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Coagulation is an organized and well-orchestrated process that depends on the intrinsic balance between procoagulants, anticoagulants, and fibrinolytic systems. During pregnancy, this balance is affected in various ways and becomes more critical due to the physiologic changes and obligate hemorrhage after delivery. In some instances, this equilibrium will be disrupted. In this article, we describe the anesthetic implications of bleeding disorders, thrombophilias, and anticoagulation for the safe management of the parturient, with an emphasis on how this impacts decision-making by the anesthesiologist., (Copyright © 2014 Elsevier Inc. All rights reserved.)

To the obstetrician, preeclampsia is a placental syndrome becoming clinically apparent in later pregnancy and presenting with maternal hypertension, proteinuria, and in some cases liver and central nervous system dysfunction, which, if not addressed in a timely fashion can lead to significant maternal and fetal morbidity and mortality. As such, the only satisfactory cure is delivery of the fetus, after which most, if not all, of the manifestations disappear. The nephrologist, who often is consulted only when patients develop more serious manifestations such as accelerating hypertension, acute kidney injury, and microangiopathic features, often has a different perspective. She/he sees a woman with hypertension and proteinuric kidney disease with mildly reduced glomerular filtration rate. Exciting discoveries regarding the pathogenesis of this syndrome have helped to reconcile these two views; however, much remains unknown. This review focuses on the hypertension and kidney manifestations of the disease, acknowledging that complex placental pathogenic alterations are clearly an important, if not the most important, initiator of the later maternal signs and symptoms., (Copyright © 2013 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Preeclampsia is a pregnancy-specific syndrome that usually develops after 20 weeks gestation. The exact pathogenic mechanisms remain uncertain and are likely multifactorial. Preeclampsia is a heterogeneous condition with potentially maternal and fetal consequences. As part of the spectrum of hypertensive disorders of pregnancy, preeclampsia may progress rapidly and is a leading cause of maternal and perinatal morbidity and mortality worldwide. In the United States, the incidence of preeclampsia has increased. Clinical manifestations are highly variable and may occur antepartum, intrapartum, or postpartum. Hypertension and proteinuria are the traditional hallmarks for the diagnosis of preeclampsia. These signs may occur with or without multisystem dysfunction and fetal involvement. Risk factors have been identified for the development of preeclampsia; however, ideal methods for prevention, screening, and treatment remain elusive. Preeclampsia resolves after delivery of the fetus, but patients may still have hypertension postpartum. Women and fetuses affected by preeclampsia are at higher risk of developing long-term health issues. There appear to be risk factors common to hypertensive disorders of pregnancy and cardiovascular disease seen later in adulthood. Physicians providing healthcare to women are urged to recognize potential risk factors that arise from patient obstetric histories so that optimal long-term health surveillance is provided., (Copyright © 2013 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Histoarchitectural characteristics of the human placenta place the fetus at a high risk of growth restriction, abnormal fetomaternal cell traffic, and vertical transmission of pathogens. These abnormalities of the fetomaternal unit are frequently associated with hematological abnormalities in the fetus/neonate and may be the first, most common, or the only clinical manifestations of these conditions. This article reviews the pathophysiology and characteristic hematological manifestations of these conditions in the fetus and the neonate.

Adverse pregnancy outcome (APO), includes fetal loss > or =20 weeks' gestation (fetal death), severe preeclampsia <36 weeks, or severe intrauterine growth restriction (severe IUGR) defined as birth weight < or =5th percentile or < or =10th percentile for gestational age. APO affects 8% of pregnant women (320,000 annually) and collectively contributes to the largest proportion of maternal/fetal mortality and morbidity. Women with prior APO in antecedent pregnancy are at high risk of an adverse maternal or fetal outcome in the subsequent pregnancy. Maternal serum markers and Doppler ultrasound can be used to predict adverse pregnancy outcome. There are no adequate, completed randomized trials for prophylactic measures; the roles of aspirin, calcium, and low molecular weight heparin need to be evaluated.

In 1926 von Willebrand described a bleeder family in Aland; this condition became known as von Willebrand disease (VWD). von Willebrand noted that "the trait seemed especially to be seen among the women." Today, the use of a pictorial bleeding assessment chart (PBAC) has enabled the prevalence of VWD to be established among women presenting with menorrhagia, as well as the documentation of this symptom in women with known VWD and the assessment of treatment response in menorrhagia. Treatments for menorrhagia include tranexamic acid, desmopressin (DDAVP) administered either intranasally or subcutaneously, the oral contraceptive pill, the "Mirena" coil (Schering Oy, Turku, Finland), and endometrial ablation. Von Willebrand factor (VWF) shows strong cyclical variation, with peak values occurring in the luteal phase. Although increased in pregnancy, levels of VWF decline postnatally and the incidence of both primary and secondary postpartum hemorrhage is high (20% to 25%). Baseline VWF levels less than 15 IU/dL are unlikely to reach greater than 50 IU/dL in the third trimester, and therefore prophylaxis with DDAVP or VWF-containing concentrate to cover delivery should be considered.

Acute hypotension in the setting of hemorrhage most often signifies abrupt and dangerous blood loss. The physiologic changes of pregnancy are designed to protect the mother from blood loss at parturition. When this protective reserve is exceeded, hypovolemic shock occurs. Ideally, blood loss of this magnitude should not be allowed to occur. Notwithstanding, obstetric hemorrhage continues to be an important cause of maternal mortality. Most deaths due to hemorrhage are preventable. Successful treatment requires that the clinician must react with the immediate institution of effective resuscitative measures. The importance of an organized, team approach with input from relevant specialties in the scheme of management cannot be overemphasized.

In recent years, considerable progress has been made in understanding the pathogenic mechanisms involved in the allo- and autoimmune thrombocytopenias. A number of new platelet-associated alloantigens have been described and platelet autoantigens continue to be studied in more detail. Specific assays for antibodies directed against the major antigenic platelet glycoproteins are now available. Important recent clinical investigations have led to modification of the management of immune thrombocytopenia in the perinatal period, resulting in a reduced risk of hemorrhagic complications for both mother and infant. Future investigations are likely to further improve the outcome of these pregnancies.