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51 results in Fetal Therapy

Page 1 of 3

  • Chapter 7 - Fetal and neonatal alloimmune thrombocytopenia

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 67-77

  • 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 20.1 - Fetal stem cell transplantation

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 389-396

  • Summary

    This chapter summarizes some basic features of stem cells, including their defining properties, the range of different stem cell types, and the ways in which they can be identified and characterized. It considers the therapeutic application of stem cells. Stem cells with only a limited period of activity underlie the formation of the embryo from a single fertilized cell through to the fully formed fetus. The precise way in which a transplantation assay of stem cells is performed depends on the type of cell being characterized and whether it is a same species assay or a xenograft. The assay of hematopoietic stem cells (HSCs) involves irradiation of the host mouse to completely ablate its resident bone marrow stem cells and hematopoietic system. Cellular therapy that can be performed in the fetus is also a special case because of the status of the immune system.

  • Chapter 18.1 - Intrauterine growth restriction

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 341-354

  • Summary

    Advances in obstetrical ultrasound, combined with ancillary magnetic resonance imaging and rapid molecular testing of amniotic fluid, have greatly improved the diagnostic capabilities when assessing the fetus with suspected intrauterine growth restriction (IUGR). Placental villi are covered by the fetally derived epithelial layer termed villous trophoblast; this is a distinct lineage under separate transcriptional control from the extravillous trophoblast (EVT) in mammalian placentae. The maternal-fetal interface, or decidua, is rich in cell lineages of the maternal immune system, in particular large granular lymphocytes and uterine natural killer (NK) cells. The net effect of abnormal maternal perfusion of the placental villi is one or more of the following: spiral artery thrombosis and unstable perfusion. The developmentally abnormal placenta, characterized by decidual bed pathology, structurally abnormal villi with defective or damaged areas of syncytiotrophoblast is prone to thrombosis.

  • Chapter 19.1 - Congenital diaphragmatic hernia

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 370-375

  • Summary

    In congenital diaphragmatic hernia (CDH) pulmonary hypoplasia is variable depending on the size of the diaphragmatic defect and the amount and timing of visceral herniation. In CDH pulmonary hypoplasia may arise from loss of lung fluid, decreased fetal breathing secondary to diaphragmatic dysfunction, and decreased intrathoracic volume. The lungs in CDH appear to be arrested in the saccular phase of development with poorly developed airspaces and thickened interalveolar septums. Pulmonary hypoplasia and decreased lung compliance contribute to the increased susceptibility to ventilation-induced lung injury seen in CDH. Persistent pulmonary hypertension of the newborn is the failure of the normal circulatory transition after birth. Four major components of surfactant proteins have been identified: surfactant protein A and D are hydrophilic and protein B and C are hydrophobic. A surfactant deficiency is clearly seen in the experimental lamb model of CDH.

  • Chapter 10.2 - Manipulation of amniotic fluid volume

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 137-144

  • Summary

    This chapter first discusses the measurement of amniotic fluid and the technique of measuring the depth of amniotic pool. It then describes the causes, diagnosis, and treatment of both polyhydramnios and oligohydramnios. Amniotic fluid can be semi-quantified reliably using two-dimensional ultrasound measurement of the depth of amniotic pocket and presented with amniotic fluid index (AFI) or maximum vertical pool or pocket (MVP). Combination of clinical and ultrasound assessment often allows accurate diagnosis of the underlying causes of oligohydramnios and polyhydramnios, which are heterogeneous and are usually not treatable or reversible prenatally. The aim of management is to prevent the adverse consequences resulting from extreme deviations of amniotic fluid volume. In polyhydramnios, serial amnioreduction may help to relieve the maternal pressure symptoms. In oligohydramnios caused by ruptured membranes, serial amnioinfusion may be considered to prevent pulmonary hypoplasia. Both interventions are only supported by small and uncontrolled observational studies.

