A case of consumption coagulopathy during pregnancy due to leiomyoma degeneration

A case of consumption coagulopathy during pregnancy due to leiomyoma degeneration | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report A case of consumption coagulopathy during pregnancy due to leiomyoma degeneration Asako Kumagai, Jun Takeda, Misato Kawata, Shun Masaoka, Yuka Yamamoto, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4705152/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Consumption coagulopathy during pregnancy is a very rare condition associated with an elevated risk of maternal and neonatal morbidity and mortality. The incidence of pregnancies complicated by leiomyomas is increasing as infertility treatments advance. Degeneration is a complication of leiomyomas during pregnancy. We encountered a leiomyoma degeneration-induced consumption coagulopathy during pregnancy that may have caused fetal periventricular leukomalacia (PVL). Case presentation: a 42-year-old nulliparous woman with two leiomyomas was admitted to the hospital at 17 weeks and 5 days with leiomyoma degeneration and threatened preterm labour. Blood examination revealed severe inflammation, very low fibrinogenlevels, increased D-dimer levels, and prolonged PT-INR. These data suggested consumption coagulopathy; therefore, fresh frozen plasma (FFP) and dried human fibrinogen were administered, and the patient recovered from consumption coagulopathy. She was discharged once the inflammation improved by 19 weeks of gestation. At 41 weeks, the baby was delivered using forceps because of a non-reassuring fetal status (NRFS). The newborn had severe asphyxia, and magnetic resonance imaging (MRI) on day 6 revealed a PVL. In this case, the timing of the coagulopathy consumption was too early for the development of PVL but the duration from delivery was too short to develop PVL. Conclusion: Consumption coagulopathy might cause not only acute placental hypoxia, but also chronic placental hypoxia, which might have caused PVL in the most susceptible interval. consumption coagulopathy degenerated leiomyoma periventricular leukomalacia pregnancy threatened miscarriage Figures Figure 1 Figure 2 Introduction Leiomyomas are benign tumours that arise in smooth muscle layers. It is the most common tumour in a female reproductive organ, its frequency increases up to 70–80% in women by age 50 ( 1 ). Leiomyomas can cause infertility and/or miscarriage; however, owing to the rapid progress and spread of infertility treatment and/or the rise in childbearing age, pregnancies complicated with uterine leiomyomas are increasing. About 10–30% of pregnant women with leiomyoma experience pregnancy complications such as preterm delivery, intrauterine growth restriction, placental abruption, placenta previa, caesarean section, abdominal pain due to degeneration and/or torsion, and postpartum haemorrhage ( 1 ). Generally, the size, number, and position of leiomyomas affect the risk of pregnancy-related complications. In 40–60% of the cases, the size of the leiomyoma is stable during pregnancy ( 2 ) ( 3 ). In the remaining cases, leiomyomas grow during pregnancy, mostly in the first trimester, up to 10 weeks of gestation ( 4 , 5 ). In women with leiomyomas > 5 cm in diameter, pain due to leiomyoma degeneration is the most common symptom during pregnancy ( 6 ). The mechanism of degeneration is thought to be that the rapid growth of leiomyomas results in an insufficient blood supply, which induces tissue ischemia and necrosis. Bradykinin is released from damaged tissues and manifests as pain ( 7 ). In most cases, bed rest, hydration, and painkillers relieve symptoms ( 8 ). Although extremely rare, leiomyoma degeneration can cause enhanced fibrinolytic-type disseminated intravascular coagulopathy (DIC), which requires intensive care. Enhanced fibrinolytic-type DIC due to leiomyoma degeneration during pregnancy has only been reported in two studies ( 9 ) ( 10 ). In both cases, consumption coagulopathy was improved by the surgical removal of the leiomyoma. Here, we report a case of consumption coagulopathy that developed in a pregnant woman with a degenerated uterine leiomyoma. Unlike previous reports, we managed to continue the pregnancy until full term without removing the leiomyoma; however, the newborn developed periventricular leukomalacia (PVL). There are no previous reports regarding the relevance of consumption coagulopathy during pregnancy to PVL, or definite evidence to support that consumption coagulopathy during pregnancy caused the PVL in this case. In this report, we describe details of how consumption coagulopathy occurred and was treated, as well as the evaluation of PVL after birth, and discuss the possible mechanism by which consumption coagulopathy during pregnancy could cause PVL in newborns. Case presentation The patient was 42 years old nulliparous woman. She conceived via in vitro fertilization-embryo transfer. She visited our outpatient clinic at eight weeks of gestation for further prenatal care. During the first visit, we confirmed a 60 mm leiomyoma on the posterior wall of the lower corpus of the uterus. Her pregnancy course was uneventful; however, she developed lower abdominal pain and vaginal bleeding at 17 weeks and 5 days of gestation. Irregular uterine contractions were observed, but cervical length was maintained. Magnetic resonance imaging (MRI) of the uterus revealed two leiomyomas measuring 54 mm in diameter on the anterior wall and 52 mm on the posterior wall of the uterus. The one on the posterior wall was located at the placental attachment site. T2-weighted images showed heterogeneous low and high signal intensities in leiomyomas of the anterior and posterior walls, respectively (Fig. 1 a, b). She was admitted to our hospital because of a suspected threatened miscarriage and degeneration of a posterior wall leiomyoma. Blood tests after admission revealed an elevated white blood cell count 24,400 /µL, C-reactive protein 1.72 mg/dL, and D-dimer 300 mg/dL, as well as reduced