FAQs on Asherman’s syndrome

What is Asherman’s syndrome?
Asherman’s syndrome is the mainly iatrogenic condition where scarring in the uterus, usually from instrumentation during uterine surgery, leads to the formation of intrauterine adhesions (IUA) and/or fibrosis (endometrial atrophy). IUA may connect opposing walls in the uterus and/or cervix, sometimes obliterating the entire cavity. Scarring occurs when the basal endometrium is accidentally removed/damaged. The uterus is lined by the endometrium composed of two layers: the functional layer, which is shed each month during menstruation, and the underlying basal layer from which the functional layer regenerates. Beneath the endometrium is a muscle layer, the myometrium. Sometimes even parts of the myometrium are inadvertantly removed during surgery. Scarring may also occur without the formation of adhesions and is known as fibrosis or unstuck Asherman’s syndrome where functional endometrium is replaced by flat scar tissue which does not respond to hormones.

How common is Asherman’s syndrome?
Asherman’s syndrome is thought to be present in 5% of the female population (prevalence). It is often under diagnosed or misdiagnosed. Between 19 and 23.6 % of women who undergo diagnosis for repeated miscarriage or infertility were reported to have the condition (1-4). The incidence of AS following D&C for miscarriage varies between 7-30%, (5-9) and after D&C following delivery is 25% (10). Among women with D&C for RPOC, repeat D&C and D&C for retained placenta the incidence of Asherman’s syndrome was found to be 40% (11).

Who is at a risk for Asherman’s syndrome?
-Women who have undergone any intra uterine surgery/procedures
-Women who are at an increased risk for miscarriages (because standard care for them is unfortunately still D&C despite the existence of alternatives). This can include those with Mullerian malformations (they are also at a risk for the condition from corrective surgery, see Causes, below), women over 35, and women with other known causes of recurrent miscarriage (note: recurrent miscarriage can also be a symptom of Asherman’s syndrome if they are of unknown cause)
-Women who had complications at delivery such as retained placenta or post partum hemorrhaging (PPH).

However, any woman who has ever had a miscarriage or a delivery complication is potentially at risk of acquiring Asherman’s syndrome if these were treated with D&C. A single suction D&C can lead to Asherman’s syndrome.

What are the causes?
-D&C/D&E/MVA also known as ‘surgical evacuation’ or ‘curettage’ for ANY reason is the most common cause (over 90% (12)). These are carried out for the following reasons:
-miscarriage ('silent', 'delayed', 'missed')
-evacuation of hydatiform mole
-termination of pregnancy (TOP) ie. abortion
-retained products of conception (RPOC) also known as 'incomplete miscarriage' which may occur after failed expectant management (wait and watch approach), medical management (misoprostol) or surgical evacuation (D&C). The procedure is referred to as evacuation of retained products of conception, or ERPC.
-retained post partum placenta
-post partum hemorrhaging (PPH)
-diagnostic purposes (eg. endometrial biopsy)
-polypectomy (polyp removal)
-myomectomy (fibroid removal)
Note that there are better alternatives to D&C in all of the above situations (hysteroscopy, misoprostol).
-Any other intrauterine surgery such as:
-hysteroscopic polypectomy*
-hysteroscopic myomectomy* (13)
-hysteroscopic correction of structural abnormalities of the uterus* (Mullerian malformations including septate uterus) (13)
-B lynch suture (for PPH) (14)
- possibly uterine artery ligation or other procedures which reduce blood flow to the uterus (for PPH or fibroids) (15)
-cesarean section (12)
*If lesions are deep, it may be impossible not to injure the basal endometrium even when surgery is performed under direct vision (eg. hysteroscopy).

Infection at the time of surgery can be a contributing factor but is not necessary for the development of Asherman’s syndrome.
Although persistent RPOC should always be removed (preferably with hysteroscopic curettage), there is no evidence that it alone can lead to Asherman’s syndrome.

-Infection in the absence of surgery such as:
-Genital/endometrial tuberculosis* (16) which is caused by particular bacteria
-Shistosomiasis* (17) which is caused by a parasite
-very rarely it has been reported in women with puerperal endometritis or PID with no history of surgery. (18)

*Rare in industrialized countries.

-Other causes:
-douching with a caustic substance (19) (eg. for inducing an abortion-NEVER try this for any reason)
-uterine packing (eg. to stop postpartum bleeding) (19)
-manual removal of placenta (19)
-irradiation (eg. for cancer treatment) (18)

Note that endometrial ablation is a technique used to intentionally induce severe Asherman’s syndrome in women who suffer from excessive bleeding. It should not be performed in women who desire future pregnancy because even if it can be reversed severe complications and birth defects may ensue if pregnancy occurs.

