Hemorrhage in Early Pregnancy and Antepartum Hemorrhage Contemporary Diagnosis, Management, and Maternal–Fetal Outcomes
1. Sohil
2. Osmonova Gulnaz Zhenishbaevna
(1. Student, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic
2. Teacher, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic.)
Abstract
Obstetric hemorrhage remains a principal contributor to severe maternal morbidity, maternal mortality, and compromised fetal outcomes worldwide. Bleeding during pregnancy is broadly categorized by gestational age into early pregnancy hemorrhage, occurring prior to twenty weeks of gestation, and antepartum hemorrhage, occurring from twenty weeks of gestation until delivery. Early pregnancy hemorrhage is primarily driven by spontaneous pregnancy loss, ectopic implantation, gestational trophoblastic disease, and lower genital tract lesions. Antepartum hemorrhage is overwhelmingly dominated by placental structural anomalies, specifically placental abruption, placenta previa, morbidly adherent placenta spectrum, and vasa previa. Advances in high-resolution transvaginal ultrasonography, point-of-care biomolecular testing, color Doppler imaging, and viscoelastic point-of-care hematologic assays have fundamentally revolutionized diagnostic accuracy and clinical triage. Management strategies have shifted toward multi-tiered, multidisciplinary protocolized algorithms incorporating modern mass transfusion protocols, cell salvage, systemic hemostatic agents, and minimally invasive radiological endovascular therapies alongside definitive surgical procedures. Maternal complications encompass hypovolemic shock, disseminated intravascular coagulation, multiorgan dysfunction syndrome, and surgical morbidity including peripartum hysterectomy. Fetal and neonatal consequences range from severe intrauterine hypoxia and extreme prematurity to neurological disability and intrauterine death. This article provides a comprehensive synthesis of the contemporary pathophysiological concepts, diagnostic pathways, clinical management frameworks, and maternal–fetal outcomes associated with obstetric bleeding across the entire gestational continuum.
Introduction
Vaginal bleeding during pregnancy represents one of the most critical and time-sensitive presentations in clinical obstetrics. Obstetric hemorrhage spans a vast continuum, ranging from benign, self-limiting spotting in early gestation to catastrophic, life-threatening maternal blood loss requiring emergent surgical and hematologic resuscitation. Global epidemiological assessments indicate that maternal hemorrhage accounts for nearly twenty-seven percent of all maternal deaths worldwide, with the vast majority occurring in low- and middle-income resource settings, although it remains a substantial driver of severe maternal morbidity in high-income nations as well. Beyond maternal mortality, acute or recurrent gestational bleeding generates profound downstream repercussions for the developing fetus, significantly increasing the risk of spontaneous or iatrogenic preterm birth, intrauterine growth restriction, neonatal encephalopathy, and perinatal mortality.
The diagnostic and therapeutic paradigm for gestational bleeding is heavily dependent on gestational age. Early pregnancy hemorrhage, conventionally defined as bleeding occurring before twenty weeks of gestation, requires a clinical focus on confirming intrauterine viability, excluding extrauterine implantation, and assessing the completeness of tissue expulsion. Conversely, antepartum hemorrhage, defined as bleeding from or into the genital tract occurring from twenty weeks of gestation up to the delivery of the fetus, shifts the clinical imperative toward evaluating utero-placental architecture, preserving maternal hemodynamic integrity, monitoring fetal oxygenation, and optimizing the timing and route of delivery.
Recent advancements in reproductive medicine, maternal-fetal imaging, and critical care hematology have significantly transformed clinical practice. The integration of high-resolution transvaginal sonography, rapid high-sensitivity quantitative serum human chorionic gonadotropin assays, non-invasive cell-free fetal DNA screening, and color Doppler mapping has markedly enhanced diagnostic precision. Simultaneously, resuscitation science has evolved with the implementation of ratio-based mass transfusion protocols, real-time viscoelastic coagulation testing, intravenous iron therapy, and minimally invasive endovascular techniques such as uterine artery embolization. Despite these diagnostic and therapeutic innovations, managing gestational hemorrhage requires continuous clinical vigilance, standardized protocolization, and coordinated multidisciplinary collaboration. This review provides a rigorous, contemporary synthesis of the etiology, diagnostic algorithms, evidence-based management frameworks, and dual maternal–fetal outcomes associated with bleeding throughout pregnancy.
