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Importance Psychological reactions to perinatal loss, although often self-limited, may lead to significant psychological morbidities. Obstetrician-gynecologists and other maternal health providers play a key role in recognizing the range of psychological responses to perinatal loss and providing education, support, and treatment options to their patients. Objective This review aims to define psychological reactions associated with perinatal loss, examine psychotherapy and psychopharmacologic treatments for psychiatric morbidities, discuss interpregnancy interval following perinatal loss, and highlight brief, psychological interventions that can be implemented by maternal health providers. Evidence acquisition Search terms "perinatal loss psychology," "reproductive loss grief," "perinatal psychopharmacology," "psychopharmacology grief," and "interpregnancy interval" were utilized to search PubMed, Google Scholar, and PsycINFO. Results Grief is an expected, normal response to perinatal loss. Psychological morbidities, including major depressive disorder, generalized anxiety disorder, and posttraumatic stress disorder, are also associated with perinatal loss. Risk factors for these conditions include history of a psychiatric illness, childlessness, unknown cause of perinatal loss, limited social support, and marital/relationship discord. Careful interviewing and brief screening measures can help identify patients who may suffer from depressive or anxiety disorders following reproductive loss. Patients with perinatal loss can benefit from psychological and possibly pharmacologic treatments. Recommended interpregnancy interval after perinatal loss should be customized by gestational age and cause of loss. Conclusions and relevance Patients with perinatal loss emotionally benefit from their reproductive health care providers acknowledging the psychological aspects of reproductive loss, inquiring about their emotional needs, and providing information regarding grief and mental health referrals.

The placenta is a remarkable organ that coordinates and regulates maternal-fetal interactions during pregnancy to optimize fetal development. A host of obstetric complications are associated with placental dysfunction, and existing methods for evaluating in vivo placental function fail to reliably detect at-risk pregnancies prior to maternal or fetal morbidity. Although routinely used as a monitoring tool, the predictive power of ultrasound for identifying compromised pregnancies is poor. Recent preclinical studies performed in our laboratory, using blood oxygen-level dependent magnetic resonance imaging (BOLD-MRI) in the pregnant nonhuman primate (NHP), established a strong correlation between placental T2* values and maternal-fetal oxygen transport. Here we extend this work to a large, longitudinal, two-site study of quantitative in vivo T2* mapping in human pregnancies across 11 to 38 weeks of gestation to characterize the evolution of placental oxygenation in uncomplicated pregnancies and to elucidate the relationship between aberrant placental T2* and adverse obstetric outcomes attributable to placental dysfunction. This methodology has high discriminatory power and strong potential diagnostic utility.

Miscarriage is a frequent complication of human pregnancy: ∼50% to 70% of spontaneous conceptions are lost prior to the second trimester. Etiology of miscarriage includes genetic abnormalities, infections, immunological and implantation disorders, uterine and endocrine abnormalities, and lifestyle factors. Given such variability, knowledge regarding causes, pathophysiological mechanisms, and morphologies of primary early pregnancy loss has significant gaps; often, pregnancy losses remain unexplained. Pathologic evaluation of miscarriage tissue is an untapped source of knowledge. Although miscarriage specimens comprise a significant part of pathologists' workload, information reported from these specimens is typically of minimal clinical utility for delineating etiology or predicting recurrence risk. Standardized terminology is available, though not universally used. We reintroduce the terminology and review new information about early pregnancy losses and their morphologies. Current clinical terminology is inconsistent, hampering research progress. This review is a resource for diagnostic pathologists studying this complex problem.

Introduction: Significant variability in morbidity and mortality persists for children with single ventricle congenital heart disease (SV-CHD) despite standardization in medical and surgical care. Multiple risk factors for poor outcomes have been described, but they only explain a fraction of the disparity in outcomes. The Developmental Origins of Health and Disease (DOHaD) theory proposes that fetal adaptation to an adverse in utero environment alters the ability to respond to post-natal stressors and may explain additional risk for poor outcomes. This study assessed maternal risk factor association with disparate outcomes following SV palliation. Hypothesis: Maternal factors related to weight, diabetes, hypertension, and smoking may be associated with an increased risk of poor outcomes in children with SV-CHD. Methods: This retrospective observational cohort study included all term maternal-infant pairs with a diagnosis of SV-CHD who underwent surgical palliation from 2006-2015 at Primary Children’s Hospital. Pairs lacking maternal variables of interest or infant follow-up data up to 1 year were excluded. The association of death or transplant with maternal risk factors [abnormal pre-pregnancy BMI, abnormal weight gain during pregnancy (≤ 7 kg or ≥ 20 kg), any type of hypertension or diabetes and smoking] was analyzed using a multivariable logistic regression model. Results: Of 190 infants who qualified, 135 (71%) maternal-infant dyads had complete data for inclusion. Systemic right ventricular morphology was present in 69% and 31% had systemic left ventricular morphology. Death or transplant occurred in 48 infants (36%) during an average follow-up of 2.2 years (0.1-11.7 years). Abnormal weight gain during pregnancy was present in 34 (25%) mothers, of which 24 had excessive (>20 kg) and 10 had inadequate ( Conclusions: Abnormal maternal weight gain (excessive or inadequate) during pregnancy is a novel risk factor that may contribute to worse outcomes in SV-CHD.