platelet (Plt) 136,000 /µL, fibrinogen 62 mg/dL and antithrombin (AT) 73%. The prothrombin time-international normalized ratio (PT-INR) increased to 1.5. Blood pressure (BP), pulse (P), and body temperature (BT) were 122/77 mmHg, 77/min, and 36.2 ℃, respectively. The sequential organ failure assessment (SOFA) score at admission was 2 points (PaO2/FiO2 > 400, total-bilirubin 1.28 mg/dL, Glasgow Coma Scale (GCS) 15, and creatinine 0.63 mg/dL), and 1 point (PaO2/FiO2 > 400, Plt 115,000/µL, total-bilirubin 0.57 mg/dL, BP 106/60 mmHg, GCS 15 and creatinine 0.96 mg/dL) after 24 h. These data suggest an infection with degenerated leiomyoma and consumption coagulopathy without signs of sepsis. The obstetrical disseminated intravascular coagulation (DIC) score was 5 points (cut off value ≧ 8 points) in the obstetrical DIC criteria defined by The Japan Society of Obstetrical, Gynaecological and Neonatal Haematology (Table 1) ( 11 ). DIC score was 6 points in basic type (cut off value ≧ 6 points) and 4 points in infection type (cut off value ≧ 5 points) of DIC criteria defined by The Japanese Society of Thrombosis and Haemostasis (JSTH) ( 12 ). We administered tazobactam/piperacillin (18 g/day) and ampicillin (8 g/day) for leiomyoma infection, and freeze-dried human fibrinogen (3 g) and FFP (4 U) for hypofibrinogenemia. As the pain got worse with the uterine contractions, we administered ritodrine hydrochloride 100 µg/min for two days until the uterine contractions and abdominal pain were relieved. The vital signs revealed that the shock index (SI) was mostly < 1, despite treatment with ritodrine hydrochloride. Her response to antibiotics and blood transfusion was prompt, and she was discharged on day 14. Vaginal and blood cultures at admission were negative. After discharge, there was no recurrence of abdominal pain or cervical shortening during pregnancy. At 41 weeks and 0 days, she was readmitted because of the onset of labour. After the cervix was fully dilated, a non-reassuring fetal status (NRFS) pattern was observed on the cardiotocography; therefore, the baby was delivered using forceps. The baby was a 3428 g male with an Apgar score of 3 and 4 at 1 and 5 min, respectively, and an umbilical artery pH of 7.120. Neonatal resuscitation was initiated immediately, and the respiratory status recovered 6 min and 30 s after birth. Since the neonatal asphyxia was severe (arterial blood pH 6.971 and base deficit − 16 mmol/L within 60 min after birth), hypothermia therapy was administered. Hypothermia therapy was terminated at 48 h, as scheduled. A brain MRI was performed at 6 days of age. Axial T1-weighted, T2-weighted, fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted images of the lateral ventricle showed low, high, high, and high signal intensities, respectively, indicating PVL gliosis (Fig. 2 ). The infant was closely monitored in the neonatal intensive care unit for possible complications of neonatal asphyxia and PVL and was discharged at 24 days of age. The growth and neurological/brain development of the baby were within normal ranges after discharge, and there were no symptoms of cerebral palsy at the age of two. Pathological findings of the placenta revealed syncytial nodules and chorangiosis but no signs of infarction or inflammation of the amniotic membrane or umbilical cord. Discussion Obstetric DIC, which occurs in 0.03 ~ 0.35% of pregnancies, is the leading cause of maternal and neonatal death worldwide ( 13 ). In most cases, obstetric DIC occurs secondary to placental abruption, amniotic fluid embolism, preeclampsia, HELLP syndrome, or postpartum haemorrhage. In these cases, DIC was mostly caused by consumption or dilutional coagulopathy. In our case, blood examination revealed extremely low fibrinogen and high D-dimer levels, indicating enhanced fibrinolytic-type DIC. The DIC score was only positive for the basic criteria defined by the JSTH, but did not meet the criteria for either obstetrical DIC or infectious DIC. Therefore, the consumption coagulopathy in our case was thought to have initiated secondary to leiomyoma degeneration. Consumption coagulopathy due to leiomyoma degeneration is rare, with only five cases reported in the English literature ( 14 ). Consumption coagulopathy induced by degenerated leiomyoma during pregnancy is even rarer, and only two cases have been reported ( 15 ). In all these previous reports, signs of enhanced fibrinolytic-type DIC were observed. All previous cases required surgical removal to resolve the consumption coagulopathy, and the pathological findings of these cases revealed multiple infarctions with thrombi in the leiomyoma ( 15 , 16 ). Kitao et al. suggested that acute degeneration of leiomyomas might damage the endothelial cells of the vessel, which activates the consumption of coagulation factors and platelets; then, thrombin and plasmin might be released into the circulation and finally activate fibrinolysis. In general, enhanced fibrinolytic-type DIC increases the risk of haemorrhagic events; however, none of the leiomyoma degeneration-oriented consumption coagulopathies, including our case, experienced massive haemorrhage. In our case, abnormal vaginal bleeding at admission that was not accompanied by shortening of the cervical length might have been a sign of abnormal coagulation-fibrinolysis conditions. The perinatal outcomes of patients with coagulopathy during pregnancy were poor. Not to speak of obstetrical DIC, in the previous cases of consumption coagulopathy due to leiomyoma degeneration, the patient went through preterm delivery ( 9 ). To our knowledge, this is the first report of successful continuation of pregnancy without obstetric complications. This suggests that prompt evaluation of blood tests, including coagulation factors, in the acute phase of leiomyoma degeneration as well as the immediate use of blood preparations are recommended before the situation worsens, especially when abnormal bleeding is observed. However, in this case, a new complication, PVL, arose as a possible complication