Diagnostic and Pathophysiological Framework of Early Pregnancy Hemorrhage
Early pregnancy hemorrhage presents a frequent diagnostic challenge, affecting approximately fifteen to twenty-five percent of all clinically recognized pregnancies during the first trimester. The physiological mechanisms underpinning early gestational bleeding vary widely, ranging from benign physiological implantation bleeding to pathological processes involving non-viable intrauterine tissue, ectopic trophoblastic invasion, or neoplastic disease.
Early pregnancy loss, encompassing threatened, inevitable, incomplete, complete, and missed abortion, represents the most frequent cause of first-trimester bleeding. Chromosomal abnormalities, predominantly numerical aneuploidies such as autosomal trisomies, monosomy X, and triploidy, account for over fifty percent of early pregnancy failures. Pathophysiologically, non-viable conceptuses induce localized decidual necrosis, microvascular disruption, and retrochorionic hematoma formation, culminating in uterine contractions, cervical dilatation, and overt vaginal bleeding. Threatened miscarriage manifests as vaginal bleeding through a closed cervical os with demonstrated intrauterine fetal cardiac activity. Inevitable miscarriage presents with persistent bleeding accompanied by cervical effacement and dilatation, whereas incomplete miscarriage involves partial expulsion of products of conception, leaving retained trophoblastic tissue that prevents effective uterine myometrial contraction and causes sustained hemorrhage.
Ectopic pregnancy represents the most critical life-threatening cause of early pregnancy hemorrhage, occurring in approximately one to two percent of all pregnancies. Ectopic gestations occur when a fertilized ovum implants outside the endometrial cavity, most commonly within the ampullary or isthmic segments of the fallopian tube. Trophoblastic erosion into non-adapted tubal vasculature lacking the capacious decidual bed of the endometrium ultimately leads to tubal wall distension, tubal rupture, and severe intra-abdominal hemorrhage. A subset of patients presents with ectopic pregnancy bleeding secondary to decidual breakdown in the endometrial cavity, driven by declining serum progesterone and human chorionic gonadotropin levels, which can clinically mimic an early intrauterine miscarriage. Interstitial, cervical, scar, and abdominal ectopic pregnancies present even greater diagnostic and therapeutic challenges due to their proximity to major pelvic arterial networks, conferring a high risk of catastrophic internal hemorrhage upon disruption.
Gestational trophoblastic disease represents a spectrum of proliferative trophoblastic disorders comprising hydatidiform mole, invasive mole, choriocarcinoma, and placental site trophoblastic tumor. Complete hydatidiform moles, typically possessing a 46,XX paternal diploid karyotype, and partial moles, presenting with a triploid karyotype, exhibit abnormal placental villous trophoblastic hyperplasia and marked hydropic swelling. Pathophysiologically, diffuse arteriovenous malformations and high-pressure intervillous bleeding within the vesicular molar mass cause recurrent, dark red vaginal hemorrhage, often accompanied by marked disproportionate uterine enlargement and significantly elevated serum quantitative human chorionic gonadotropin levels.
Non-obstetric causes of early pregnancy hemorrhage must also be systematically evaluated. Lower genital tract pathologies, such as cervical ectropion, cervical polyps, infectious cervicitis, vaginitis, and lower genital tract trauma, frequently present with post-coital or contact vaginal spotting. Although non-fatal, these conditions can obscure coexisting intra-uterine or extra-uterine pathologies and necessitate careful visual inspection of the cervix and vagina during diagnostic evaluation.
