Cases reported "Hydrops Fetalis"

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1/15. Fetal brain infection with human parvovirus B19.

    Intrauterine parvovirus B19 infection is known to be one of the causes of hydrops fetalis. However, there are few reports of the pathologic changes in the central nervous system. Postmortem examination of a fetus revealed multinucleated giant cells of macrophage/microglia lineage and many small calcifications around the vessels, predominantly in the cerebral white matter. parvovirus B19 genome dna was detected in the nucleus of the multinucleated giant cells and solitary endothelial cells by polymerase chain reaction amplification and in situ polymerase chain reaction methods. capsid antigen was also demonstrated in the cytoplasm of the endothelial cells by immunofluorescent assay. Thus, intrauterine B19 parvovirus infection could be associated with marked neuropathologic changes in the fetal brain at the midembryonal period. Neurologic follow-up of complications may be necessary for children who survive the intrauterine infection.
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2/15. A case of non-immune hydrops fetalis with congenital cystic adenomatoid malformation of the left lung in a twin.

    hydrops fetalis is a rare condition that occurs in one out of every 1,400-4,000 pregnancies. There are two types, immune and non-immune. It can be caused by a maternal-fetal incompatibility due to the Rh factor or, more rarely, the Kell factor or due to other antigens to red corpuscles. Non-immune types of hydrops have a complex multiform pathogenesis and in 50% of the cases they are of idiopathic nature. The causes that could determine non-immune hydrops are manifold and in 50% of the cases they are of an idiopathic nature. Independently of the clinical condition, the presented case could be classified in those forms of pathogenesis in which there is the presence of a congenital cystic adenomatoid malformation (CAM), not encountered in the fetal ultrasound performed at the sixteenth week of pregnancy. The particularity of our case is due to the association of the fetal hydrops of the CAM type in only one of the two twins. The presented case is classified in those forms of hydrops that are expressed with a clinical trend towards a worse prognosis, characterized by the intrauterine death of the fetus or the birth of a hydropic fetus that does not survive because of respiratory insufficiency and cardiocirculatory collapse.
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3/15. Fatal hydrops fetalis caused by anti-D in a mother with partial D.

    BACKGROUND: Rare cases of hemolytic disease of the newborn occur in women with genetic variants of the D antigen. A partial D variant might be suspected when typing for the D antigen shows weaker-than-normal reactions (weak D). Historically, patients with a weak D phenotype have not been considered candidates for Rh immune globulin prophylaxis. CASE: A gravida 2, para 1 woman with A-positive blood type, delivered an infant who died from severe hemolytic disease of the newborn 6 days after birth. Anti-D, undetectable at the first prenatal visit, was identified (titer 1:64) at delivery. The mother's red cells were partial D(VI) phenotype. CONCLUSION: Although severe hemolytic disease in patients with partial D is rare, this neonatal death illustrates the need for a change in management of women with weak D.
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4/15. Maternal ABO-mismatched blood for intrauterine transfusion of severe hemolytic disease of the newborn due to anti-Rh17.

    BACKGROUND: Clinically significant antibodies to high-incident antigens present a challenge in hemolytic disease of the newborn. Antigen-negative blood may be difficult to obtain for intrauterine transfusion (IUT). In these instances, maternal blood is de facto compatible regardless of an ABO mismatch. CASE REPORT: A group B/D-- woman with a history of hemolytic disease of the newborn due to anti-Rh17 (titer 256) presented to the obstetrical clinic at 12 weeks gestation for management of her third pregnancy. She consented to donate blood for possible IUT. STUDY DESIGN AND methods: Washed maternal packed cells were suspended in saline to 75 percent Hct and irradiated before transfusion. The fetus was transfused via the intrahepatic vein. RESULTS: Ultrasound examination at 19 weeks indicated a hydropic fetus. The fetal blood group was O Rh , direct antiglobulin test 4 , and hemoglobin 22 g per L. A total of 368 mL of maternal blood was transfused during seven procedures. Labor was induced at 38 weeks, and a 2560-g male infant was delivered by Caesarian-section due to fetal distress. The infant grouped as B Rh , direct antiglobulin test negative. No group O red blood cells were detected. The hemoglobin level was 143 g per L rising to 209 g per L at discharge 3 days later. The indirect bilirubin was 55 micromol/L and remained stable during the hospital stay. phototherapy was discontinued after 1 day, and the infant was discharged without an exchange or top-up transfusion. CONCLUSIONS: Maternal ABO-mismatched blood is an alternate source for IUT in instances when antigen-compatible allogenic blood is unavailable.
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5/15. Nonimmune hydrops fetalis and fetal congenital syphilis. A case report.