  • Chapter 17.1 - Fetal tumors

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 320-328

  • Summary

    Many of the tumors that are regarded as malignant in older children may behave in a more benign fashion in the fetus and neonate, including neuroblastoma, congenital myeloproliferative disorder in Trisomy 21, congenital fibrosarcoma, and hereditary retinoblastoma. A number of genetic, chromosomal, and syndromic associations are reported for fetal and neonatal tumors. Germ cell tumors comprise both benign and malignant tumors and can arise in both gonadal and extragonadal locations; the latter are usually found in the midline, including the sacrococcygeal area, mediastinum, and neck. Teratomas contain tissues derived from all three embryonic layers (viz. ectoderm, mesoderm, and endoderm) with a wide range of histological patterns. Neuroblastoma represents a classical embryonal tumor of neuronal lineage that may occur in the adrenal medulla and any other sites of sympathetic ganglia, from the neck to the presacral region.

  • Chapter 13.2 - Fetal infections

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 208-237

  • Summary

    This chapter focuses on pathogenic organisms that may be responsible for fetal infection during pregnancy and may have significant effects on outcome. Many infections have associated serious consequences including fetal/perinatal mortality and significant morbidity. Infection with parvovirus can cause fetal hydrops and/or cardiac involvement. Prenatal diagnosis of fetal parvovirus infection requires samples of fetal blood, serous body effusions, and amniotic fluid to be sent to recognized reference laboratories. Chickenpox in adults is often more symptomatic and leads to the risk of varicella pneumonia, which carries a significant mortality. Diagnosis of primary cytomegalovirus (CMV) infection in pregnant women is based on serological testing with the appearance of specific IgG. The main host cells infected by CMV are the endothelial cells and the polymorphic nuclear leukocytes. CMV can be detected in the amniotic fluid by conventional viral isolation, rapid culture, or molecular assays.

  • Chapter 21 - Gene therapy

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 417-432

  • Summary

    Proof-of-principle prenatal gene therapy studies have shown long-term expression of proteins at therapeutic levels and induction of immune tolerance in both small and large animals and cured congenital disease in some animal models. This chapter describes current progress with fetal gene therapy and discusses how this therapy may be eventually translated into the clinic. The genodermatoses may be good candidates for prenatal gene therapy, where gene transfer to the skin via the amniotic fluid may provide an obvious advantage to cumbersome postnatal therapy. Most of this work is performed in animals, mostly in mice that can provide transgenic models of human disease necessary to demonstrate proof-of-principle. The most commonly tested vectors in prenatal gene therapy pre-clinical studies have been adenovirus and adeno-associated virus, lentivirus and retrovirus vectors. Targeting of vectors to organs or specific tissues is the ultimate goal, and will most likely require the use of several combined approaches.

  • Chapter 9.3 - Structural heart disease

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 123-127

  • Summary

    This chapter summarizes the current state of trans-catheter fetal cardiac interventions (FCI) for a select group of congenital heart defects (CHDs). The ethical issues and risks that pertain to the mother, as the healthy patient and innocent bystander are non-trivial. However, there are other situations in medical therapy that involve procedures to a healthy patient for the sake of another. Therapy for FCI involves ultrasound-guided uterine and fetal cardiac puncture with an 18- or 19-gauge cannula, predominantly percutaneous, and can be performed with the mother awake. The fetal cardiac lesion that has been the main focus of FCI over the past two decades is severe aortic stenosis (AS) in early and mid-gestation that has been shown in several publications to evolve into HLHS at birth. Hypoplastic left heart syndrome (HLHS) with highly restrictive or intact atrial septum (IAS) is one of the most challenging lesions in managing patients with CHD.

