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Background: Sacrococcygeal teratomas (SCT) are often highly vascularized and may result in high-output cardiac failure, polyhydramnios, fetal hydrops, and demise. Delivery is guided by the SCT to fetus volume ratio (SCTratio), SCT growth rate, and cardiac output indexed for weight (CCOi). Methods: We compared measurements and outcome in 12 consecutive fetuses referred with SCT. Adverse outcomes were: fetal surgery, delivery < 32 gestational weeks or neonatal demise. Only SCTratio and CCOi were used to manage the cases. SCT vascularization index (VI%) was derived from the 3D virtual organ computer-aided analysis (VOCAL) software. The SCTModel (modified from acardiac twins) calculated a hypothetical SCT draining vein size and derived a risk line, using diameters of the superior and inferior vena cava, the azygous and umbilical veins. VI% and a model of systemic and umbilical venous volumes (SCTModel) were tested as indicators for outcome in SCT. Results: Fetuses were monitored from 20.1 to 36.4 gestational weeks and 5/12 had adverse outcomes: 1 had successful open fetal surgery at 23.8 weeks and delivered at term, 4 delivered at < 32 weeks with 3/4 having neonatal demise between 25 and 29 weeks. VI% was significantly higher in cases with adverse outcomes (mean 10.3 [8.9–11.6] vs. 4.4 [3.4–5.3], p < 0.0001). The additional fraction of the fetal cardiac output required to perfuse the SCT-draining vein (XSCO%) (p = 0.46), SCTratio (p = 0.08), and CCOi (p = 0.64) were not significant. All cases with adverse outcome had VI% > 8%. The SCTModel risk line predicted nonadverse outcomes well but lacked data in 2/5 cases with adverse outcomes. Conclusions: VI% is a significant indicator of SCT cases with adverse outcomes and combined with SCTratio may guide timing of delivery better than current measures.

A rare case of a low incidence red cell antigen causing severe fetal allo-immune red cell disease is presented. Discussion of how this can be diagnosed and successfully managed antenatally using middle cerebral artery Doppler ultrasound and maternal antibody titre levels for fetal surveillance and timing of intervention with intrauterine transfusion.

Introduction: The Ballantyne syndrome (or mirror syndrome) is a gestational proteinuric hypertension associated with fetal hydrops. This report describes a case in which Ballantyne syndrome reversion occurred despite fetal hydrops persistence. Case Report: A 24-year-old woman showed fetoplacental hydrops at 28 2/7 gestational weeks. Severe Rh(D) alloimmunization and fetal hemolytic anemia (fetal hematocrit 15.4%) were confirmed by cordocentesis, and an intrauterine transfusion was performed. She also revealed hypertension (160/100 mm Hg), edema and proteinuria (845 mg/day). After four intrauterine transfusions, blood pressure was normalized; urinary proteinuria was not significant, and the edema vanished completely. Fetal hydrops persisted until delivery at 32 gestational weeks, but a partial reduction of placental hydrops was noted. Discussion: Total or partial reduction of the placental edema may be responsible for the reversal of the Ballantyne syndrome despite the fetal hydrops persistence.

Objective: We report the management and outcome of 6 cases of non-immune fetal hydrops secondary to parvovirus B19 infection presenting over a 5-month period. Methods: The Queen Mothers Hospital is a tertiary referral centre for fetal medicine. All cases were suspected on the basis of ultrasound evidence of hydrops. Two cases were managed conservatively owing to the presence of an active fetus with evidence of resolving hydrops. Fetal blood sampling intra-uterine transfusion and drainage of ascitic fluid were performed in 3 cases. The 6th case unfortunately resulted in an intra-uterine death prior to fetal blood sampling. Results: Maternal parvovirus specific B19 was identified in all cases. Fetal parvovirus B19 IgM was identified in the 3 cases in whom fetal blood sampling was performed. A single intra-uterine transfusion was performed in these 3 cases; fetal hydrops resolved in 2 of these pregnancies progressing to the birth of a healthy baby at term, whereas 1 case was complicated by intra-uterine death. Fetal hydrops resolved in both cases managed conservatively, leading to the birth of a healthy baby at term. Conclusions: Parvovirus B19 infection should always be suspected in cases of non-immune hydrops. Conservative management will be appropriate in some cases and should involve weekly ultrasonography. The outlook for pregnancies presenting with gross hydrops remains guarded, even if intra-uterine transfusion is performed successfully.

Introduction: Fetal thyrotoxicosis, often caused by maternal Grave’s disease, can have adverse effects on fetal outcomes, such as growth impairment or fetal hydrops. Therefore, intrauterine treatment is recommended. Objective: To describe the experience of intrauterine medical treatment of fetal thyrotoxicosis. Case: A 19-year-old woman with a history of Grave’s disease in a euthyroid clinical status after subtotal thyroidectomy became pregnant 2 months after thyroidectomy. At gestational age 28 weeks, persistent fetal tachycardia was identified and the diagnosis of fetal thyrotoxicosis was established by fetal thyroid function test on umbilical cord blood obtained by cordocentesis. Intrauterine treatment for hyperthyroidism was initiated with antithyroid drugs (150 mg/day of propylthiouracil) via maternal oral administration. Fetal heart rate, size of fetal thyroid gland and umbilical cord blood sampling for thyroid function test were monitored. Fetal heart rate became normal and fetal thyroid function tested on fetal cord blood at 1 month after antithyroid fetal therapy was also normal. Fetal thyrotoxicosis improved but the mother had some degree of hypothyroidism from fetal therapy and needed thyroid hormone replacement. The remaining course of gestation was uneventful. The patient had spontaneous labor and delivery at 38 weeks of gestation resulting in normal female baby, 2,900 g, and had no clinical of neonatal thyrotoxicosis. Maternal thyroid medications were stopped immediately after birth. Conclusion: Intrauterine treatment of fetal thyrotoxicosis with medication via the maternal circulation can possibly improve fetal outcome.

