with ITP, there was no case of fetal or neonatal ICH and no infant with any central nervous system abnormality (Wyszynski, 2016). Fetal bleeding complications are considered rare, and fetal blood sampling is not recommended (Neunert, 201i1). Delivery mode is based on standard obstetrical indications.
This term refers to excessive accumulation of serous fluid. Strictly defined, hydrops etalis is edema of the fetus. Traditionally, the diagnosis was made after delivery of a massively edematous neonate, often stillborn (Fig. 1i5-4). With sonography, hydrops has become a prenatal diagnosis. It is deined as two or more fetal efusions-pleural, pericardial, or ascites-or one efusion plus anasarca. As hydrops progresses in severity, edema is invariably a component, and is usually accompanied by placentomegaly and hydramnios. Clinically significant edema is defined sonographically as skin thickness > 5 mm, and placentomegaly if the placenta thickness is at least 4 em in the second trimester or 6 em in the third trimester (Bellini, 2009; Society for Maternal-Fetal Medicine, 2015b). Hydrops may result from a wide range of conditions with varying pathophysiologies, each with the potential to make the fetus severely ill. It is divided into two categories. If found in association with red cell alloimmunization, it is termed immune, otherwise, it is nonimmune.
he incidence of immune hydrops has dramatically declined with the advent of anti-D immune globulin, MCA Doppler studies for detection of severe anemia, and prompt fetal transfusion when needed (p. 304). However, fewer than 10 percent of hydrops cases are caused by red cell alloimmunization (Bellini, 2012; Santolaya, 1992).
The pathophysiology underlying hydrops remains unknown. Immune hydrops is postulated to share several physiological abnormalities with nonimmune hydrops. As shown in
FIGURE 15-4 Hydropic, macerated stillborn infant and characteristically large placenta. The etiology was B1o9 parvovirus infection. (Used with permission from Dr. April Bleich.) 15-5, these include decreased colloid oncotic pres sure, increased hydrostatic (or central venous) pressure, and enhanced vascular permeability. Immune hydrops results from transplacental passage of maternal antibodies that destroy fetal red cells. The resultant anemia stimulates marrow erythroid hyperplasia and extramedullary hematopoiesis in the spleen and liver. The latter likely causes portal hypertension and impaired hepatic protein synthesis, which lowers plasma oncotic pressure (Nicolaides, 1985). Fetal anemia also may raise central venous pressure (Weiner, 1989). Finally, tissue hypoxia from anemia may increase capillary permeability, such that luid collects in the fetal thorax, abdominal cavity, andlor subcutaneous tissue.
he degree of anemia in immune hydrops is typically severe.
In a series of 70 pregnancies with fetal anemia from red cell alloimmunization, Mari and coworkers (2000) found that all those with immune hydrops had hemoglobin values <5 g/dL. As discussed on page 304, immune hydrops is treated with fetal blood transfusions.