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Published 24 June 2009, doi:10.1136/bmj.b2282
Cite this as: BMJ 2009;338:b2282
J Cheung, foundation year 1 doctor1, R Shaw, consultant obstetrician and gynaecologist1
1 Derby City General Hospital, Derby DE22 3NE
R Shaw robert.shaw{at}nottingham.ac.uk
A 28 year old woman was referred by her general practitioner with secondary amenorrhoea. She had had an uneventful pregnancy with the normal delivery of a baby girl 18 months previously. She was readmitted to hospital shortly after delivery because of postpartum haemorrhage and underwent evacuation of retained products of conception. The patient was taking the progesterone only contraceptive pill after delivery, but treatment was stopped after 10 months because of an absence of any menstruation. Since discontinuing oral contraception, she had not menstruated for a further 9 months. Otherwise, she had no relevant medical history and no family or drug history. Her menstrual cycle was normal before pregnancy and her body mass index was 22.5. Examination showed no evidence of galactorrhoea or abdominal mass. The vagina and cervix were normal on speculum examination. On palpation, the uterus was of normal size and anteverted, with no adnexal masses. These findings were confirmed by transvaginal ultrasound, which also showed that the texture of the myometrium was slightly heterogeneous in places with irregular endometrial thickness (up to 6 mm in isolated pockets). Biochemical investigations showed normal thyroid function and normal serum levels of prolactin. Serial hormone tests over 3 weeks—including serum concentration of luteinising hormone, follicle stimulating hormone, oestradiol, and progesterone—indicated normal cyclical ovarian activity.
Short answers
Long answers
1 Ashermans syndrome
Ashermans syndrome describes the occurrence of intrauterine adhesions. Any insult to the endometrium can predispose to the formation of intrauterine adhesions at opposing surfaces of the uterus, which can partially or completely obliterate the uterus.1 Although Ashermans syndrome is uncommon, the incidence of this disorder has been rising steadily,2 possibly as a result of the increased incidence of elective abortion.3 4 There are several classification systems that can be used to grade the severity of intrauterine adhesions and to predict prognosis (table 1).
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Clinical presentations include secondary amenorrhoea or oligomenorrhoea, recurrent miscarriage, infertility, and, possibly, dysmenorrhoea.12 13 It is important to suspect Ashermans syndrome in women with any of these signs, especially in those who have a history of dilatation and curettage, in order to avoid delays in diagnosis and treatment.
2 Investigations
Pregnancy is the most frequent cause of amenorrhoea in women of childbearing age (whether on oral contraception or not); therefore, pregnancy should be excluded before any further investigations are undertaken.
Ashermans syndrome is diagnosed by hysteroscopy and hysterosalpingography (table 2).
Hysterosalpingography uses contrast media to allow indirect visualisation of endometrial lesions such as filling defects or uterine wall irregularities. In contrast, hysteroscopy enables direct visualisation of the uterine cavity with a hysteroscope and is considered the diagnostic method of choice. This technique confirms the diagnosis and determines the severity of Ashermans syndrome,13 and is associated with a higher accuracy than hysterosalpingography.14 15 16
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The severity of Ashermans syndrome determines the success of treatment. Success rates are measured by the restoration of normal menstruation, subsequent live term deliveries, and reduced miscarriage rates. A normal menstruation pattern is achieved in up to 100% of cases;4 19 24 26 however, adhesiolysis can result in lower pregnancy and live birth rates.19 20 24 Women who become pregnant after treatment are at high risk of obstetric complications, including miscarriage, premature labour, spontaneous uterine rupture, abnormal placentation, severe intrauterine growth retardation, and postpartum haemorrhage.24 27 28 Placenta accreta is the most common complication,29 and delivery by caesarean section followed by hysterectomy is often necessary.24 29 It is, therefore, essential to inform patients about their risk of life threatening complications in pregnancy after treatment for intrauterine adhesions and to monitor and manage their pregnancies closely in hospitals.
Intrauterine adhesions can recur after treatment in patients with Ashermans syndrome. The risk of recurrence seems to correlate with the severity of the intrauterine adhesions before treatment and is possibly associated with an innate predisposition to intrauterine adhesions.6 30 Methods of preventing further adhesions include physical barriers and pharmacological agents.31 Barrier methods work by separating the dissected adjacent uterine surfaces during the initial healing phase, when the risk of adhesion re-formation is highest.31 Techniques include the intrauterine contraceptive device,4 23 32 Foley catheter balloon,4 6 19 32 and amnion graft.33 Pharmacological methods include treatment with oestrogen and progestogen, which stimulate regrowth of the endometrium.26 34 Two new pharmacological agents—hyaluronic acid and SprayGel (Confluent Surgical, Inc, Waltham, MA)—have been developed that act as a gel barrier in the uterine cavity and are then absorbed into the circulatory system for excretion.35 36 Although which preventative methods are most effective is under debate,3 32 37 postoperative prevention of further intrauterine adhesions is key for successful treatment of Ashermans syndrome.
Patient outcome
Following hysteroscopy, adhesiolysis, and fitting of an intrauterine device worn for three months (to prevent recurrent adhesions), this patient returned to normal menstruation. She subsequently conceived within 4 months and had a normal delivery.
Cite this as: BMJ 2009;338:b2282
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed.