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Thursday, April 8, 2010
Complications in post Ashermans syndrome Pregnancies (Part II)
Continued from Part I
Click here for pregnancies in the presence of intrauterine adhesions (synechiae).
Cervical incompetence or insufficiency is when the involuntary muscle of the cervix is structurally weak and unable to sustain the weight of the growing fetus. Effacement (shortening and thinning of the cervical walls) occurs prematurely and in the absence of contractions, resulting in bulging of the amniotic membranes, leading to rupture and premature birth. This often occurs during the second trimester before the fetus is able to survive outside the uterus. Cervical incompetence is associated with AS although it is thought to result not from having had scarring but rather as a consequence of frequent dilations of the cervix during procedures such as D&C and hysteroscopy- which itself is used to correct AS. The less widely and less often the cervix is dilated, the better, as frequent dilations of over 8mm put women at an increased risk of cervical incompetence in subsequent pregnancies. In order to monitor for CI, transvaginal ultrasound measurements of the cervix should be undertaken beginning during second trimester at around 16 weeks. Women cannot sense or predict its occurrence and it is also difficult for Obgyns to predict and prevent even with close monitoring as it may have a very sudden onset. It is thought that the increased rate of second trimester pregnancy loss in women with past AS is due to CI. In one study, 3 of 15 pregnancies (20%) were complicated with second trimester fetal loss (9) probably caused by CI. Cervical incompetence may be managed with bed rest and cervical cerclage (9). Cerclage is a cervical stitch sewn to prevent the cervix from opening and it may be placed vaginally or abdominally. Cerclage is a controversial obstetric procedure and studies are continuing to investigate how effective it is. Therapeutic cerclage is used when the cervix is showing signs that it is dangerously shortened ( under 2cm) or funneling, however it is not always effective at this stage and pregnancy loss may still occur. ‘Prophylactic’ cerclages are usually indicated in women with a past history of CI ie. whom have already experienced CI in a previous pregnancy. Because cerclage itself carries the risk of infection, inflammation, and rupture of membranes, it is not routinely recommended in women with past AS. Instead, monitoring of cervical length and therapeutic cerclage if needed is recommended. Interestingly, a study on women with short cervix during pregnancy (under 1.5 cm measured around 22 weeks of gestation) found that progesterone supplementation reduced spontaneous delivery before 34 weeks compared to placebo (25).
Possibilities for prevention of CI include the reduction/replacement of D&C with drugs or expectant management, the use of smaller instruments necessitating less dilation during hysteroscopic surgery (11), and the use of misoprostol for cervical priming (instead of mechanical force for dilation).
IUGR (intrauterine growth restriction, or fetal growth restriction) refers to a condition where the fetus is smaller than expected for its gestational age (less than the 10th percentile). Newborns with IUGR are termed small for gestational age (SGA). IUGR is caused by a reduction in oxygen and nutrients delivered to the growing fetus due to a lack of adequate blood flow to the placenta. As the endometrium of women with past AS may be damaged, blood flow to the uterus and placenta may be suboptimal, leading to poor placenta perfusion. There are also other causes of IUGR including high blood pressure, diabetes, cigarette smoking, substance abuse, malnutrition, and kidney disease. A lack of oxygen reduces the fetal heart rate and puts the life of the fetus at great risk. IUGR may be early or late-onset, however the earlier the onset, the greater the risks. Risks include premature delivery, stillbirth, and long-term growth problems in children. Diagnosis is made by ultrasound measurements of the fetal size and fetal weight estimation. Doppler flow studies can be used in conjunction with ultrasound to measure the quantity and velocity of blood flow in the fetal brain and umbilical cord. IUGR cannot be predicted or reversed, however its possible presence should be closely monitored in women with a past history of AS. Placenta previa, another potential complication of AS, is also associated with IUGR. Bed rest and increased maternal nutrition may help, as may aspirin therapy to improve blood flow. If IUGR is threatening the well being of the fetus, early delivery may be necessary ie. via C-section. Yasmin and Adeghe (26) report a case of early-onset symmetrical fetal growth restriction in a patient with treated AS. At 20 weeks the fetal measurements corresponded with 18 weeks. A detailed scan at 29 weeks revealed measurements under the 3rd centile with oligohydroamnios and uterine artery flow suggested poor placental perfusion. The baby was delivered via C-section at 29 weeks. The placenta was calcified and partially adherent to the uterine wall. Interestingly, there are no other published studies mentioning IUGR as a complication of AS, although one would not expect it to be a rare consequence. It is possible that some cases of IUGR in women with a history of AS have been attributed to other causes, as there are potentially many confounding risk factors.
Premature or preterm birth is defined as spontaneous labour followed by birth before 37 weeks of gestation. The duration of most pregnancies is around 40 weeks, with babies born between 37 and 42 weeks considered full term. There are several factors which are linked to prematurity which makes it difficult to always know the exact cause. Certain life style factors (smoking, drinking/drugs, stress etc.), and medical conditions (diabetes, hypertension, infections, underweight or obesity etc.) are associated with prematurity. Certain women are also predisposed to premature delivery: those with twin/triplet ie. multiple pregnancies, women with previous premature birth, and women with uterine or cervical abnormalities (congenital or acquired). The overall rate of premature birth in the US is 12.8% (27). However, in women with a past history of AS rates of premature delivery from 17.912-50% have been reported (9, 10, 28, 29, 30) In some cases, but not all, prematurity occurred in conjunction with abnormal placentation (eg. adherant placenta, placenta accrete and/or previa etc). Other studies have linked prematurity to induced surgical (ie. D&C) abortion but not to medical abortion, which supports a correlation between endometrial trauma and premature delivery. Note that most terminations are now carried out medically (however, unfortunately, standard management of missed or incomplete miscarriage continues to be D&C in many countries, more for cultural reasons rather than medical ones).
Premature birth is the leading cause of neonatal mortality and morbidity. Infants born prematurely are at an increased risk for both short and long-term health complications. The earlier the birth, the higher the risk for health complications. Complications are more likely to occur and with more severity in infants born before 32 weeks than after. As medical care continues to improve, infants are surviving at earlier gestational ages, however the current limit for viability is generally around 24 weeks. Potential health complications of ‘premies’ include:
-neurological problems (eg. cerebral palsy, apnea of prematurity, retinopathy of prematurity),
-respiratory problems (eg. respiratory distress syndrome),
-cardiovascular problems (eg. patent ductus arteriosus),
-gastrointestinal/metabolic disorders (eg. rickets, inguinal hernia),
-hematological conditions (eg. jaundice, anemia) and
-infections (eg. sepsis, UTI).
Pregnancy loss due to cervical insufficiency (CI), which occurs without labour and has a different etiology, is not considered premature birth. However, cervical cerclage and progesterone supplementation may be used to prevent/manage both conditions. Progesterone derivatives have been shown to reduce the frequency of premature delivery both in women with previous premature delivery (31) and women with short cervix (25).
The most common factor predisposing to uterine rupture is a uterine scar. This may be caused by D&C, C-section or hysteroscopic surgery (eg. myomectomy, reparation of congenital uterine malformations etc.). Not surprisingly, there have been several reports of uterine rupture among women with a past history of AS (7, 32, 33, 34, 35). In most of these cases, prior uterine perforation occurred during hysteroscopic adhesiolysis , however in rupture has also been reported in women without prior perforation (33). The thinning, weakened and increased fibrosis of the myometrium undoubtedly predispose to rupture of the uterus (2, 36).
This long list of potentially serious complications supports the recommendation that women who have had AS, even after correction, should be carefully monitored by a high risk Obstetrician, and preferably one who is aware of the reported complications in order to optimize the well-being of the pregnancy and the patient. These serious complications also add to a growing list of reasons why prevention of AS from occurring is more compelling than relying solely on treatment of the condition. In all of these complications endometrial damage is the common denominator which has the potential to affect placental attachment, uterine/cervical strength and/or placental perfusion. Finally, it is interesting to note that while complications and sequelae readily attributed to C-sections are being closely monitored and the number of C-sections is being audited by hospitals and organizations such as the WHO with a view to reducing their frequency (37), the same is not being done for D&C. Why not? A reduction in D&C rates would lead to fewer obstetric complications necessitating C-sections. Furthermore, the public health costs of diagnosis, surgical correction, treatment for infertility and obstetric complications resulting from D&C should be reason enough to reduce the reliance on this procedure-not to mention the impact on women's health and well-being.