Diagnostic evaluation of early pregnancy hemorrhage relies heavily on combining quantitative serum human chorionic gonadotropin measurements with high-resolution transvaginal ultrasonography. The concept of the discriminatory zone—the serum quantitative human chorionic gonadotropin concentration above which a normal intrauterine gestational sac should consistently be visualized by transvaginal ultrasound—serves as a core diagnostic threshold. While historically set between one thousand five hundred and two thousand international units per liter, contemporary guidelines advocate for a higher conservative discriminatory threshold of two thousand five hundred to three thousand500 international units per liter before declaring a pregnancy non-viable or extrauterine, thereby preventing inadvertent iatrogenic disruption of a desired early intrauterine pregnancy.
Transvaginal sonographic criteria for non-viable early pregnancy have been standardized. A definitive diagnosis of pregnancy failure is established when transvaginal ultrasound demonstrates a crown-rump length of seven millimeters or greater without cardiac activity, or a mean sac diameter of twenty-five millimeters or greater without an embryo. When sonographic findings remain inconclusive, serial quantitative serum human chorionic gonadotropin levels measured forty-eight hours apart are required. A normal early intrauterine pregnancy typically exhibits an rising serum human chorionic gonadotropin level, with minimum expected percentage increases varying based on initial values, whereas ectopic gestations and non-viable intrauterine pregnancies characteristically demonstrate suboptimal serum human chorionic gonadotropin rises or plateauing levels.
Etiology and Pathophysiology of Antepartum Hemorrhage
Antepartum hemorrhage, occurring from twenty weeks of gestation to delivery, affects approximately two to five percent of all pregnancies and represents an acute obstetric emergency. The pathophysiological mechanisms underlying antepartum hemorrhage are predominantly anatomical and structural, involving abnormal placental insertion, premature separation of a normally implanted placenta, structural fetal vessel abnormalities, or uterine structural failure.
Placental abruption, defined as the premature detachment of a normally implanted placenta from the uterine myometrium before the delivery of the fetus, accounts for approximately thirty percent of all cases of antepartum hemorrhage. The primary pathophysiological event is the rupture of maternal decidual spiral arteries, leading to retroplacental hematoma formation. As the hematoma expands, it further shears off adjacent villous tissue, compromising maternal-fetal gas exchange and utero-placental perfusion. Placental abruption is classified as revealed when blood dissects down between the membranes and uterine wall to exit through the cervix, or concealed when the retroplacental hematoma remains entirely sequestered behind the placenta. Concealed abruptions are particularly treacherous, as severe maternal hypovolemia and fetal compromise can occur in the absence of significant visible vaginal blood loss. In severe concealed abruption, extensive extravasation of blood into the uterine myometrium and beneath the serosa gives rise to a Couvelaire uterus, compromising myometrial contractility and exacerbating postpartum uterine atony. Etiological risk factors for abruption include chronic maternal hypertension, preeclampsia, abdominal trauma, sudden uterine decompression following premature rupture of membranes or delivery of a first twin, tobacco use, cocaine abuse, and prior history of placental abruption.
Placenta previa occurs when the placenta implants over or in close proximity to the internal cervical os. Modern sonographic classification categorizes placenta previa as complete, where the placenta completely covers the internal os, or low-lying placenta, where the placental edge lies within twenty millimeters of the internal os without covering it. Pathophysiologically, as the lower uterine segment thins, elongates, and undergoes physiological remodeling during the third trimester, shear forces disrupt the anchoring placental attachment at the lower segment. This separation opens retroplacental venous sinuses, resulting in recurrent episodes of painless, bright red maternal bleeding. Because the bleeding originates from the maternal systemic circulation, significant placenta previa hemorrhage rapidly compromises maternal hemodynamic stability.
Morbidly adherent placenta spectrum, historically termed placenta accreta spectrum, represents an increasingly prevalent cause of life-threatening antepartum and intrapartum hemorrhage, driven primarily by rising global rates of cesarean delivery. Placenta accreta spectrum encompasses placenta accreta vera, where chorionic villi attach directly to the myometrium without invading it; placenta increta, where villi deeply invade the myometrium; and placenta percreta, where villi penetrate through the full thickness of the myometrium, invading the uterine serosa and potentially adjacent pelvic viscera such as the urinary bladder. Pathophysiologically, placenta accreta spectrum arises from a defect in the decidua basalis, usually at the site of a prior uterine scar, preventing normal nitabuch layer formation and permitting unchecked trophoblastic invasion into myometrial vascular spaces. Patients with coexisting placenta previa and a history of multiple prior cesarean sections are at the highest risk for placenta accreta spectrum, frequently presenting with massive, uncontained hemorrhage during third-trimester conservative management or attempted manual removal of the placenta.