of consumption coagulopathy during pregnancy. It can also cause long-term neurodevelopmental disorders. PVL is white matter brain damage that is mainly attributed to hypoxia and inflammation ( 17 ). The preterm brain is susceptible to PVL formation, with the most susceptible interval at 24–32 weeks of gestation, in which cerebral white matter axons are in the rapid growth phase ( 18 ). The lesion becomes visible 1–2 weeks after onset. In our case, because the PVL lesion was already visible on day 6, the timing of PVL formation was estimated to be before the onset of labour. The most probable period for the development of PVL is at 17–18 weeks of gestational age, when severe inflammation and consumption coagulopathy developed. However, these periods were too early for white matter neurodevelopment, and therefore, unlikely for PVL formation. Another possibility is that hypoxia due to leiomyoma degeneration may have persisted long after the recovery from consumption coagulopathy. Regarding the placental pathological findings, syncytial nodules and chorangiosis, which are often observed in the placenta during preeclampsia, maternal diabetes, and fetal growth restriction, indicate an adaptive response to chronic intrauterine hypoxia ( 19 ). Acute intrauterine hypoxia may have occurred during the period of severe inflammation and consumption coagulopathy, and chronic intrauterine hypoxia may have been caused by insufficient blood supply to the placenta due to a large leiomyoma throughout the pregnancy period. Continuous chronic hypoxia following an acute event may be a second cause of PVL formation. We report a case of pregnancy complicated by consumption coagulopathy due to a degenerated leiomyoma. Unlike previous reports, the pregnancy in our case lasted until full term after the patient recovered from consumption coagulopathy by transfusion of blood preparations. However, consumption coagulopathy may have induced chronic intrauterine hypoxia and affected the infant’s brain development. The fact that the continuation of pregnancy was possible even after consumption coagulopathy without removing the degenerated leiomyoma is a new finding; however, the limitation of this study is that we could not confirm a direct relationship between the degenerated leiomyoma and consumption coagulopathy without a pathological study of the leiomyoma. Consumption coagulopathy during pregnancy, not due to obstetrical causes, is rare, but the degeneration of a leiomyoma during pregnancy is a common condition for those who have large leiomyomas. We need to be aware of the possibility that pregnancy complicated by a large leiomyoma could cause severe hypoxia and inflammation, which might be attributed to poor prenatal outcomes and/or permanent neurodevelopmental disorders in newborns. Declarations Ethical approval and consent to participate: The patient provided informed consent for the treatment of coagulopathy, degenerated leiomyoma, and the delivery of forceps. The prognosis of the pregnancy complicated by degenerated leiomyoma and the prognosis of the baby with PVL were shared with the patient and her partner. Consent for publication: The patient provided informed consent for the publication of this case report. Availability of data and materials: The data and images are available on request from the corresponding author, JT. Competing interest: none Funding: none Authors contribution: KA and TJ conceived the study. KA wrote the manuscript with the support of TJ. KA, KM, and MS collected the data. YY and IA supervised the study. All the authors discussed the outcomes of the study and contributed to the manuscript. Acknowledgement: none References Coutinho LM, Assis WA, Spagnuolo-Souza A, Reis FM. Uterine Fibroids and Pregnancy: How Do They Affect Each Other?. Reprod Sci 2022;29(8):2145-2151. https://doi.org/10.1007/s43032-021-00656-6 Aharoni A, Reiter A, Golan D, Paltiely Y, Sharf M. Patterns of growth of uterine leiomyomas during pregnancy. A prospective longitudinal study. Br J Obstet Gynaecol 1988;95(5):510-513. https://doi.org/10.1111/j.1471-0528.1988.tb12807.x Cagan M, Tanacan A, Donmez HG, Fadiloglu E, Unal C, Beksac MS. The Effect of Small Size Uterine Fibroids on Pregnancy Outcomes in High-risk Pregnancies. Rev Bras Ginecol Obstet 2020;42(9):535-539. https://doi.org/10.1055/s-0040-1713913 Sarais V, Cermisoni GC, Schimberni M, et al. Human Chorionic Gonadotrophin as a Possible Mediator of Leiomyoma Growth during Pregnancy: Molecular Mechanisms. Int J Mol Sci 2017;18(9):2014. Published 2017 Sep 20. https://doi.org/10.3390/ijms18092014 Laughlin SK, Baird DD, Savitz DA, Herring AH, Hartmann KE. Prevalence of uterine leiomyomas in the first trimester of pregnancy: an ultrasound-screening study. Obstet Gynecol 2009;113(3):630-635. https://doi.org/10.1097/AOG.0b013e318197bbaf De Carolis S, Fatigante G, Ferrazzani S, et al. Uterine myomectomy in pregnant women. Fetal Diagn Ther 2001;16(2):116-119. https://doi.org/10.1159/000053893 Dray A, Perkins M. Bradykinin and inflammatory pain. Trends Neurosci 1993;16(3):99-104. https://doi.org/10.1016/0166-2236(93)90133-7 Lee HJ, Norwitz ER, Shaw J. Contemporary management of fibroids in pregnancy. Rev Obstet Gynecol. 