomed Material Res. 2002;63:10-14. Abstract
Related Links:Good news: Grow endometrium by stem cells. (Times of India)
Recommendation Grading:
Level A: Recommendations are based on good and consistent scientific evidence.
Level B: Recommendations are based on limited or incomsistent scientific evidence.
Level C: Recommendations are based primarily on consensus and expert opinion.
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
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, 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.
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