144
Letters to the Editor—Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 191 (2015) 140–145
Shintaro Makino* Chihiro Hirai Atsuo Itakura Satoru Takeda Juntendo University Faculty of Medicine, Japan Hideki Yoshikawa Hitachi, Ltd., Central Research Laboratory, Medical Systems Research Department, Japan Zisheng Li Hitachi, Ltd., Central Research Laboratory, Intelligent Media Systems Research Department, Japan Ken-ichi Kawabata Hiroki Tanaka Hitachi, Ltd., Central Research Laboratory, Medical Systems Research Department, Japan *Corresponding author. Tel.: +81 338133111 E-mail address: [email protected] (S. Makino).
even of abnormally invasive placentation [1]. This first case of an amniotic fluid embolism following UAE for fibroids, which we report here, raises the question of a possible causal relation. Amniotic fluid embolisms are rare obstetric events. Their incidence ranges from 2.0 to 7.7 per 100,000 deliveries [2,3]. In our case, the clinical presentation and blood samples showing disseminated intravascular coagulation, together with the autopsy results, strongly suggests such an embolism [2]. The pathogenesis of amniotic fluid embolism remains poorly understood. Nevertheless, it likely results from the passage of amniotic fluid into the maternal circulation before or during delivery, by rupture of the uteroplacental barrier [4]. The three possible sites of such rupture are the endocervical veins, the placental implantation site, and any uterine lesion due to trauma [4]. UAE for symptomatic leiomyomas is known to cause abnormal placental development that leads to miscarriages, abnormal placental implantation, and PPH [1]. The mechanism responsible is probably compromised endometrial perfusion and a myometrial defect remaining after the expulsion of the infarcted fibroid [1]. These two phenomena might well also promote the passage of amniotic fluid into the maternal circulation, by weakening the site of placental insertion. To date, only 200 pregnancies have been
30 September 2014 http://dx.doi.org/10.1016/j.ejogrb.2015.04.009
Amniotic fluid embolism after uterine artery embolization for uterine fibroids Dear Editors, We present the case of a 37-year-old Asian woman who died of an amniotic fluid embolism after delivery of her fifth child. Her medical history was remarkable for chronic hepatitis C, diagnosed five years earlier. Uterine artery embolization for uterine fibroids was performed after her fourth delivery. The course of her fifth pregnancy was normal. At 41 weeks and five days of gestation, it was decided to induce labor because of the prolonged (postterm) pregnancy. Prostaglandins were used for this purpose for 24 h, followed by oxytocin and amniotomy. Seven hours after oxytocin administration began the patient reported thoracic pain and itching of the extremities. Her hemodynamic state was normal. Severe fetal heart rate decelerations at 8 h after oxytocin administration led to a cesarean delivery of a 3890-g boy. The cesarean was immediately complicated by a postpartum hemorrhage (PPH). After uterine artery ligation failed to stem the bleeding, a total hysterectomy was performed 1 h after the birth. At that point, blood loss was estimated at 2400 mL. The patient received transfusions of 8 units of packed red blood cells, 9 units of fresh frozen plasma, and clotting factors. Severe hypotension was observed, and blood testing showed disseminated intravascular coagulation. Two hours after birth, cardiac arrest occurred. Despite transfusion, noradrenaline, closed cardiac massage, and countershocks, the patient, died. An autopsy was performed. Microscopic examination showed numerous emboli in both lungs. They were composed of keratin (fetal squamae), amniotic fluid (mucinous material), and hair (Fig. 1A and B). The cause of death was determined to be a massive bilateral amniotic fluid embolism. Uterine artery embolization (UAE) to treat symptomatic uterine fibroids is relatively contraindicated in women wishing to retain their childbearing ability, because of the potentially higher risk of miscarriage, cesarean delivery, postpartum hemorrhage (PPH), and
Fig. 1. (A) Amniotic fluid embolism (mucinous material) (arrow). Lung parenchyma. Hematoxylin–eosin–saffron staining. Original magnification 200. (B) Fetal squames in a vascular lumen (arrow). Lung parenchyma. Hematoxylin–eosin– saffron staining. Original magnification 200.
