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Fetal Therapy
  • Edited by Mark D. Kilby, Department of Fetal Medicine, University of Birmingham , Anthony Johnson, Baylor College of Medicine, Texas , Dick Oepkes, Department of Obstetrics, Leiden University Medical Center
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Book description

Fetal treatment, particularly complex fetal therapy, is an emergent and expanding field. This comprehensive text focuses on areas of fetal disease and pathophysiology that can be treated in utero and the benefits and problems with such therapy. Both medical (non-invasive) and surgical procedures are discussed, drawing on the expertise of an internationally renowned author team. Each chapter includes a comprehensive overview of the basic science underlying fetal pathology, as well as discussing the highest level of technical performance of fetal interventions. Contributions from fetal therapy 'centers-of-excellence' around the world collectively emphasize the need for an evidence-based approach to the field. This volume is useful both as a quick reference guide to the latest fetal therapy options and as an in-depth study book for maternal-fetal medicine and neonatology specialists at any stage of their career who are seeking to acquire essential background knowledge. Indispensable on any bookshelf in fetal medicine units.

Reviews

'It is both scientific and pragmatic and should satisfy a variety of curiosities in this fascinating field of therapeutic medicine. As such, it is a "must have" for fetal medicine specialists and trainees, but also medical libraries.'

Source: The Obstetrician and Gynaecologist

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Contents


Page 1 of 2


  • Section 1 - General principles
  • View abstract

    Summary

    Initial therapies such as intrauterine transfusion for severe hemolytic disease of the fetus were undertaken based on sound physiological principles and an understanding of the basic pathogenesis but were never subjected to randomized clinical trials. More recent targeted interventions for such conditions as treatment for severe twin-to-twin transfusion syndrome (TTTS), myelomeningocele (MMC) and congenital diaphragm hernia (CDH) have been the subject of well-designed randomized investigations. This chapter elucidates the history and the basis for the treatment of these fetal interventions. Routine induction of labor at a premature gestation was the only therapy that could be offered to attempt to curb the inevitable death due to hemolytic disease of the fetus and newborn (HDFN) that occurred in 30% of cases. The human fetus has indeed become a patient and development of treatments is a work in progress.
  • Chapter 2 - Insights into pathogenesis of adult cardiovascular disease from fetal animal studies
    pp 12-23
  • View abstract

    Summary

    This chapter reviews the current status of research into the notion that the current epidemic of non-communicable disease, particularly adult cardiovascular disease (CVD), originates during early development. It describes the potential of animals as models of human fetal development and presents the evidence from human and animal studies. The fetus offers the potential for detection of an individual's risk of disease even earlier in life, and may provide future early routes for intervention. However, in light of the ethical restrictions on human fetal investigations, suitable animal model alternatives are crucial in advancing this area of research. There is now considerable human and animal evidence to suggest that risk of later CVD is initiated by fetal phenotypic changes in response to a suboptimal intrauterine environment. Such prenatal adaptive responses may start as a response which is made to enhance immediate fetal survival or to optimize phenotype for the predicted later environment.
  • Chapter 3 - Human embryology
    pp 24-38
  • View abstract

    Summary

    There are five major signaling pathways that control embryogenesis, comprising the Hedgehog, Wnt, TGFβ/Bmp, Notch, and fibroblast growth factor (FGF) signaling families. Together these control cell proliferation, cell survival, changes in cell shape, migration, adhesion, and cell differentiation. Mutation in components of these pathways results in a number of human syndromes. This chapter discusses the five key signaling pathways that control embryonic development. It describes the various roles, mechanisms of action of each pathway and highlights syndromes that are due to mutations in components of these signaling pathways. The chapter explains how mutations in transcription factors, matrix molecules, and epigenetic factors can affect embryonic development. During embryonic development, the vertebrae and axial musculature develop from somites, which are epithelial balls that periodically bud off from the unsegmented paraxial mesoderm. Deregulation of the notch pathway affects somite development by deregulating the clock and preventing the formation of boundaries.
  • Chapter 4 - Ethics of fetal therapy
    pp 39-44
  • View abstract

    Summary

    This chapter provides an ethical framework to guide clinical investigation and the translation of its results into clinical practice. It describes the ethical framework for fetal therapy in clinical research as well as in practice. Medical ethics identifies the ethical obligations of physicians and healthcare organizations to patients as well as the obligations of patients. The ethical concept of the fetus as a patient is based on both the ethical principle of beneficence and the ethical principle of respect for the pregnant woman's autonomy. Innovation in fetal therapy research begins with the design of an intervention and its implementation in animal models, followed by a single case and then case series. Three criteria must be satisfied in order to conduct such preliminary investigations in fetal research in an ethically responsible fashion, by taking into account beneficence-based obligations to the fetal patient and beneficence-based obligations to the pregnant woman.
  • Chapter 5 - Fetal therapy choices
    pp 45-54
  • View abstract