Vasa previa represents a rare but highly dangerous fetal condition occurring in approximately one in two thousand five hundred pregnancies. Vasa previa occurs when unprotected fetal blood vessels, running within the fetal membranes unsupported by the umbilical cord or placental tissue, traverse the lower uterine segment over the internal cervical os. This typically occurs in the setting of velamentous cord insertion, succenturiate placental lobes, or low-lying placentas. Pathophysiologically, when the fetal membranes rupture spontaneously or iatrogenically during labor, these exposed fetal vessels are susceptible to laceration, resulting in rapid fetal exsanguination. Because total fetal blood volume at term is extraordinarily small, approximately eighty to ninety milliliters per kilogram, even minor bleeding from a ruptured vasa previa can rapidly cause fetal hypovolemic shock, severe fetal bradycardia, sinusoidal fetal heart rate patterns, and intrauterine fetal death within minutes.
Other contributors to antepartum hemorrhage include uterine rupture, cervical abnormalities, and heavy bloody show. Uterine rupture involves a full-thickness disruption of the myometrium and serosa, most commonly occurring along a previous cesarean section scar during trial of labor, resulting in massive maternal intra-abdominal and vaginal hemorrhage, sudden cessation of uterine contractions, loss of fetal station, and profound fetal distress. Non-placental genital tract lesions, including cervical erosion, cervical carcinoma, advanced cervical polyps, and vaginal lacerations, must also be systematically excluded during clinical evaluation.
Clinical Management Frameworks and Interventions
The clinical management of gestational hemorrhage requires a structured, multi-tiered approach structured according to gestational age, hemorrhage severity, maternal hemodynamic stability, and fetal condition. Modern management emphasizes rapid resuscitation, precise diagnostic localization, targeted pharmacological and surgical therapies, and proactive multidisciplinary coordination.
Management of early pregnancy hemorrhage focuses on patient stability, determining viability, and choosing among expectant, medical, and surgical interventions. In threatened miscarriage with confirmed intrauterine fetal viability, management is predominantly conservative, emphasizing reassurance, bed rest, and serial clinical evaluations. The administration of exogenous progesterone therapy in early pregnancy bleeding remains a subject of active research; however, modern clinical evidence supports offering oral micronized progesterone to women presenting with first-trimester bleeding who have a history of one or more prior miscarriages.
When early pregnancy loss is non-viable, expectant, medical, or surgical management options are offered based on clinical stability and patient preference. Expectant management allows spontaneous tissue expulsion over one to two weeks, but is associated with higher rates of unpredictable bleeding and emergency surgical evacuation. Medical management utilizes misoprostol, a prostaglandin E1 analogue, administered vaginally, orally, or sublingually, often pretreated twenty-four hours prior with oral mifepristone, an antiprogesterone agent. Pretreatment with mifepristone significantly enhances uterine contractility and cervical ripening, resulting in higher complete expulsion rates and reducing the need for secondary surgical intervention compared to misoprostol monotherapy. Surgical management, via electric or manual vacuum aspiration, is indicated for patients presenting with heavy ongoing hemorrhage, hemodynamic instability, clinical infection, or patient preference for immediate definitive resolution. Surgical intervention should be conducted using gentle aspiration techniques to minimize the risk of intrauterine adhesion formation and cervical trauma.
Management of ectopic pregnancy is dictated by clinical stability, ectopic size, serum human chorionic gonadotropin levels, and ultrasound features. Hemodynamically unstable patients or those with evidence of tubal rupture require immediate emergency laparoscopy or laparotomy for salpingectomy. In select hemodynamically stable patients with unruptured ectopic masses measuring less than thirty-five millimeters, absence of fetal cardiac activity, and initial serum human chorionic gonadotropin levels below five thousand international units per liter, medical management with systemically administered methotrexate—a folic acid antagonist—serves as a safe, fertility-preserving alternative to surgery.