Letters to the Editor—Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 191 (2015) 140–145
reported to follow UAE [1]. It is therefore quite unlikely that a causal relation between UAE for fibroids and amniotic fluid embolisms will be proved, especially in view of the rarity of the latter. Although our patient had several known risk factors for AFE (age over 35, induction of labor, ethnic minority), we would like to alert physicians that UAE for fibroids may increase the risk of a subsequent amniotic fluid embolism, even if in our case, it could be only an association.
[3] Abenhaim HA, Azoulay L, Kramer MS, Leduc L. Incidence and risk factors of amniotic fluid embolisms: a population-based study on 3 million births in the United States. Am J Obstet Gynecol 2008;199(July (1)):49.e1–e8. [4] Kramer MS, Rouleau J, Liu S, Bartholomew S, Joseph KS. Amniotic fluid embolism: incidence, risk factors, and impact on perinatal outcome. BJOG 2012; 119(June (7)):874–9.
Pauline Jeanneteaua,* Guillaume Legendrea Philippe Descampsa Loı¨c Sentilhesa a Department of Obstetrics and Gynecology, Angers University Hospital, Angers, France
Conflict of interest None. Financial support b
None. References [1] Kitson SJ, Macphail S, Bulmer J. Is pregnancy safe after uterine artery embolisation? BJOG 2012;119(April (5)):519–21. http://dx.doi.org/10.1111/j.14710528.2012.03286.x. [2] Knight M, Tuffnell D, Brocklehurst P, Spark P, Kurinczuk JJ. Incidence and risk factors for amniotic-fluid embolism. Obstet Gynecol 2010;115(May (5)): 910–7.
145
Audrey Rousseaub Department of Pathology, Angers University Hospital, Angers, France
*Corresponding author at: Department of Obstetrics and Gynecology, Angers University Hospital , 4 rue Larrey, 49000 Angers, France. Tel: +33 2 41 35 42 16; Fax: +33 2 41 35 42 54 29 October 2014 http://dx.doi.org/10.1016/j.ejogrb.2015.05.006
Letters to the Editor—Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 191 (2015) 140–145
Shintaro Makino* Chihiro Hirai Atsuo Itakura Satoru Takeda Juntendo University Faculty of Medicine, Japan Hideki Yoshikawa Hitachi, Ltd., Central Research Laboratory, Medical Systems Research Department, Japan Zisheng Li Hitachi, Ltd., Central Research Laboratory, Intelligent Media Systems Research Department, Japan Ken-ichi Kawabata Hiroki Tanaka Hitachi, Ltd., Central Research Laboratory, Medical Systems Research Department, Japan *Corresponding author. Tel.: +81 338133111 E-mail address: [email protected] (S. Makino).
even of abnormally invasive placentation [1]. This first case of an amniotic fluid embolism following UAE for fibroids, which we report here, raises the question of a possible causal relation. Amniotic fluid embolisms are rare obstetric events. Their incidence ranges from 2.0 to 7.7 per 100,000 deliveries [2,3]. In our case, the clinical presentation and blood samples showing disseminated intravascular coagulation, together with the autopsy results, strongly suggests such an embolism [2]. The pathogenesis of amniotic fluid embolism remains poorly understood. Nevertheless, it likely results from the passage of amniotic fluid into the maternal circulation before or during delivery, by rupture of the uteroplacental barrier [4]. The three possible sites of such rupture are the endocervical veins, the placental implantation site, and any uterine lesion due to trauma [4]. UAE for symptomatic leiomyomas is known to cause abnormal placental development that leads to miscarriages, abnormal placental implantation, and PPH [1]. The mechanism responsible is probably compromised endometrial perfusion and a myometrial defect remaining after the expulsion of the infarcted fibroid [1]. These two phenomena might well also promote the passage of amniotic fluid into the maternal circulation, by weakening the site of placental insertion. To date, only 200 pregnancies have been
30 September 2014 http://dx.doi.org/10.1016/j.ejogrb.2015.04.009