A highly unusual case of a pregnancy complicated by diffuse placental chorioangiomatosis that resulted in a live-birth and short-term fetal survival is reported. The potential for antenatal diagnosis and intrauterine treatment to optimise fetal outcome is discussed.

A new lethal case of nemaline myopathy is reported. The diagnosis was made by postmortem muscle biopsy. The child died before his first day of life. This is one of the very rare cases of nemaline myopathy with severe antenatal ultrasonographic signs: fetal hydrops and arthrogryposis. In a review of the literature other cases of the congenital rapidly fatal form are found, some of them with clinical decrease of fetal movements but only few authors report ultrasonographic signs. The diagnostic, histopathogenic, genetic and evolutive aspects of this heterogeneous disorder are analyzed. This congenital nonprogressive myopathy is not as benign as previously thought and may be an etiology of the lethal form of arthrogryposis multiplex congenita. The existence of ultrasonographic antenatal signs seems to be a factor of poor prognosis. In spite of recent genetic discoveries, there is at present no specific antenatal diagnosis. Consequently, muscle biopsy in lethal cases is very important to allow a genetic counselling; however, in utero fetal biopsy has never been performed in such cases.

Three cases of placental chorioangiomas, from 6.5 to 10 cm in diameter, were diagnosed prenatally by ultrasound and color Doppler imaging at 21–34 weeks of gestation. In 1 case, due to fetal hydrops a

Severe fetal hydrops associated with cystic adenomatoid malformation of the lung inexplicably resolved spontaneously at 33-34 weeks' gestation. Following postnatal resection of the lesion which was of the macrocystic variety, the infant's respiratory status deteriorated, requiring 1 week of complicated support with extracorporeal membrane oxygenation. The baby survived and was discharged.

Fetal hydrops due to Rh (D) alloimmunization can be reversed by ultrasound-guided intravascular transfusions with improvement in perinatal morbidity and mortality. We report a case of in utero intravascular transfusion in hydropic twins which reversed all the hydropic findings within 3 days. A simple intraperitoneal transfusion was performed in each twin 2 weeks later, and only one neonatal exchange transfusion was required for the ultimate survival of both twins.

Objective: To evaluate the influence of fetal hydrops and other variables on fetal hematocrit (Hct) decrease after the first intrauterine transfusion (IUT) in alloimmunized pregnancies. Methods: From 1996 to 2006, the data of all alloimmunized pregnancies submitted to IUT were assessed. Exclusion criteria included: fetuses submitted to intraperitoneal transfusion; pregnancies complicated by other fetal abnormalities; pregnancies submitted to only one IUT, and cases in which posttransfusion or pretransfusion blood samples were not obtained. Linear regression models were implemented to assess the relationship between the rate of Hct fall after the first IUT and the following variables: fetal hydrops; antibody titer; gestational age at the first IUT; number of days between the first and second IUT; pretransfusion and posttransfusion fetal Hct values. Results: Fifty fetuses fulfilled the study criteria. The fetal Hct decrease after the first IUT was 1.21 (range 0.18–2.3) %/day. The variables independently associated with the fetal Hct drop after the first IUT were the fetal hydrops (p = 0.000), the pretransfusion fetal Hct (p = 0.001) and the posttransfusion fetal Hct (p = 0.016). Conclusion: Fetal hydrops, pretransfusion fetal Hct and posttransfusion fetal Hct seem to influence the fetal Hct decrease between the first and second IUT. These findings may be helpful for estimating the rate of fetal Hct drop and programming the following IUT.

We report a successful treatment of a B19 parvovirus-induced fetal hydrops diagnosed at 16 weeks of gestation. This disease could be corrected by means of a unique intraperitoneal blood transfusion performed at 18 weeks, once diagnosis was established. The delivery occurred at 36 weeks, leading to the birth of a healthy baby. This case suggests that transfusion should be attempted, as the spontaneous fetal recovery remains uncertain and shows that intraperitoneal blood transfusion is an effective therapeutic option of the B19 parvovirus-induced anemia, in the absence of a viral myocarditis.

The management of fetal hydrops in the second trimester is changing as the underlying etiologies are better understood. We report a case which was diagnosed at 18 weeks gestation. There was no underlying anatomical abnormality. Fetal blood sampling confirmed a normal karyotype and there was no evidence of fetal infection. Bilateral thoracocentesis and paracentesis caused temporary improvement of the fetal condition but subsequent fluid reaccumulation was noted within the left pleural cavity. A pleuroamniotic shunt inserted at 22 weeks caused permanent resolution of the hydrops. The infant was normal at 1-year follow-up.