Management of antepartum hemorrhage requires an immediate, protocolized multidisciplinary response involving obstetricians, maternal-fetal medicine specialists, obstetric anesthesiologists, neonatologists, blood bank specialists, and critical care nursing staff. Initial clinical assessment must prioritize maternal hemodynamic stabilization according to standard advanced trauma life support principles. Vital signs, including heart rate, continuous non-invasive or invasive arterial blood pressure, respiratory rate, and pulse oximetry, must be continuously monitored alongside quantitative measurement of cumulative blood loss. Continuous electronic fetal monitoring via cardiotocography should be instituted immediately for gestations past the limit of viability. A crucial clinical dictum in antepartum hemorrhage is the absolute prohibition of digital vaginal examination until ultrasound imaging has definitively excluded placenta previa and vasa previa, as digital palpation through the cervical os can inadvertently disrupt a low-lying placenta or vasa previa, triggering catastrophic, uncontained hemorrhage.
Hemodynamic resuscitation in major antepartum hemorrhage centers on the early activation of a specialized massive transfusion protocol. Traditional volume resuscitation using large volumes of crystalloid solutions is discouraged, as excessive crystalloid infusion exacerbates dilutional coagulopathy, hypothermia, and metabolic acidosis—the lethal triad of trauma and hemorrhage. Modern resuscitation frameworks favor early, ratio-based administration of packed red blood cells, fresh frozen plasma, and platelets in a balanced one-to-one-to-one ratio, aiming to mimic whole blood replacement. Real-time viscoelastic testing, such as rotational thromboelastometry or thrombelastography, provides rapid point-of-care assessment of specific coagulation deficits, enabling targeted administration of fibrinogen concentrate, cryoprecipitate, or prothrombin complex concentrates. Tranexamic acid, a synthetic lysine analogue that inhibits fibrinolysis, should be administered early in cases of severe obstetric bleeding, as clinical trials demonstrate significant reductions in hemorrhage-related maternal mortality without increasing thromboembolic risks.
In cases of placental abruption, management depends on maternal stability, fetal condition, and gestational age. If maternal shock or acute fetal distress is present, immediate emergency delivery, typically via emergency cesarean section, is required regardless of gestational age, accompanied by aggressive maternal resuscitation and correction of consumptive coagulopathy. Conversely, in a hemodynamically stable mother with a reassuring fetal status presenting with a partial abruption at a preterm gestation, expectant management in a high-dependency maternal-fetal care unit may be considered to allow for antenatal corticosteroid administration for fetal lung maturation and magnesium sulfate for neuroprotection, alongside close, continuous monitoring.
Management of placenta previa is guided by bleeding severity and gestational age. Asymptomatic placenta previa or low-lying placenta identified in the second trimester requires follow-up transvaginal ultrasound imaging at thirty-two to thirty-six weeks of gestation to evaluate for placental migration. For patients with persistent, uncomplicated placenta previa, elective delivery by cesarean section is recommended between thirty-six and thirty-seven weeks of gestation. In cases of acute, major antepartum bleeding secondary to placenta previa, emergent cesarean section is mandatory. When placenta accreta spectrum is suspected or confirmed antenatally, delivery should be scheduled between thirty-four and thirty-five weeks of gestation at a specialized tertiary care center equipped with a multidisciplinary surgical team, cell salvage equipment, interventional radiology support, and immediate access to massive transfusion resources. Planned cesarean hysterectomy with the placenta left in situ remains the primary definitive surgical management for advanced placenta accreta spectrum, avoiding manual placental extraction attempts that invariably provoke massive, uncontrolled hemorrhage.
Vasa previa management relies entirely on accurate, early prenatal ultrasound diagnosis using color and pulsed-wave Doppler imaging. When diagnosed antenatally, patients with vasa previa should be admitted to a tertiary facility between thirty and thirty-four weeks of gestation for close surveillance, antenatal corticosteroid administration, and planned elective cesarean delivery between thirty-four and thirty-six weeks of gestation, prior to the onset of labor or spontaneous membrane rupture. If a patient presents with sudden vaginal bleeding following membrane rupture accompanied by immediate fetal distress, emergency cesarean delivery within minutes offers the only chance for fetal survival.