2010;3(1):20-27. Kitao K, Ohara N, Funakoshi T, et al. Consumptive coagulopathy that developed in a pregnant woman with degenerated uterine leiomyoma: case report. Clin Exp Obstet Gynecol 2005;32(4):250. Hnat RF, Anderson GG, Alonzo DR. Diffuse intravascular coagulation associated with a degenerating myoma during pregnancy. Obstet Gynecol 1967;29(2):207-210. The Japan society of Obstetrical, g.a.N.H. Obstetric DIC score. Available from: http://www.jsognh.jp/dic/ . Asakura H, Takahashi H, Uchiyama T, et al. Proposal for new diagnostic criteria for DIC from the Japanese Society on Thrombosis and Hemostasis. Thromb J 2016;14:42. Published 2016 Sep 28. https://doi.org/10.1186/s12959-016-0117-x Erez O, Othman M, Rabinovich A, Leron E, Gotsch F, Thachil J. DIC in Pregnancy - Pathophysiology, Clinical Characteristics, Diagnostic Scores, and Treatments. J Blood Med 2022;13:21-44. Published 2022 Jan 6. https://doi.org/10.2147/JBM.S273047 Taneichi A, Fujiwara H, Mizoguchi Y, et al. Disseminated intravascular coagulopathy caused by uterine leiomyoma with sarcoma-like findings on magnetic resonance imaging. Case Rep Obstet Gynecol 2014;2014:978743. https://doi.org/10.1155/2014/978743 Kitao K, Ohara N, Funakoshi T, et al. Consumptive coagulopathy that developed in a pregnant woman with degenerated uterine leiomyoma: case report. Clin Exp Obstet Gynecol 2005;32(4):250. Caputo R, Kanbour-Shakir A. Chronic disseminated intravascular coagulation caused by a uterine leiomyoma. A case report. J Reprod Med 1993;38(9):737-740. Abiramalatha T, Bandyopadhyay T, Ramaswamy VV, et al. Risk Factors for Periventricular Leukomalacia in Preterm Infants: A Systematic Review, Meta-analysis, and GRADE-Based Assessment of Certainty of Evidence. Pediatr Neurol 2021;124:51-71. https://doi.org/10.1016/j.pediatrneurol.2021.08.003 Volpe JJ. The encephalopathy of prematurity--brain injury and impaired brain development inextricably intertwined. Semin Pediatr Neurol 2009;16(4):167-178. https://doi.org/10.1016/j.spen.2009.09.005 Sung DK, Baergen RN. Focal Chorangiosis: Does It Have Clinical and Pathologic Significance?. Pediatr Dev Pathol 2019;22(5):406-409. https://doi.org/10.1177/1093526619830866 Table Table 1 is available in the Supplementary Files section Additional Declarations No competing interests reported. Supplementary Files Table1DICscore.xlsx Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4705152","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":339703912,"identity":"f18ae97a-fc11-4d80-802b-219457f71e4c","order_by":0,"name":"Asako Kumagai","email":"","orcid":"","institution":"Juntendo University Faculty of Medicine","correspondingAuthor":false,"prefix":"","firstName":"Asako","middleName":"","lastName":"Kumagai","suffix":""},{"id":339703913,"identity":"ee4c86ae-544b-4fad-a1d9-47a4639e7421","order_by":1,"name":"Jun Takeda","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA+ElEQVRIiWNgGAWjYBACxgYGZgYGNgY5IAMEmCHCEvi0tEG0GAO1gHQRoQWoGqwlsYEBWQs+wDy/+bHBhzK79OYZuccffNxhLcfAfvgBg+UOfA5jM06ccS45t3FGXmLjzDPpxgw8aQYMkmfw+sX4MG8bM1BLjmEzb9thoAtzGBgk2/BpYf98+G9bfTojSMtfkBb+N4S08BgnM7YdTgBrYQRpkSBoS06xYc+544aNPW8MZ/a2pRuzSTwzOIDPL4bNxzdL/CirljdszzH48LPNWo6fP/nhY0k8IWbYgM5gA+LDkg3YFEOAPAYD7NyPeLSMglEwCkbBiAMAgJ9QEHYzRoYAAAAASUVORK5CYII=","orcid":"","institution":"Juntendo University Faculty of Medicine","correspondingAuthor":true,"prefix":"","firstName":"Jun","middleName":"","lastName":"Takeda","suffix":""},{"id":339703914,"identity":"b7915a63-8d71-454b-a422-9a304a08736b","order_by":2,"name":"Misato Kawata","email":"","orcid":"","institution":"Juntendo University Faculty of Medicine","correspondingAuthor":false,"prefix":"","firstName":"Misato","middleName":"","lastName":"Kawata","suffix":""},{"id":339703915,"identity":"74938e82-2de1-4e5a-9557-4564a2839bf4","order_by":3,"name":"Shun Masaoka","email":"","orcid":"","institution":"Juntendo University Faculty of Medicine","correspondingAuthor":false,"prefix":"","firstName":"Shun","middleName":"","lastName":"Masaoka","suffix":""},{"id":339703916,"identity":"1aa6d64c-fb0b-41ca-ae68-7b1c46b24abb","order_by":4,"name":"Yuka Yamamoto","email":"","orcid":"","institution":"Juntendo University Faculty of Medicine","correspondingAuthor":false,"prefix":"","firstName":"Yuka","middleName":"","lastName":"Yamamoto","suffix":""},{"id":339703917,"identity":"fdd4ef69-46bc-4523-930a-4070281beebf","order_by":5,"name":"Astuo Itakura","email":"","orcid":"","institution":"Juntendo University Faculty of Medicine","correspondingAuthor":false,"prefix":"","firstName":"Astuo","middleName":"","lastName":"Itakura","suffix":""}],"badges":[],"createdAt":"2024-07-08 11:24:11","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4705152/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4705152/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":62818898,"identity":"83d603dc-3ff2-4647-9e57-aca94ef21897","added_by":"auto","created_at":"2024-08-19 23:50:54","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":1741009,"visible":true,"origin":"","legend":"\u003cp\u003eSagittal T2 weighted magnetic resonance image of the pelvic cavity\u003c/p\u003e\n\u003cp\u003ea) Heterogeneous low signal intensity in a 54 mm leiomyoma on the anterior wall of the uterus indicated an un-degenerated leiomyoma.\u003c/p\u003e\n\u003cp\u003eb) Heterogeneous high signal intensity in a 52 mm leiomyoma on the posterior wall of the uterus indicated a degenerated leiomyoma. A degenerated leiomyoma is located beneath the placenta.\u003c/p\u003e\n\u003cp\u003eThe white arrows indicate the place of leiomyomas.\u003c/p\u003e","description":"","filename":"DICfig1.png","url":"https://assets-eu.researchsquare.com/files/rs-4705152/v1/54afea5ebdd022fe1b07dc87.png"},{"id":62819633,"identity":"9f0f1f3f-ce86-47a2-ab01-b5e1868fb63d","added_by":"auto","created_at":"2024-08-19 23:58:54","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":2226361,"visible":true,"origin":"","legend":"\u003cp\u003eAxial magnetic resonance image of a newborn on day 6\u003c/p\u003e\n\u003cp\u003eIn the left lobe at the level of the lateral ventricle, a) T1-weighted images showed a low intensity region, b) T2-weighted images showed high intensity region, c) fluid attenuated inversion recovery images showed high intensity region and d) diffusion weighted images showed high intensity region. The white arrows indicate the place of periventricular gliosis, characteristic of periventricular leukomalacia.