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The incidence of twin and higher order multiple pregnancies increased dramatically with the advent of Assisted Reproductive Technology (ART) in the 1970s, but practice guidelines have led to decreasing numbers from 2014 onwards. All types of twins have increased in incidence, but dizygous much more so than monozygous. Monochorionic placentation is peculiar to monozygotic pregnancies. Higher orders of chorionicity can occur in monozgotic pregnancies, but are much more common in gestations of plural zygosity. There are many factors that affect the incidence of multiple gestation: individual, genetic, and environmental. However, prudent ART management is the simplest and most effective way of reducing the incidence. Multifetal pregnancy reduction is an operative intervention that can reduce the unwanted medical and social sequelae of multiple pregnancy, counseling about such an intervention should be non-directional and carried out by a specialist.
A thrombophilic defect is an abnormality in the coagulation system that predisposes an individual to thrombosis. This chapter examines the role that the acquired thrombophilic defects play in the magnitude of early pregnancy loss, with particular reference to Primary Antiphospholipid syndrome, hyperhomocysteinemia and Acquired protein C resistance. Antiphospholipid syndrome (APS) is now recognized to be the most important treatable cause of recurrent miscarriage. The potential of thromboelastography as a clinical tool to overcome many of the above limitations in hemostasis testing in our recurrent pregnancy-loss population is promising. The success of thromboprophylactic treatment for women with recurrent miscarriage associated with APS has resulted in women with unexplained recurrent miscarriage frequently demanding similar treatment. Recurrent miscarriage is a distressing condition that affects at least 1% of couples trying to achieve a successful pregnancy. Recurrent miscarriage is a heterogeneous condition and no single abnormality will account for all cases.
Hypertensive disorders are among the most common medical complications of pregnancy, with an incidence of approximately 6-10%. This spectrum of conditions includes essential hypertension, pre-eclampsia and HELLP syndrome. For patients with pre-existing hypertension, management ideally commences prior to conception, and continues through pregnancy to the postnatal period. This book provides information on the evidence-based management of women with hypertension throughout pregnancy, supported by important background information on the etiology, risk-factors and pathophysiology of these disorders. Illustrated with accompanying algorithms, tables and lists for quick reference on diagnostic criteria, drugs and side-effects, this book will help clinicians rapidly gain access to the information they need to care for these patients. This will to be of interest to all grades of obstetric trainees as well as specialists, obstetric anesthetists and anesthetic trainees, midwives and maternal-fetal physicians.
Eclampsia refers to the occurrence of one or more generalized convulsions and/or coma in the setting of pre-eclampsia and in the absence of other neurologic conditions. Pre-eclampsia is a multisystem disorder of pregnancy and the puerperium, complicating approximately 6–8% of all pregnancies (ACOG, 1996, 2002). Pre-eclampsia is characterized by new onset hypertension (sitting blood pressure ≥140/90), proteinuria (≥2+ in a random urine sample or ≥300 mg in a 24-h collection) with or without non-dependent edema after 20 weeks' gestation. Eclampsia was at one time thought to be the end result of pre-eclampsia, hence the nomenclature. It is now clear, however, that seizures are but one clinical manifestation of “severe” pre-eclampsia. Other manifestations include, among others, HELLP syndrome (Hemolysis, Elevated Liver enzymes and Low Platelets), disseminated intravascular coagulopathy (DIC), renal failure, hepatocellular damage, pancreatitis, congestive cardiac failure, pulmonary edema and fetal intrauterine growth restriction.
The pathophysiology of pre-eclampsia is poorly understood. It is a disease of human pregnancy; more precisely, it is a disease of the placenta since it is also described in pregnancies where there is trophoblast but no fetal tissue (complete molar pregnancies) (Goldstein and Berkowitz, 1994). The blueprint for the development of pre-eclampsia is laid down early in pregnancy. The pathologic hallmark of pre-eclampsia appears to be a failure of the second wave of trophoblast invasion from 8 to 18 weeks' gestation, a process that is responsible for destruction of the muscularis layer of the spiral arterioles and, as such, establishment of the definitive uteroplacental circulation (Brosens et al., 1972; Cross et al., 1994; Meekins et al., 1994).
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