Anti-D immunoglobulin administration is a critical supportive management component in all non-sensitized Rh-D-negative women experiencing early pregnancy hemorrhage or antepartum hemorrhage. Because fetomaternal hemorrhage can trigger maternal alloimmunization against Rh-D positive fetal red cells, lead to hemolytic disease of the fetus and newborn in subsequent pregnancies, standard doses of anti-D immunoglobulin must be administered within seventy-two hours of any bleeding episode, with Kleihauer-Betke testing or flow cytometry performed in third-trimester antepartum hemorrhage to quantify fetomaternal blood volume transfer and adjust anti-D dosing accordingly.
Maternal and Fetal Outcomes
Obstetric hemorrhage across all gestational ages continues to exert a major impact on maternal and fetal morbidity and mortality. Maternal outcomes are directly linked to the speed of diagnosis, the volume and rate of blood loss, and the rapidity of comprehensive resuscitation and definitive clinical management. Acute hypovolemic shock resulting from severe blood loss leads to tissue hypoperfusion, end-organ ischemia, and acute kidney injury secondary to acute tubular necrosis. Consumptive coagulopathy and disseminated intravascular coagulation are particularly common in severe placental abruption, driven by the systemic release of tissue factor from the damaged retroplacental bed into the maternal circulation. Disseminated intravascular coagulation rapidly depletes circulating fibrinogen, platelets, and clotting factors, creating a dangerous cycle of intractable bleeding.
Advanced maternal surgical complications associated with severe antepartum hemorrhage, particularly in cases of placenta accreta spectrum, include extensive pelvic tissue trauma, accidental ureteral or bladder laceration, intraoperative cardiac arrest, and the necessity for emergency peripartum hysterectomy. Maternal psychological morbidity, including post-traumatic stress disorder, postpartum depression, and severe anxiety, is also significantly elevated following life-threatening obstetric bleeding episodes. In resource-limited global regions lacking immediate access to blood transfusion services, surgical facilities, and critical care units, maternal mortality from uncontained early pregnancy ectopic rupture or late antepartum hemorrhage remains disproportionately high.
Fetal and neonatal outcomes following gestational hemorrhage are similarly serious and heavily dictated by gestational age, the extent of placental separation, and the degree of maternal hemodynamic instability. In early pregnancy, acute hemorrhage associated with ectopic pregnancy or incomplete miscarriage results in total pregnancy loss. In surviving gestations complicated by first-trimester threatened miscarriage, prospective cohort studies demonstrate an increased long-term risk of subsequent adverse late-pregnancy outcomes, including higher incidences of second-trimester pregnancy loss, premature rupture of membranes, fetal growth restriction, low birth weight, and placental abruption.
Antepartum hemorrhage poses immediate and severe risks to fetal survival and long-term health. Placental abruption causes acute disruption of maternal-fetal gas exchange, resulting in fetal hypoxia, metabolic acidosis, intrauterine asphyxia, severe neurological injury such as hypoxic-ischemic encephalopathy, and intrauterine fetal demise. Even in non-fatal cases of partial abruption or recurrent placenta previa bleeding, chronic utero-placental insufficiency often causes severe intrauterine growth restriction and oligohydramnios.
Iatrogenic and spontaneous preterm birth represents a primary driver of neonatal morbidity associated with antepartum hemorrhage. The necessity for urgent early delivery to preserve maternal life in major placenta previa, placenta accreta spectrum, or placental abruption frequently exposes the neonate to the sequelae of extreme prematurity. Neonatal complications include respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, patent ductus arteriosus, neonatal sepsis, long-term neurodevelopmental delay, and cerebral palsy. In vasa previa, failure to diagnose the condition prior to rupture results in catastrophic fetal exsanguination, with perinatal mortality rates exceeding sixty percent in unmanaged presentations, whereas early antenatal detection and planned cesarean delivery yield neonatal survival rates exceeding ninety-five percent.