\u003c/p\u003e","description":"","filename":"DICfig2.png","url":"https://assets-eu.researchsquare.com/files/rs-4705152/v1/f30b9a0c3137428f2d81bd6d.png"},{"id":69994360,"identity":"07c42667-3f72-4f2d-a108-6f2f109ff78c","added_by":"auto","created_at":"2024-11-27 09:54:11","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":4900153,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4705152/v1/ca943c27-7658-4ddd-b292-1f8bcf748653.pdf"},{"id":62818899,"identity":"98d51563-34f4-4763-8285-f92a82c59774","added_by":"auto","created_at":"2024-08-19 23:50:54","extension":"xlsx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":10843,"visible":true,"origin":"","legend":"","description":"","filename":"Table1DICscore.xlsx","url":"https://assets-eu.researchsquare.com/files/rs-4705152/v1/ccb8743736d64ea25d917cf1.xlsx"}],"financialInterests":"No competing interests reported.","formattedTitle":"A case of consumption coagulopathy during pregnancy due to leiomyoma degeneration","fulltext":[{"header":"Introduction","content":"\u003cp\u003eLeiomyomas are benign tumours that arise in smooth muscle layers. It is the most common tumour in a female reproductive organ, its frequency increases up to 70\u0026ndash;80% in women by age 50 (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Leiomyomas can cause infertility and/or miscarriage; however, owing to the rapid progress and spread of infertility treatment and/or the rise in childbearing age, pregnancies complicated with uterine leiomyomas are increasing. About 10\u0026ndash;30% of pregnant women with leiomyoma experience pregnancy complications such as preterm delivery, intrauterine growth restriction, placental abruption, placenta previa, caesarean section, abdominal pain due to degeneration and/or torsion, and postpartum haemorrhage (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Generally, the size, number, and position of leiomyomas affect the risk of pregnancy-related complications. In 40\u0026ndash;60% of the cases, the size of the leiomyoma is stable during pregnancy (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e) (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). In the remaining cases, leiomyomas grow during pregnancy, mostly in the first trimester, up to 10 weeks of gestation (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). In women with leiomyomas\u0026thinsp;\u0026gt;\u0026thinsp;5 cm in diameter, pain due to leiomyoma degeneration is the most common symptom during pregnancy (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). The mechanism of degeneration is thought to be that the rapid growth of leiomyomas results in an insufficient blood supply, which induces tissue ischemia and necrosis. Bradykinin is released from damaged tissues and manifests as pain (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). In most cases, bed rest, hydration, and painkillers relieve symptoms (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Although extremely rare, leiomyoma degeneration can cause enhanced fibrinolytic-type disseminated intravascular coagulopathy (DIC), which requires intensive care. Enhanced fibrinolytic-type DIC due to leiomyoma degeneration during pregnancy has only been reported in two studies (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e) (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). In both cases, consumption coagulopathy was improved by the surgical removal of the leiomyoma. Here, we report a case of consumption coagulopathy that developed in a pregnant woman with a degenerated uterine leiomyoma. Unlike previous reports, we managed to continue the pregnancy until full term without removing the leiomyoma; however, the newborn developed periventricular leukomalacia (PVL). There are no previous reports regarding the relevance of consumption coagulopathy during pregnancy to PVL, or definite evidence to support that consumption coagulopathy during pregnancy caused the PVL in this case. In this report, we describe details of how consumption coagulopathy occurred and was treated, as well as the evaluation of PVL after birth, and discuss the possible mechanism by which consumption coagulopathy during pregnancy could cause PVL in newborns.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eThe patient was 42 years old nulliparous woman. She conceived via in vitro fertilization-embryo transfer. She visited our outpatient clinic at eight weeks of gestation for further prenatal care. During the first visit, we confirmed a 60 mm leiomyoma on the posterior wall of the lower corpus of the uterus. Her pregnancy course was uneventful; however, she developed lower abdominal pain and vaginal bleeding at 17 weeks and 5 days of gestation. Irregular uterine contractions were observed, but cervical length was maintained. Magnetic resonance imaging (MRI) of the uterus revealed two leiomyomas measuring 54 mm in diameter on the anterior wall and 52 mm on the posterior wall of the uterus. The one on the posterior wall was located at the placental attachment site. T2-weighted images showed heterogeneous low and high signal intensities in leiomyomas of the anterior and posterior walls, respectively (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003ea, b). She was admitted to our hospital because of a suspected threatened miscarriage and degeneration of a posterior wall leiomyoma. Blood tests after admission revealed an elevated white blood cell count 24,400 /\u0026micro;L, C-reactive protein 1.72 mg/dL, and D-dimer 300 mg/dL, as well as reduced platelet (Plt) 136,000 /\u0026micro;L, fibrinogen 62 mg/dL and antithrombin (AT) 73%. The prothrombin time-international normalized ratio (PT-INR) increased to 1.5. Blood pressure (BP), pulse (P), and body temperature (BT) were 122/77 mmHg, 77/min, and 36.2 ℃, respectively. The sequential organ failure assessment (SOFA) score at admission was 2 points (PaO2/FiO2\u0026thinsp;\u0026gt;\u0026thinsp;400, total-bilirubin 1.28 mg/dL, Glasgow Coma Scale (GCS) 15, and creatinine 0.63 mg/dL), and 1 point (PaO2/FiO2\u0026thinsp;\u0026gt;\u0026thinsp;400, Plt 115,000/\u0026micro;L, total-bilirubin 0.57 mg/dL, BP 106/60 mmHg, GCS 15 and creatinine 0.96 mg/dL) after 24 h. These data suggest an infection with degenerated leiomyoma and consumption coagulopathy without signs of sepsis. The obstetrical disseminated intravascular coagulation (DIC) score was 5 points (cut off value\u0026thinsp;≧\u0026thinsp;8 points) in the obstetrical DIC criteria defined by The Japan Society