    Nonimmune hydrops fetalis occurred secondary to a syphilitic infection. Ultrasonographic evaluation and cordocentesis were used to confirm the antenatal infection. An IgM antibody specific for treponema pallidum wall antigen (anti-47-kDa) was used to document the fetal infection. High-dose intravenous penicillin was administered in an attempt to achieve adequate fetal levels.
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6/15. hydrops fetalis caused by homozygous alpha-thalassemia and Rh antigen alloimmunization: report of a survivor and literature review.

    Hematologic causes of hydrops fetalis include homozygous alpha-thalassemia and immune hemolytic anemias. We report the case of a boy with hydrops fetalis who had homozygous alpha-thalassemia and alloimmune hemolytic anemia due to anti-E and anti-C blood group antibodies. He received intrauterine red blood cell transfusions and postnatal chronic transfusion with iron chelation therapy. A non-myeloablative sibling stem cell transplant failed. He is now 5 years and 6 months of age, hypothyroid with short stature, but in overall good health. He is one of the oldest reported homozygous alpha-thalassemia survivors and, to our knowledge, the only survivor with immune- and nonimmune-induced hydrops fetalis.
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7/15. Anti-C(w) alloimmunization presenting as hydrops fetalis.

    C(w) is a low frequency red cell antigen that belongs to the Rh blood groups system. While not uncommon, anti-C(w) is rarely associated with clinically significant haemolytic disease of the newborn (HDN). When it does occur, it is often subclinical or of mild to moderate clinical severity. In the majority of pregnancies it is considered to be a naturally occurring antibody and has not been reported to cause hydrops fetalis or stillbirth. We report a case of anti-C(w) alloimmunization, which was associated with significant anaemia and hydrops fetalis, presenting at 35 wk gestation. Conclusion: Pregnancies affected by anti-C(w) merit closer scrutiny. Consideration should be given to performing more frequent antenatal ultrasound assessments to detect hydrops fetalis. This may help to support the need for more invasive procedures (cordocentesis and intrauterine transfusions).
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8/15. Intravenous drug abuse causes Rh immunization.

    Intravenous drug abuse causes many health problems. From March 1989 to January 1990 of 27 Rh-negative women (28 pregnancies) referred to our centre, 4 women (5 pregnancies) were Rh immunized due to the sharing of needles and blood with their Rh-positive partners. Severe hydrops was present in 4 of their 5 fetuses when they were first seen at 17-35 weeks of gestation. Only the fetus first seen at 35 weeks survived. That infant was moribund at birth and now has evidence of leukomalacia and porencephaly. The fifth fetus, not hydropic, required two intravascular fetal transfusions in order to survive. A fifth woman, immunized in a similar manner, had a spontaneous abortion. These fetuses represent some of the earliest and severest examples of hydrops fetalis ever seen at our centre. The severity of their fetal hemolytic disease is probably due to the fact that their mothers' exposure to Rh(D) antigen by blood sharing was continuous and ongoing. Because of their aberrant behaviour, these women have suffered irreversible reproductive damage.
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9/15. Increased severity of fetal hemolytic disease with known rhesus alloimmunization after first-trimester transcervical chorionic villus biopsy.

    Fetomaternal hemorrhage secondary to chorionic villus biopsy has the potential to accelerate fetal hemolytic disease in the pregnant patient previously sensitized to red cell antigens. A case of poor fetal outcome after first-trimester transcervical chorionic villus sampling in an alloimmunized patient is reported. An increase in antibody titers was associated with the demise of a hydropic fetus early in the second trimester. Maternal red cell alloimmunization is suggested as an absolute contraindication for chorionic villus sampling performed for genetic indications.
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10/15. Immune hydrops fetalis attributable to anti-HJK.

    We describe a new low-frequency antigen as the cause of immune hydrops fetalis in a fetus presenting at 27 weeks with a hematocrit of 6%. The fetus was treated successfully by intravascular transfusion. This antigen, temporarily identified as HJK, has been detected in only one family.
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