  • 15.1 - Fetal lung growth, development, and lung fluid

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 271-281

  • Summary

    This chapter focuses on how normal lung development is regulated before birth, and how it is affected by the intrauterine environment. Lung development is completed during early postnatal life; therefore, after infancy there is limited scope for repairing abnormal lung development. At least four or five distinct stages of lung development are recognized, based on microscopic appearance: these are the embryonic, pseudoglandular, canalicular, and saccular-alveolar stages. A final stage of microvascular maturation can also be recognized. For the lung to develop normally it must be able to expand to a higher degree than is seen after birth; this requires adequate intrathoracic space, fetal breathing movements (FBM), and the ongoing production of lung liquid across the airway epithelium. Changes in the environment of the developing lung that chronically affect the degree of lung expansion will result in either lung hypoplasia or hyperplasia.

  • Chapter 15.2 - Fetal lung growth, development, and lung fluid

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 282-300

  • Summary

    This chapter discusses the most common pulmonary pathologies, including fetal pleural effusions (FPE), pulmonary adenomatoid malformations, and congenital high airway obstruction sequence (CHAOS). It reviews the evidence-based methods of fetal therapy, and available data on fetal and neonatal outcome following antenatal intervention. The appearance of lung septations or solid components suggests an alternate diagnosis, such as congenital pulmonary airway malformation (CPAM) or congenital diaphragmatic hernia (CDH). The most commonly identified prenatal anomalies are congenital cystic adenomatoid malformations (CCAM) and bronchopulmonary sequestration (BPS). CCAM lesions were originally classified based on postnatal histological features: type I macrocystic, type II mixed macrocystic and microcystic, and type III microcystic. CHAOS presents as a syndrome of predicted ultrasound findings, resulting from the various causes of laryngeal or tracheal obstruction in the fetus. The chapter describes three fetal intervention cases with an antenatal diagnosis of CHAOS.

  • Chapter 14.1 - Fetal urinary tract obstruction

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 238-245

  • Summary

    Fetal urinary tract obstruction accounts for the largest identifiable cause of kidney failure in infants and children. The site of obstruction along the urinary tract varies from the ureteropelvic junction (UPJ), to the ureterovesical junction and urethra. Congenital obstructive lesions may be associated with abnormal renal development, resulting in renal agenesis, hypoplasia. The effects of urinary tract obstruction to impair nephrogenesis and to injure already-formed nephrons clearly compound perinatal risk factors as well as those accumulating throughout life. The role of angiotensin II in normal kidney development is well established, and numerous cases of renal maldevelopment and injury are reported in fetuses born to mothers exposed to angiotensin II inhibitors. The functional response of the fetal kidney to urinary tract obstruction depends on the location and timing of the obstruction. Numerous factors combine to determine the immediate and long-term impact of fetal urinary tract obstruction in affected infants.

  • Chapter 11.1 - Twin-to-twin transfusion syndrome

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 145-155

  • Summary

    Twin-to-twin transfusion syndrome (TTTS) is a relatively unusual condition as genetically concordant twins develop phenotypically discordant features as a consequence of monochorionic placentation and the conjoined angioarchitecture. This chapter describes the underlying scientific basis for the development of the clinical picture of TTTS and discusses the interplacental vascular connections. Human hemochorial placentation involves vasculogenesis, the formation of blood vessels from non-vascular (hemangioblastic) precursors, in combination with angiogenesis, the remodeling of existing blood vessels to create new ones. The chapter provides the specific placental angioarchitecture in TTTS and explains the role angiogenic growth factors. Vascular endothelial growth factor (VEGF)-A and placental growth factor (PlGF) are shown to be potent angiogenic factors, being critical for placental angiogenesis, and also as permeability factors leading to vascular leakage. Objective ultrasound measurements of fetal cardiac function include: cardiothoracic ratio; ventricular chamber dimensions and freewall thickness; valvular regurgitation; and assessment of systolic and diastolic function.