(numbering continued from Part I)
2.Yu, D, Wong, YM, Cheong, Y, Xia, E, and Li, TC. Asherman syndrome--one
century later. Fertil Steril 2008;89(4):759-79. Abstract
9. 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. Abstract11. Fernandez H, Al Najjar F, Chauvenaud-Lambling et al. (2006). "Fertility after treatment of Asherman's syndrome stage 3 and 4". J Minim Invasive Gynecol 13 (5): 398–402. Link to complete article
25. Fonseca EB, Celik E, Parra M, Singh M, Nicolaides KH; Fetal Medicine Foundation Second Trimester Screening Group. Progesterone and the Risk of Preterm Birth Among Women with a Short Cervix. New England Journal of Medicine, 2007;375:(5)2, 2007; 462-469. Link to pdf
26. Yasmin H, Adeghe JH. Severe early-onset intrauterine growth restriction (IUGR) in a woman with Asherman's syndrome. J Obstet Gynaecol. 2004 ;24(3):312-4. Abstract
27. Martin, J.A., et al. Births: Final Data for 2006. National Vital Statistics Reports, volume 57, number 7, January 7, 2008.
28. Yu D, Factors affecting reproductive outcome of hysteroscopic adhesiolysis for Asherman’s syndrome. Fertil Steril 2007; 89(3):715-22. Abstract.
29. P.McComb, B.Wagner. Simplified therapy for Asherman"s syndrome. Fertility and Sterility; 68(6):1047-1050. Abstract
30. Protopapas A, Shushan A, Magos A. Myometrial scoring: a new technique for the management of severe Asherman's syndrome. 1998;69(5):860-4.Abstract
31. Meis PJ, Klebanoff M, Thom E, Dombrowski MP, Sibai B, Moawad AH, Spong CY, Hauth JC, Miodovnik M, Varner MW, Leveno KJ, Caritis SN, Iams JD, Wapner RJ, Conway D, O'Sullivan MJ, Carpenter M, Mercer B, Ramin SM, Thorp JM, Peaceman AM, Gabbe S; National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Prevention of Recurrent Preterm Delivery by 17 Alpha-Hydroxyprogesterone Caproate. New England Journal of Medicine, 2003;348(24):2379-85. Link to pdf
32. Deaton JL, Maier D, Andreoli J Jr. Spontaneous uterine rupture during pregnancy after treatment of Asherman's syndrome. Am J Obstet Gynecol. 1989;160(5 Pt 1):1053-4. Abstract
33. Shiau CS, Hsieh CC, Chiang CH, Hsieh TT, Chang MY, Chang Gung. Intrapartum spontaneous uterine rupture following uncomplicated resectoscopic treatment of Asherman's syndrome. Med J. 2005 Feb;28(2):123-7. Abstract with link to free article
34. Gürgan T, Yarali H, Urman B, Dagli V, Dogan L. Uterine rupture following hysteroscopic lysis of synechiae due to tuberculosis and uterine perforation. Hum Reprod. 1996;11(2):291-3. Abstract35. Hulka JF.Uterine rupture after treatment of Asherman's syndrome. Am J Obstet Gynecol. 1990 May;162(5):1352-3.
36. Felmus LB, Pedowitz P, Nassberg S. Spontaneous rupture of the apparently normal uterus during pregnancy. A review. Obstet Gynecol Surv 1953;8(2):155-172.
37. Nils Chaillet, Eric Dubé, Marylène Dugas, Diane Francoeur, Johanne Dubé, Sonia Gagnon, Lucie Poitras, Alexandre Dumont. Identifying barriers and facilitators towards implementing guidelines to reduce caesarean section rates in Quebec. Bulletin of the World Health Organisation 2007;85(10):733-820. Complete article