    Summary

    This chapter discusses the difficulties and the possibilities for doctors in supporting parents/patients in making difficult decisions using the case of fetal lung anomalies. It also discusses the difficulties in parental understanding of the information given and the way people use information while making a decision. The following aspects are important when delivering information to parents and family: People in general are able to only process a limited amount of information at a single interview; people process information in an intuitive and emotional way; and people, in general, find it difficult to understand risk information. In most clinical cases there is a trade-of between benefits and risks for the choice of different treatment options. The affective impact of the mental images of risks about the outcome of a decision contributes to a binary perception of risks.
  • Section 2 - Fetal disease
  • View abstract

    Summary

    This chapter discusses the role of fetal therapy for fetal anemia, which has been one of the success stories of fetal medicine. There is a risk of red cell alloimmunization in any pregnancy where the mother is exposed to fetal red cells that possess antigens for which her own red cells are negative. A number of pregnancy-related events are associated with a risk of fetomaternal hemorrhage (FMH). A number of techniques have evolved over time to facilitate assessment of pregnancies at risk of 'hemolytic disease of the fetus and newborn' (HDFN). The aim of assessment is to identify the anemic fetus requiring intrauterine transfusion (IUT) before hydrops fetalis develops. However, monitoring an identified at-risk pregnancy to the point at which hydrops fetalis develops would be considered a management failure. Although less common than RhD disease, profound fetal anemia, hydrops, and intrauterine death can result from Kell alloimmunization.
  • Chapter 7 - Fetal and neonatal alloimmune thrombocytopenia
    pp 67-77
  • View abstract

    Summary

    This chapter focuses on fetal and neonatal alloimmune thrombocytopenia (FNAIT), which is one of the major causes of both severe thrombocytopenia and intracranial hemorrhage (ICH) in fetuses and term neonates. FNAIT is caused by maternal immunization against human platelet antigens (HPAs) on fetal platelets, inherited from the father and different from those present in the mother. The chapter also focuses on the current insights in the etiology, diagnosis, and management of pregnancies at known risk of FNAIT. The diagnosis of FNAIT is unequivocal when paternal incompatibility with corresponding maternal alloantibodies is present. The primary goal of the management of a neonate with FNAIT is to prevent or stop thrombocytopenic bleeding. In suspected cases of FNAIT, babies with severe thrombocytopenia can be transfused with random platelets transfusions, until the diagnosis is established and matched platelets are available.
  • Chapter 8.1 - Fetal dysrhythmias
    pp 78-86
  • View abstract

    Summary

    Antiarrhythmic agents affect the generation and/or propagation of the cardiac rhythm by their actions on one or several ion channel currents and/or the autonomous nervous system. This chapter focuses on five antiarrhythmic agents: digoxin, flecainide, sotalol, amiodarone and adenosine. Due to their relative safety and efficacy, these agents are considered the foundation of transplacental and/or direct pharmacological therapy of fetal supraventricular tachyarrhythmias (SVT). SVT itself can be produced by four different mechanisms, namely: atrioventricular reentry (AVRT), atrial flutter (AF), atrial ectopic tachycardia (AET), and permanent junctional reciprocating tachycardia (PJRT). AVRT and PJRT involve the atrial and ventricular myocardium, the AV node, and accessory pathway(s) in the reentrant circuit. Suppression of AET and AF is possible by drugs like flecainide, sotalol, and amiodarone that directly act on atrial cells. The fetal response to antiarrhythmic therapy not unexpectedly is affected by fetal hemodynamics, arrhythmia mechanism, and the choice of drug management.
  • Chapter 8.2 - Fetal dysrhythmias
    pp 87-99
  • View abstract

    Summary

    This chapter provides a logical approach to diagnosis of fetal dysrhythmias and discusses the current management of fetal dysrhythmias. Echocardiography, the main diagnostic tool in the fetus, allows recording of the mechanical consequences of the electrical stimulation, registered as myocardial wall movement and blood flow signals. Other techniques such as fetal electrocardiography (f-ECG) or fetal magnetocardiography (f-MCG) allow recording of the electrical cardiac impulses. Rhythm irregularities are common and often associated with premature contraction of the atrium. The most frequent tachycardias are supraventricular tachyarrhythmias including supraventricular tachycardia (SVT) and atrial flutter (AF). Neither heart rate nor fetal heart rate (FHR) variability allows clear distinction among the various types although they may aid diagnosis. Fetal bradycardia may be a manifestation of fetal distress and require emergency Cesarean section. Hydrops increases morbidity and mortality for both tachycardias and bradycardias.
  • Chapter 9.1 - Structural heart disease
    pp 100-112
  • View abstract

    Summary

    In essence cardiac development shows basic similarities of the major processes involved in between species; therefore, mechanisms unraveled in animal models can be reliably used in understanding normal human cardiac development and congenital heart disease (CHD). This chapter provides an update on recent advances in heart development in which it is important to distinguish a first heart field (FHF) and a second heart field (SHF). It provides a general introduction into embryology and then talks about the most common heart malformations in a developmental context. This is followed by a discussion on each specific malformation. The chapter explains the separation of the SHF in an anterior/secondary (arterial pole) and posterior (venous pole) population. It then introduces a number of processes that are essential in the formation of the four-chambered heart with a proper alignment of the atria, ventricles, and great arteries.