of Obstetrical, Gynaecological and Neonatal Haematology (Table\u0026nbsp;1) (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). DIC score was 6 points in basic type (cut off value\u0026thinsp;≧\u0026thinsp;6 points) and 4 points in infection type (cut off value\u0026thinsp;≧\u0026thinsp;5 points) of DIC criteria defined by The Japanese Society of Thrombosis and Haemostasis (JSTH) (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e). We administered tazobactam/piperacillin (18 g/day) and ampicillin (8 g/day) for leiomyoma infection, and freeze-dried human fibrinogen (3 g) and FFP (4 U) for hypofibrinogenemia. As the pain got worse with the uterine contractions, we administered ritodrine hydrochloride 100 \u0026micro;g/min for two days until the uterine contractions and abdominal pain were relieved. The vital signs revealed that the shock index (SI) was mostly\u0026thinsp;\u0026lt;\u0026thinsp;1, despite treatment with ritodrine hydrochloride. Her response to antibiotics and blood transfusion was prompt, and she was discharged on day 14. Vaginal and blood cultures at admission were negative. After discharge, there was no recurrence of abdominal pain or cervical shortening during pregnancy.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eAt 41 weeks and 0 days, she was readmitted because of the onset of labour. After the cervix was fully dilated, a non-reassuring fetal status (NRFS) pattern was observed on the cardiotocography; therefore, the baby was delivered using forceps. The baby was a 3428 g male with an Apgar score of 3 and 4 at 1 and 5 min, respectively, and an umbilical artery pH of 7.120. Neonatal resuscitation was initiated immediately, and the respiratory status recovered 6 min and 30 s after birth. Since the neonatal asphyxia was severe (arterial blood pH 6.971 and base deficit \u0026minus;\u0026thinsp;16 mmol/L within 60 min after birth), hypothermia therapy was administered. Hypothermia therapy was terminated at 48 h, as scheduled. A brain MRI was performed at 6 days of age. Axial T1-weighted, T2-weighted, fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted images of the lateral ventricle showed low, high, high, and high signal intensities, respectively, indicating PVL gliosis (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The infant was closely monitored in the neonatal intensive care unit for possible complications of neonatal asphyxia and PVL and was discharged at 24 days of age. The growth and neurological/brain development of the baby were within normal ranges after discharge, and there were no symptoms of cerebral palsy at the age of two. Pathological findings of the placenta revealed syncytial nodules and chorangiosis but no signs of infarction or inflammation of the amniotic membrane or umbilical cord.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eObstetric DIC, which occurs in 0.03\u0026thinsp;~\u0026thinsp;0.35% of pregnancies, is the leading cause of maternal and neonatal death worldwide (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). In most cases, obstetric DIC occurs secondary to placental abruption, amniotic fluid embolism, preeclampsia, HELLP syndrome, or postpartum haemorrhage. In these cases, DIC was mostly caused by consumption or dilutional coagulopathy. In our case, blood examination revealed extremely low fibrinogen and high D-dimer levels, indicating enhanced fibrinolytic-type DIC. The DIC score was only positive for the basic criteria defined by the JSTH, but did not meet the criteria for either obstetrical DIC or infectious DIC. Therefore, the consumption coagulopathy in our case was thought to have initiated secondary to leiomyoma degeneration. Consumption coagulopathy due to leiomyoma degeneration is rare, with only five cases reported in the English literature (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Consumption coagulopathy induced by degenerated leiomyoma during pregnancy is even rarer, and only two cases have been reported (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). In all these previous reports, signs of enhanced fibrinolytic-type DIC were observed. All previous cases required surgical removal to resolve the consumption coagulopathy, and the pathological findings of these cases revealed multiple infarctions with thrombi in the leiomyoma (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). Kitao et al. suggested that acute degeneration of leiomyomas might damage the endothelial cells of the vessel, which activates the consumption of coagulation factors and platelets; then, thrombin and plasmin might be released into the circulation and finally activate fibrinolysis. In general, enhanced fibrinolytic-type DIC increases the risk of haemorrhagic events; however, none of the leiomyoma degeneration-oriented consumption coagulopathies, including our case, experienced massive haemorrhage. In our case, abnormal vaginal bleeding at admission that was not accompanied by shortening of the cervical length might have been a sign of abnormal coagulation-fibrinolysis conditions.\u003c/p\u003e \u003cp\u003eThe perinatal outcomes of patients with coagulopathy during pregnancy were poor. Not to speak of obstetrical DIC, in the previous cases of consumption coagulopathy due to leiomyoma degeneration, the patient went through preterm delivery (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). To our knowledge, this is the first report of successful continuation of pregnancy without obstetric complications. This suggests that prompt evaluation of blood tests, including coagulation factors, in the acute phase of leiomyoma degeneration as well as the immediate use of blood preparations are recommended before the situation worsens, especially when abnormal bleeding is observed. However, in this case, a new complication, PVL, arose as a possible complication of consumption coagulopathy during pregnancy. It can also cause long-term neurodevelopmental disorders. PVL is white matter brain damage that is mainly attributed to hypoxia and inflammation (\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). The preterm brain is susceptible to PVL formation, with the most susceptible interval at 24\u0026ndash;32 weeks of gestation, in which cerebral white matter axons are in the rapid growth phase (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). The lesion becomes visible 1\u0026ndash;2 weeks after onset. In our case, because the PVL lesion was already visible on day 6, the timing of PVL formation was estimated to be before the onset of labour. The most probable period for the development of PVL is at 17\u0026ndash;18 weeks of gestational age, when severe inflammation and consumption coagulopathy developed. However, these periods were too early for white matter neurodevelopment, and therefore, unlikely for PVL formation. Another possibility is that hypoxia due to leiomyoma degeneration may have persisted long after the recovery from consumption coagulopathy. Regarding the placental pathological findings, syncytial nodules and chorangiosis, which are often observed in the placenta during preeclampsia, maternal diabetes, and fetal growth restriction, indicate an adaptive response to chronic intrauterine hypoxia (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e). Acute intrauterine hypoxia may have occurred during the period of severe inflammation and consumption coagulopathy, and chronic intrauterine hypoxia may have been caused by insufficient blood supply to the placenta due to a large leiomyoma throughout the pregnancy period. Continuous chronic hypoxia following an acute event may be a second cause of PVL formation.\u003c/p\u003e \u003cp\u003eWe report a case of pregnancy complicated by consumption coagulopathy due to a degenerated leiomyoma. Unlike previous reports, the pregnancy in our case lasted until full term after the patient recovered from consumption coagulopathy by transfusion of blood preparations. However, consumption coagulopathy may have induced chronic intrauterine hypoxia and affected the infant\u0026rsquo;s brain development. The fact that the continuation of pregnancy was possible even after consumption coagulopathy without removing the degenerated leiomyoma is a new finding; however, the limitation of this study is that we could not confirm a direct relationship between the degenerated leiomyoma and consumption coagulopathy without a pathological study of the leiomyoma. Consumption coagulopathy during pregnancy, not due to obstetrical causes, is rare, but the degeneration of a leiomyoma during pregnancy is a common condition for those who have large leiomyomas. We need to be aware of the possibility that pregnancy complicated by a large leiomyoma could cause severe hypoxia and inflammation, which might be attributed to poor prenatal outcomes and/or permanent neurodevelopmental disorders in newborns.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthical approval and consent to participate:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe patient provided informed consent for the treatment of coagulopathy, degenerated leiomyoma, and the delivery of forceps. The prognosis of\u0026nbsp;the\u0026nbsp;pregnancy complicated by degenerated leiomyoma and the prognosis of the baby with PVL were shared with the patient and her partner.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe patient provided informed consent for the publication of this case report.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe data and images are available on request from the corresponding author, JT.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interest:\u003c/strong\u003e none\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u003c/strong\u003e none\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors contribution:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eKA and TJ conceived the study. KA wrote the manuscript with\u0026nbsp;the\u0026nbsp;support of TJ. KA, KM, and MS collected the data. YY and IA supervised the\u0026nbsp;study. All\u0026nbsp;the authors discussed the outcomes\u0026nbsp;of the study and contributed\u0026nbsp;to the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgement:\u003c/strong\u003e none\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eCoutinho LM, Assis WA, Spagnuolo-Souza A, Reis FM. Uterine Fibroids and Pregnancy: How Do They Affect Each Other?. Reprod Sci 2022;29(8):2145-2151. https://doi.org/10.1007/s43032-021-00656-6\u003c/li\u003e\n \u003cli\u003eAharoni\u0026nbsp;A, Reiter A, Golan D, Paltiely Y, Sharf M.\u0026nbsp;Patterns of growth of uterine leiomyomas during pregnancy. A prospective longitudinal study.\u0026nbsp;Br J Obstet Gynaecol 1988;95(5):510-513. https://doi.org/10.1111/j.1471-0528.1988.tb12807.x\u003c/li\u003e\n \u003cli\u003eCagan M, Tanacan A, Donmez HG, Fadiloglu E, Unal C, Beksac MS.\u0026nbsp;The Effect of Small Size Uterine Fibroids on Pregnancy Outcomes in High-risk Pregnancies.\u0026nbsp;Rev Bras Ginecol Obstet 2020;42(9):535-539.\u0026nbsp;https://doi.org/10.1055/s-0040-1713913\u003c/li\u003e\n \u003cli\u003eSarais V, Cermisoni GC, Schimberni M,\u0026nbsp;et al.\u0026nbsp;Human Chorionic Gonadotrophin as a Possible Mediator of Leiomyoma Growth during Pregnancy: Molecular Mechanisms.\u0026nbsp;Int J Mol Sci 2017;18(9):2014. Published 2017 Sep 20. https://doi.org/10.3390/ijms18092014\u003c/li\u003e\n \u003cli\u003eLaughlin\u0026nbsp;SK, Baird DD, Savitz DA, Herring AH, Hartmann KE.\u0026nbsp;Prevalence of uterine leiomyomas in the first trimester of pregnancy: an ultrasound-screening study.\u0026nbsp;Obstet Gynecol 2009;113(3):630-635.\u0026nbsp;https://doi.org/10.1097/AOG.0b013e318197bbaf\u003c/li\u003e\n \u003cli\u003eDe Carolis S, Fatigante G, Ferrazzani S,\u0026nbsp;et al.\u0026nbsp;Uterine myomectomy in pregnant women.\u0026nbsp;Fetal Diagn Ther 2001;16(2):116-119. https://doi.org/10.1159/000053893\u003c/li\u003e\n \u003cli\u003eDray A,\u0026nbsp;Perkins\u0026nbsp;M.\u0026nbsp;Bradykinin and inflammatory pain.\u0026nbsp;Trends Neurosci 1993;16(3):99-104.