What are the symptoms of Asherman’s syndrome?
Symptoms of Asherman’s syndrome include:
-a reduction in menstrual flow. This need not be total secondary amenorrhea, it can be secondary oligomehorrhea or hypomenorrhea.
-pain (dysmenorrhea) and bloating along with reduced or no bleeding during menstrual interval (due to trapped blood)
-a reduction in the length of the menstrual period. For example, menstruation used to be 5 days but suddenly becomes 2.
- Increased dark blood (reddish brown to black) or no more bright red blood. Dark blood means it is oxidized and indicates that it is not fresh. This may occur because it takes longer for the lining to exit the body due to obliteration from adhesions or because the lining is thinner so there is less of it.

Other signs of Asherman’s syndrome may include consequences of the condition such as:
-infertility, especially ‘of unknown cause’ and secondary infertility (ie. You were able to conceive before but suddenly cannot anymore, especially after a D&C or other intrauterine surgery)
-recurrent miscarriage (see how AS causes infertility) especially if there is no other explanation (eg chromomal abnormality in fetus or one of the parents, immune factors, blood clotting factors etc.).
-endometriosis. The backflow of trapped blood is thought to be a cause of endometriosis.
-invasive placenta (placenta accreta, placenta increta, placenta previa)*
-retained postpartum placenta*
-thin endometrium at mid cycle.
-Repeated implantation failure (RIF) eg. 3 or more failed IVF attempts for no apparent reason (good quality blastocysts retrieved, uncomplicated embryo transfer etc.)
-tubal pregnancy with no medical history of PID or endometriosis (if uterine adhesions interfere with the entrance to the fallopian tubes, the fertilized egg can remain trapped inside the tube).

*These may indicate that the endometrium has been injured, and where there is injury, there may be intrauterine adhesions.

What other conditions can have symptoms similar to Asherman’s syndrome?
Before undergoing hysteroscopy it is advisable to rule out other potential causes of menstrual dysfunction and/or infertility such as thyroid problems, pituitary gland tumours, poly cystic ovarian syndrome (PCOS), premature ovarian failure (POF), menopause, etc. The following tests are useful:
-TSH (thyroid stimulating hormone)
-LH (leutenizing hormone)
-FSH (follicle stimulating hormone)
-AMH (anti mullerian hormone)
-Mid cycle ultrasound to rule out polycystic ovaries or other abnormalities and to confirm ovulation and check endometrial thickness. A thin (<6) and uneven endometrium at ovulation can signal Asherman’s syndrome.

How is Asherman’s syndrome diagnosed?
It is important to obtain an accurate diagnosis. Hysteroscopy is ‘gold standard’ as it allows a direct view inside the uterine cavity with a narrow telescope. Your Asherman’s syndrome specialist should indicate the severity of your condition to provide you with a prognosis and tailor the treatment protocol accordingly. Asherman’s syndrome is classified into grades according to severity, extent and location of intrauterine adhesions. There are several classification systems, none of which is formally endorsed.

Hysterosalpingography (HSG) and sonohysterography (SHG) are indirect methods which rely on X-ray and ultrasound images, respectively, of the uterus and fallopian tubes as they fill with a solution injected into the cervix. These indirect methods should be used for diagnosis only if hysteroscopy is not available. Although these techniques are not as accurate for diagnosis of AS, they provide information on the patency of the fallopian tubes which may be obstructed by adhesions inside the uterus or tubal adhesions from other causes (eg. infections, tubal surgery or endometriosis). If intrauterine adhesions physically block one or both fallopian tube openings (tubal ostium), HSG should be carried out after treatment is completed to ascertain whether communication between the uterus and the tubes has been successfully reestablished.

How is Asherman’s syndrome treated?
Recently, guidelines for the treatment of Asherman’s syndrome have been drawn up by a panel of experts (for details click here). There is still a long way to go in optimizing treatment as scientifically rigorous studies are lacking. Moderate and severe cases should always be treated before conception. Mild adhesions may be treated depending on extent and effect on reproductive function. Risks may not outweigh benefits for few mild adhesions (<15% of the uterine cavity) if they are in the fundus. Hysteroscopic adhesiolysis and estrogen therapy (with or without progesterone ie. Provera, to induce a withdrawal bleed) is the accepted treatment protocol. In more severe cases a physical barrier such as a uterine balloon/catheter, IUD (without inflammatory copper or inhibitive progesterone) or gel (eg. Seprafilm) may be placed in the uterus after adhesiolysis to keep the walls apart during the recovery period. Varying lengths and doses of estrogen (eg. progynova or premarin) are also used to plump up the endometrium, thereby reducing the likelihood of adhesion reformation. According to some specialists, microscissors possibly minimizes the destruction of the endometrium compared to electrosurgery or ND:YAG laser. The latter are used in endometrial ablation to deliberately cause IUA in women who complain of excessive bleeding (20), however other surgeons claim that they can be used safely in experienced hands. The recent compilation of guidelines for managing intrauterine adhesions does not mention risks from electrosurgery or a preference for the type of tools are used to dissect adhesions, however caution should be exercised with surgery using energy sources.