  • Chapter 11.2 - Twin-to-twin transfusion syndrome

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 156-165

  • Summary

    Monochorionic (MC) twin and triplet pregnancies pose complex clinical problems and high risks of types that are not seen in dichorionic (DC) twin pregnancies. Fetal growth discordance (FGD) and twin-to-twin transfusion syndrome (TTTS) are the most common problems. The MC twin placenta is usually a truly single, not fused, placenta that is produced by a single zygote and intended for the metabolic support of a singleton fetus. There are three vascular consequences of the insertion of two or more umbilical cords into an MC placenta: cord insertions, single umbilical artery, and interfetal vascular connections. TTTS is usually caused by a relatively low number of small diameter arteriovenous connections (AVCs) in combinations that result in net chronic blood seepage into the recipient twin. All types of vascular connections are involved in major complications in MC twins, including TTTS, donor/recipient role reversal after treatment, and neurological damage of a single surviving fetus.

  • Section 1 - General principles

  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp -

  • 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 16.2 - Neural tube defects

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 311-319

  • Summary

    The increasing use of screening ultrasonography and amniocentesis has resulted in early detection of neural tube defects (NTDs), and the use of fetal MRI has improved accuracy of the diagnosis. Spina bifida is considered a potential candidate for in-utero treatment, since the condition is routinely detected before 20 weeks of gestation. Technical difficulties associated with the small size of the fetus and fragility of the tissues generally preclude surgery before 18 weeks' gestation, and after 27 weeks there appears to be no benefit of fetal surgery. Initial screening is carried out with review of data already obtained locally by the treating obstetrician, supplemented by high-resolution ultrasound and MRI performed by the fetal team. The mortality rate for fetal surgery for spina bifida was 6% at Children's Hospital of Philadelphia (CHOP) prior to the trial, but in the Management of Myelomeningocele (MOMS) trial, the mortality was only 3%.

  • Chapter 12.2 - Twin reversed arterial perfusion (TRAP) sequence

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 193-199

  • Summary

    This chapter describes the diagnosis, pathophysiology, treatments, and diagnosis of twin reversed arterial perfusion (TRAP). Existence of TRAP requires two conditions: pump or forward flow failure in the acardiac twin and a set of arterioarterial and venovenous placental anastomoses connecting the acardiac and pump twins' circulatory systems. Ultrasonography with color Doppler is the primary method for diagnosing TRAP. The added benefits of color Doppler sonography include ability to trace fetal vessels and document reversed flow through an arterioarterial anastomosis confirming diagnosis of TRAP. MRI has also been used as an adjunct modality in the diagnosis of TRAP. Using MRI, one can determine the extent of blood flow in the umbilical cord of the acardiac, as well as evaluate the pump twin for anomalies, cardiac decompensation, and signs of chronic hypoxia such as brain ischemia. However, no single surgical technique has been found to be unequivocally superior.

  • Chapter 14.2 - Fetal urinary tract obstruction

  • from Section 2 - Fetal disease
  • Edited by Mark D. Kilby, Anthony Johnson, Baylor College of Medicine, Texas, Dick Oepkes
  • Book:
    Fetal Therapy
    Published online:
    05 February 2013
    Print publication:
    13 December 2012, pp 246-252

  • Summary

    The natural history of congenital lower urinary tract obstruction (LUTO) is highly variable and dependent on the gender, severity, duration, and age of onset of the obstruction. Outcome is measured in terms of postnatal survival and is dependent on two factors: pulmonary development and renal function. Complete urethral obstruction or significant restriction of urethral flow results in accumulation of urine within the fetal bladder, leading to marked distention. Prolonged obstruction results in smooth muscle hypertrophy and hyperplasia within the bladder wall, and eventual impairment of contractile capacity as well as compliance and elasticity. Histological studies indicate a progressive dilatation of the distal to proximal renal tubules associated with development of peritubular and interstitial fibrosis. Component of the prenatal evaluation is the serial analysis of fetal urine, obtained by vesicocentesis. More recent studies were designed to focus on the long-term outcomes of children with specific documented urethral obstructions.

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