FIGURE 15-6 Hydropic features. A. This profile of a 23-week fetus with nonimmune hydrops secondary to B 19 parvovirus infection depicts scalp edema (arrowheads) and ascites (*). B. This 34-week fetus had hydrops secondary to an arteriovenous malformation in the brain, known as a vein of Galen aneurysm. In this coronal image, prominent pleural effusions (*) outline the lungs (L). Fetal ascites is also pres- ent (arrows), as is anasarca. C. This axial (transverse) image depicts a pericardial effusion (arrows) in a 23-week fetus with hydrops from B1o9 parvovirus infection. The degree of cardiomegaly is impressive, and the ventricular hypertrophy raises concern for myocarditis, which can accompany parvovirus infection. D. This axial (transverse) image depicts fetal ascites (*) in a 15-week fetus with hydrops secondary to large cystic hygromas. Anasarca is also seen (bracket).
abnormality such as meconium peritonms. Finally, isolated edema, particularly involving the upper torso or the dorsum of the hands and feet, may be found in Turner or Noonan syndrome or may represent congenital lymphedema syndrome (Chap. 13, p. 259).
An association between fetal hydrops and development of maternal edema in which the fetus mirrors the mother is attributed to Ballantyne. He called the condition triple edema because the fetus, mother, and placenta all became edematous. he etiology of the hydrops is not related to development of mirror syndrome. It has been associated with hydrops from D alloimmunization, twin-twin transfusion syndrome, placental chorioangioma, and with fetal cystic hygroma, Ebstein anomaly, sacrococcygeal teratoma, chylothorax, bladder outlet obstruction, supraventricular tachycardia, vein of Galen aneurysm, and various congenital infections (Braun, 2010).
In a review of more than 50 cases of mirror syndrome, Braun (2010) found that approximately 90 percent of women had edema, 60 percent had hypertension, 40 percent had proteinuria, 20 percent had liver enzyme elevation, and nearly 15 percent had headache and visual disturbances. Based on these indings, it is reasonable to consider mirror syndrome a form of severe preeclampsia (Espinoza, 2006; Midgley, 2000). Others, however, have suggested that it is a separate disease process with hemodilution rather than hemoconcentration (Carbillon, 1997; Livingston, 2007).
Some reports describe the same imbalance of angiogenic and antiangiogenic factors that is observed with preeclampsia, and this suggests a common pathophysiology (Espinoza, 2006; Goa, 2013; Llurba, 2012). hese indings, which include elevated concentrations of soluble fms-like tyrosine kinase-1 (sFlt-l), decreased placental growth factor (PIG F) levels, and elevation of soluble vascular endothelial growth factor receptor-I (s VEG FR-1) concentrations, are discussed further Chapter 40 (p. 716).