Amniotic fluid embolism after uterine artery embolization for uterine fibroids Dear Editors, We present the case of a 37-year-old Asian woman who died of an amniotic fluid embolism after delivery of her fifth child. Her medical history was remarkable for chronic hepatitis C, diagnosed five years earlier. Uterine artery embolization for uterine fibroids was performed after her fourth delivery. The course of her fifth pregnancy was normal. At 41 weeks and five days of gestation, it was decided to induce labor because of the prolonged (postterm) pregnancy. Prostaglandins were used for this purpose for 24 h, followed by oxytocin and amniotomy. Seven hours after oxytocin administration began the patient reported thoracic pain and itching of the extremities. Her hemodynamic state was normal. Severe fetal heart rate decelerations at 8 h after oxytocin administration led to a cesarean delivery of a 3890-g boy. The cesarean was immediately complicated by a postpartum hemorrhage (PPH). After uterine artery ligation failed to stem the bleeding, a total hysterectomy was performed 1 h after the birth. At that point, blood loss was estimated at 2400 mL. The patient received transfusions of 8 units of packed red blood cells, 9 units of fresh frozen plasma, and clotting factors. Severe hypotension was observed, and blood testing showed disseminated intravascular coagulation. Two hours after birth, cardiac arrest occurred. Despite transfusion, noradrenaline, closed cardiac massage, and countershocks, the patient, died. An autopsy was performed. Microscopic examination showed numerous emboli in both lungs. They were composed of keratin (fetal squamae), amniotic fluid (mucinous material), and hair (Fig. 1A and B). The cause of death was determined to be a massive bilateral amniotic fluid embolism. Uterine artery embolization (UAE) to treat symptomatic uterine fibroids is relatively contraindicated in women wishing to retain their childbearing ability, because of the potentially higher risk of miscarriage, cesarean delivery, postpartum hemorrhage (PPH), and
Fig. 1. (A) Amniotic fluid embolism (mucinous material) (arrow). Lung parenchyma. Hematoxylin–eosin–saffron staining. Original magnification 200. (B) Fetal squames in a vascular lumen (arrow). Lung parenchyma. Hematoxylin–eosin– saffron staining. Original magnification 200.
Letters to the Editor—Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 191 (2015) 140–145
reported to follow UAE [1]. It is therefore quite unlikely that a causal relation between UAE for fibroids and amniotic fluid embolisms will be proved, especially in view of the rarity of the latter. Although our patient had several known risk factors for AFE (age over 35, induction of labor, ethnic minority), we would like to alert physicians that UAE for fibroids may increase the risk of a subsequent amniotic fluid embolism, even if in our case, it could be only an association.
[3] Abenhaim HA, Azoulay L, Kramer MS, Leduc L. Incidence and risk factors of amniotic fluid embolisms: a population-based study on 3 million births in the United States. Am J Obstet Gynecol 2008;199(July (1)):49.e1–e8. [4] Kramer MS, Rouleau J, Liu S, Bartholomew S, Joseph KS. Amniotic fluid embolism: incidence, risk factors, and impact on perinatal outcome. BJOG 2012; 119(June (7)):874–9.
Pauline Jeanneteaua,* Guillaume Legendrea Philippe Descampsa Loı¨c Sentilhesa a Department of Obstetrics and Gynecology, Angers University Hospital, Angers, France
Conflict of interest None. Financial support b
None. References [1] Kitson SJ, Macphail S, Bulmer J. Is pregnancy safe after uterine artery embolisation? BJOG 2012;119(April (5)):519–21. http://dx.doi.org/10.1111/j.14710528.2012.03286.x. [2] Knight M, Tuffnell D, Brocklehurst P, Spark P, Kurinczuk JJ. Incidence and risk factors for amniotic-fluid embolism. Obstet Gynecol 2010;115(May (5)): 910–7.
145
Audrey Rousseaub Department of Pathology, Angers University Hospital, Angers, France
*Corresponding author at: Department of Obstetrics and Gynecology, Angers University Hospital , 4 rue Larrey, 49000 Angers, France. Tel: +33 2 41 35 42 16; Fax: +33 2 41 35 42 54 29 October 2014 http://dx.doi.org/10.1016/j.ejogrb.2015.05.006