Asherman’s syndrome should NEVER be treated with blind D&C as this may incur further irreparable damage.

Do I need to have a followup after treatment is completed?
It is important to assess treatment success. Moderate and severe adhesions may recur following treatment if there is not enough endometrium in part(s) of the cavity. Mild adhesions do not usually recur. Second look hysteroscopy or HSG are recommended to ensure the uterine cavity is adhesion-free, especially if the original diagnosis was moderate to severe. This increases the chances of conception and reduces the possibility of complications during pregnancy (20). HSG reveals if the tubes are patent (open), if not, IVF may be recommended. In addition, a mid-cycle ultrasound is used to measure if endometrial thickness following hormone therapy is adequate for embryo implantation. Repeat surgery may be necessary especially in more severe cases. If prognosis is poor in the opinion of an Asherman’s syndrome specialist, surrogacy or adoption may be the only options for (further) children.

How successful is treatment of Asherman’s syndrome?
Asherman’s syndrome can be treated, however overall pregnancy rates (ie. including mild to severe cases) after correction are around 60% while live birth rates are around 40%. Success of treatment is dependent on the severity of the injury ie. the grade of Asherman’s syndrome diagnosed as well as how successful treatment was. In one large study, the pregnancy rate in mild cases was 93%, in moderate cases 78% and in severe cases 57%. Live birth rates from these pregnancies were lower: 81% in mild cases, 66% in moderate cases and 32% in severe cases (21).

1. Raziel, A, Arieli, S, Bukovsky, I, Caspi, E, and Golan, A. Investigation of the uterine cavity in recurrent aborters. Fertil Steril 1994;62(5):1080-2.
2. Preutthipan, S and Linasmita, V. Reproductive outcome following hysteroscopic lysis of intrauterine adhesions: a result of 65 cases at Ramathibodi Hospital. J Med Assoc Thai 2000;83(1):42-6.
3. Ventolini, G, Zhang, M, and Gruber, J. Hysteroscopy in the evaluation of patients with recurrent pregnancy loss:
4. Dendrinos, S, Grigoriou, O, Sakkas, EG, Makrakis, E, and Creatsas, G. Hysteroscopy in the evaluation of habitual abortions. Eur J Contracept Reprod Health Care 2008;13(2):198-200.
5. 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.
6. 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.
7. 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.
8. 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.
9. 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.
10. 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.
11. 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.
12.Schenker JG, Margalioth EJ. (1982). "Intra-uterine adhesions: an updated appraisal". Fertility and Sterility 37 (5): 593–610.
13. Taskin O, Sadik S, Onoglu A, Gokdeniz R, Erturan E, Burak F, Wheeler JM. Role of endometrial suppression on the frequency of intrauterine adhesions after resectoscopic surgery. J Am Assoc Gynecol Laparosc. 2000 (3):351-4.
14. Goojha CA, Case A, Pierson R. Development of Asherman syndrome after conservative surgical management of intractable postpartum hemorrhage. Fertil Steril. 2010 [Epub ahead of print]
15. Roman H, Sentilhes L, Cingotti M, Verspyck E, Marpeau L. Uterine devascularization and subsequent major intrauterine synechiae and ovarian failure.Fertil Steril. 2005;83(3):755-7.
16.Netter AP, Musset R, Lambert A Salomon Y (1956). "Traumatic uterine synechiae: a common cause of menstrual insufficiency, sterility, and abortion". Am J Obstet Gynecol. 71 (2): 368–75.
17. Krolikowski A, Janowski K, Larsen JV. (1995). "Asherman syndrome caused by schistosomiasis". Obstet Gynecol. 85 (5Pt2): 898–9
18.Thomson AJ, Abbott JA, Kingston A, Lenart M, Vancaillie TG. Fluoroscopically guided synechiolysis for patients with Asherman's syndrome: menstrual and fertility outcomes. Fertil Steril. 2007 ;87(2):405-10.
19. Robinson, JK, Colimon, LM, and Isaacson, KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril 2008;90(2):409-14.
(note: this is a secondary reference for listed causes)
20. March CM. (1995). "Intrauterine adhesions". Obstet Gynecol Clin N Am 22(3):491-505.
21. 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.