Conclusions
Gestational bleeding across early pregnancy and the antepartum period represents a spectrum of obstetric conditions requiring prompt clinical recognition, accurate pathophysiological classification, and decisive management. While early pregnancy hemorrhage centers on verifying viability, ruling out ectopic implantation, and preventing septic or hemorrhagic complications, antepartum hemorrhage demands immediate hemodynamic resuscitation, exclusion of abnormal placental implantation, and balancing maternal stability against fetal maturity. Modern innovations in transvaginal Doppler sonography, point-of-care viscoelastic hematologic profiling, ratio-based mass transfusion protocols, and multidisciplinary surgical planning have significantly improved survival and reduced morbidity. However, eliminating preventable maternal and perinatal mortality requires ongoing clinical vigilance, widespread implementation of standardized hemorrhage protocols, and improved global access to tertiary obstetric critical care.
References
1. American College of Obstetricians and Gynecologists. (2017). Practice Bulletin No. 183: Postpartum hemorrhage. Obstetrics & Gynecology, 130(4), e168–e186. https://doi.org/10.1097/AOG.0000000000002351
2. American College of Obstetricians and Gynecologists. (2018). Practice Bulletin No. 193: Tubal ectopic pregnancy. Obstetrics & Gynecology, 131(3), e91–e103. https://doi.org/10.1097/AOG.0000000000002560
3. American College of Obstetricians and Gynecologists. (2018). ACOG Practice Bulletin No. 200: Early pregnancy loss. Obstetrics & Gynecology, 132(5), e197–e207. https://doi.org/10.1097/AOG.0000000000002899
4. Giordano, R., Cacciatore, A., Cignini, P., Lapresa, R., & Alvarez, C. (2010). Antepartum haemorrhage. Journal of Prenatal Medicine, 4(4), 45–53. Cited by: 63
5. Jauniaux, E., Chantraine, F., Silver, R. M., & Langhoff-Roos, J. (2018). FIGO consensus guidelines on placenta accreta spectrum disorders: Epidemiology. International Journal of Gynecology & Obstetrics, 140(3), 265–273. https://doi.org/10.1002/ijgo.12407 Cited by: 412
6. Jauniaux, E., Alfirevic, Z., Bhide, A. G., Belfort, M. A., Burton, G. J., Royal College of Obstetricians and Gynaecologists. (2019). Placenta praevia and placenta accreta: Diagnosis and management (Green-top Guideline No. 27a). BJOG: An International Journal of Obstetrics & Gynaecology, 126(1), e1–e48. https://doi.org/10.1111/1471-0528.15306 Cited by: 310
7. Oyelese, Y., & Smulian, J. C. (2006). Placenta previa, placenta accreta, and vasa previa. Obstetrics & Gynecology, 107(4), 927–941. https://doi.org/10.1097/01.AOG.0000207559.15715.98 Cited by: 580
8. Royal College of Obstetricians and Gynaecologists. (2011). Antepartum haemorrhage (Green-top Guideline No. 63). RCOG Press.
9. Say, L., Chou, D., Gemmill, A., Tunçalp, Ö., Moller, A. B., Daniels, J., Gülmezoglu, A. M., Temmerman, M., & Alkema, L. (2014). Global causes of maternal death: A WHO systematic analysis. The Lancet Global Health, 2(6), e323–e333. https://doi.org/10.1016/S2214-109X(14)70227-X Cited by: 2450
10. Shainker, S. A., Coleman, B., Modi, B. P., & American College of Obstetricians and Gynecologists. (2018). Clinical Consensus No. 2: Society for Maternal-Fetal Medicine (SMFM) Consult Series #44: Management of vasa previa. American Journal of Obstetrics & Gynecology, 219(4), B2–B6. https://doi.org/10.1016/j.ajog.2018.06.012
11. WOMAN Trial Collaborators. (2017). Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): An international, randomised, double-blind, placebo-controlled trial. The Lancet, 389(10084), 2105–2116. https://doi.org/10.1016/S0140-6736(17)30638-4 Cited by: 1120