\u0026nbsp;https://doi.org/10.1016/0166-2236(93)90133-7\u003c/li\u003e\n \u003cli\u003eLee\u0026nbsp;HJ,\u0026nbsp;Norwitz\u0026nbsp;ER,\u0026nbsp;Shaw\u0026nbsp;J.\u0026nbsp;Contemporary management of fibroids in pregnancy.\u0026nbsp;Rev Obstet Gynecol.\u0026nbsp;2010;3(1):20-27.\u003c/li\u003e\n \u003cli\u003eKitao K, Ohara N, Funakoshi T, et al.\u0026nbsp;Consumptive coagulopathy that developed in a pregnant woman with degenerated uterine leiomyoma: case report.\u0026nbsp;Clin Exp Obstet Gynecol 2005;32(4):250.\u003c/li\u003e\n \u003cli\u003eHnat\u0026nbsp;RF,\u0026nbsp;Anderson\u0026nbsp;GG,\u0026nbsp;Alonzo\u0026nbsp;DR.\u0026nbsp;Diffuse intravascular coagulation associated with a degenerating myoma during pregnancy.\u0026nbsp;Obstet Gynecol 1967;29(2):207-210.\u003c/li\u003e\n \u003cli\u003eThe Japan society of Obstetrical, g.a.N.H. Obstetric DIC score. Available from:\u0026nbsp;\u003ca href=\"http://www.jsognh.jp/dic/\"\u003ehttp://www.jsognh.jp/dic/\u003c/a\u003e.\u003c/li\u003e\n \u003cli\u003eAsakura H, Takahashi H, Uchiyama T,\u0026nbsp;et al.\u0026nbsp;Proposal for new diagnostic criteria for DIC from the Japanese Society on Thrombosis and Hemostasis.\u0026nbsp;Thromb J 2016;14:42.\u0026nbsp;Published 2016 Sep 28. https://doi.org/10.1186/s12959-016-0117-x\u003c/li\u003e\n \u003cli\u003eErez O, Othman M, Rabinovich A, Leron E, Gotsch F, Thachil J.\u0026nbsp;DIC in Pregnancy - Pathophysiology, Clinical Characteristics, Diagnostic Scores, and Treatments.\u0026nbsp;J Blood Med 2022;13:21-44.\u0026nbsp;Published 2022 Jan 6. https://doi.org/10.2147/JBM.S273047\u003c/li\u003e\n \u003cli\u003eTaneichi A, Fujiwara H, Mizoguchi Y,\u0026nbsp;et al.\u0026nbsp;Disseminated intravascular coagulopathy caused by uterine leiomyoma with sarcoma-like findings on magnetic resonance imaging.\u0026nbsp;Case Rep Obstet Gynecol\u0026nbsp;\u0026nbsp;2014;2014:978743.\u0026nbsp;https://doi.org/10.1155/2014/978743\u003c/li\u003e\n \u003cli\u003eKitao K, Ohara N, Funakoshi T,\u0026nbsp;et al.\u0026nbsp;Consumptive coagulopathy that developed in a pregnant woman with degenerated uterine leiomyoma: case report.\u0026nbsp;Clin Exp Obstet Gynecol 2005;32(4):250.\u003c/li\u003e\n \u003cli\u003eCaputo R,\u0026nbsp;Kanbour-Shakir\u0026nbsp;A.\u0026nbsp;Chronic disseminated intravascular coagulation caused by a uterine leiomyoma. A case report.\u0026nbsp;J Reprod Med 1993;38(9):737-740.\u003c/li\u003e\n \u003cli\u003eAbiramalatha T, Bandyopadhyay T, Ramaswamy VV,\u0026nbsp;et al.\u0026nbsp;Risk Factors for Periventricular Leukomalacia in Preterm Infants: A Systematic Review, Meta-analysis, and GRADE-Based Assessment of Certainty of Evidence.\u0026nbsp;Pediatr Neurol 2021;124:51-71.\u0026nbsp;https://doi.org/10.1016/j.pediatrneurol.2021.08.003\u003c/li\u003e\n \u003cli\u003eVolpe\u0026nbsp;JJ.\u0026nbsp;The encephalopathy of prematurity--brain injury and impaired brain development inextricably intertwined.\u0026nbsp;Semin Pediatr Neurol 2009;16(4):167-178.\u0026nbsp;https://doi.org/10.1016/j.spen.2009.09.005\u003c/li\u003e\n \u003cli\u003eSung DK, Baergen RN. Focal Chorangiosis: Does It Have Clinical and Pathologic Significance?. Pediatr Dev Pathol \u0026nbsp;2019;22(5):406-409. https://doi.org/10.1177/1093526619830866\u003cstrong\u003e\u003c/strong\u003e\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Table","content":"\u003cp\u003eTable 1 is available in the Supplementary Files section\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"consumption coagulopathy, degenerated leiomyoma, periventricular leukomalacia, pregnancy, threatened miscarriage","lastPublishedDoi":"10.21203/rs.3.rs-4705152/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4705152/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground:\u003cstrong\u003e \u003c/strong\u003eConsumption coagulopathy during pregnancy is a very rare condition associated with an elevated risk of maternal and neonatal morbidity and mortality. The incidence of pregnancies complicated by leiomyomas is increasing as infertility treatments advance. Degeneration is a complication of leiomyomas during pregnancy. We encountered a leiomyoma degeneration-induced consumption coagulopathy during pregnancy that may have caused fetal periventricular leukomalacia (PVL).\u003c/p\u003e\n\u003cp\u003eCase presentation: a 42-year-old nulliparous woman with two leiomyomas was admitted to the hospital at 17 weeks and 5 days with leiomyoma degeneration and threatened preterm labour. Blood examination revealed severe inflammation, very low fibrinogenlevels, increased D-dimer levels, and prolonged PT-INR. These data suggested consumption coagulopathy; therefore, fresh frozen plasma (FFP) and dried human fibrinogen were administered, and the patient recovered from consumption coagulopathy. She was discharged once the inflammation improved by 19 weeks of gestation. At 41 weeks, the baby was delivered using forceps because of a non-reassuring fetal status (NRFS). The newborn had severe asphyxia, and magnetic resonance imaging (MRI) on day 6 revealed a PVL. In this case, the timing of the coagulopathy consumption was too early for the development of PVL but the duration from delivery was too short to develop PVL.\u003c/p\u003e\n\u003cp\u003eConclusion: Consumption coagulopathy might cause not only acute placental hypoxia, but also chronic placental hypoxia, which might have caused PVL in the most susceptible interval.\u003c/p\u003e","manuscriptTitle":"A case of consumption coagulopathy during pregnancy due to leiomyoma degeneration","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-08-19 23:50:49","doi":"10.21203/rs.3.rs-4705152/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"73fe3a83-c3a3-4595-bbfb-d9150b41675c","owner":[],"postedDate":"August 19th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2024-11-27T09:53:52+00:00","versionOfRecord":[],"versionCreatedAt":"2024-08-19 23:50:49","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4705152","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4705152","identity":"rs-4705152","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}