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A case of vaginal listeriosis occurring in the sixth month of pregnancy is reported. It was discovered when the patient suffered from symptoms of appendicitis complicated by jaundice and an acute nephritis. It was investigated by vaginal smears and swabs, and by amniocentesis. Treatment was general and local. The fetus was not attacked, the pregnancy continued, resulting in the delivery and birth of an undamaged infant.
The fetal kidneys and bladder are usually visible by 15 weeks' gestation on sonograms. The authors present their experience with the diagnosis of renal abnormalities in the fetus.
Fetal echocardiography has proved a useful tool for prenatal detection of cardiac lesions and the diagnosis--and, in some cases, the treatment--of fetal arrhythmias. It is particularly indicated for mothers from high risk groups. Management of diagnosed heart disease leads either to termination of pregnancy or to optimal postnatal care for the baby and the mother.
The outcome of cardiac disease diagnosed before birth is paradoxically worse than that diagnosed postnatally. In part, this is because fetal screening detects cases that are already showing failure of cardiac growth which are usually progressive with secondary damage to the myocardium, lungs and brain. Fetal valvuloplasty has been proposed for cases of critical aortic and pulmonary stenosis or atresia, and atrial septostomy for a restrictive oval foramen associated with aortic stenosis, hypoplastic left heart syndrome and transposition of the great arteries. The rationale for fetal therapy is to restore forward flow and reduce intraventricular pressure, thus improving coronary perfusion and minimizing ischaemic damage. Successful valvuloplasty has reduced systemic venous pressures and reversed fetal hydrops, thus prolonging pregnancy. It has resulted in improved ventricular growth in some cases and spontaneous opening of a closed oval foramen with normalization of pulmonary venous waveforms. These signs suggest better fetal cardiopulmonary development and improved surgical outcomes.
UNLABELLED: M-mode, 2DE and PDE were performed on 630 fetuses of high risk pregnancies. Fetal gestation ages ranged from 16 to 41 weeks. 21 cases of fetal heart disease were detected during pregnancy. The detected rate of fetal cardiac disease with echocardiography in high-risk pregnancies was 3.3%. In total 21 cases of fetal cardiac disease including 3 cases of atrial septal defect, 5 ventricular septal defect, 3 fetal non-immuno hydrops with pericardial effusion, 2 atrioventricular canal defect, 2 cardiac tumor (one rhabdomyoma, another lipoblastoma), an endocardial fibroelastosis, pulmonary stenosis, a single atrium with single ventricle, a hypoplastic left ventricle with single atrium and pulmonary atresia, a hypoplastic right ventricle with pulmonary atresia and a truncus arteriosus were found. 19 cases of fetal cardiac disease were confirmed at autopsy and other two by auscultation and echocardiography after delivery. The significant high-risk factors were bradycardia in 6 cases, non-immuno hydrops in 5 cases and virus infection at early pregnancy in 3 cases. CONCLUSION: (1) 2DE and PDE are the most valuable non-invasive technique for detection of fetal structural cardiac abnormalities. (2) Sustained bradycardia, non-immuno hydrops and virus infection at early pregnancy were the significant high-risk factors of fetal heart disease. Fetal non-immuno hydrops may present congestive cardiac failure in the uterus.
Intrauterine fetal transfusion is currently the therapy of choice in cases of severe anti-D isoimmunisation. However, its efficacy is reduced in patients with early severe hydrops fetalis due to the technical difficulties in performing this procedure before 20 weeks' gestation. The purpose of this study was to determine whether early onset of high-dose gammaglobulin therapy followed by intrauterine transfusions (IUTs) is more effective than IUTs alone in the treatment of very severe isoimmunised fetuses. The population studied in this retrospective clinical research was assigned to one of the following two groups: 1) Gamma group: 30 patients receiving gammaglobulin therapy before 21 weeks' gestation and IUTs after 20 weeks; or 2) IUT group: 39 patients receiving IUT treatment starting at a gestational age of 20-25 weeks. Both groups were statistically similar regarding history of perinatal deaths and anti-D antibody titers. The number of hydropic fetuses at the first IUT and of fetal deaths were significantly higher in the IUT than in the Gamma group. No significant differences were observed between the groups in fetal hematocrit at first IUT and at birth. However, the percentage of severely anemic fetuses was higher in the IUT group. Fetal mortality rate was 36% less in the Gamma group. Our results suggest that high-dose gammaglobulin therapy followed by IUTs may improve fetal survival in these severe cases. Further randomised clinical trials are needed to confirm these results.
Fetal echocardiography has had a significant impact on the diagnosis and management of congenital heart disease. Although the fetal circulation is quite forgiving for many heart lesions, other flow abnormalities gravely affect fetal physiology. Serial studies have given us a window to observe the natural history of many lesions that progress during gestation. Although fetal cardiac surgery is not yet a viable alternative to neonatal repair, fetal intervention on noncardiac disorders has had limited success and the field is growing. Fetal diagnosis remains an integral part of the management of children with cardiac lesions.
Fetal echocardiography is a detailed examination of the fetal heart, its anatomy and function, performed with high frequency, high-resolution ultrasound probes. Advancements in echocardiographic technology have made possible accurate diagnosis of complex cardiac defects from a transabdominal approach, as early as 14-18 weeks of gestation, although optimal images are usually acquired at 20 weeks of gestation. Indications for fetal echocardiogram are maternal or fetal factors that place the fetus at increased risk for having heart defect but suspected cardiac abnormality on a level 1 scan is the most frequent referral indication and the one indication with the highest yield of positive fetal echocardiogram. Diagnosis of fetal heart disease can have major influences on the prenatnal and postnatal management and enables parents to prepare and plan for the birth of a child with a cardiac defect.
Fetal cardiology includes the assessment of the fetal heart for congenital heart disease (CHD) and arrhythmias, the management of affected fetuses, including parental counselling for the therapeutic options, the planning of the delivery and the postnatal care. This requires a close collaboration between obstetricians, neonatologists and pediatric cardiologists. Because of restricted financial sources extensive fetal echocardiographic assessment is reserved for pregnancies with increased risk for CHD, which includes a family history of CHD, suspicion of a cardiac or extracardiac fetal abnormalities at obstetric routine ultrasonography, fetal arrhythmias and chromosomal anomalies. Since most CHD occur in pregnancies without increased risk an ultrasound screening of the fetal heart during routine pregnancy ultrasound is recommended. Most forms of CHD can potentially be detected in utero, especially the severe ones with considerable fetal and postnatal morbidity and mortality. The prenatal diagnosis of a major cardiac malformation requires further assessments for extracardiac and chromosomal disorders. The deliveries of patients with major cardiac anomalies in a tertiary obstetric center close to a pediatric cardiac facility allows optimal perinatal and postnatal management. This may be of crucial importance for cardiac malformations which are arterial duct dependent postnatally. Many CHD have genetic causes. Well established is the association of CHD and the trisomies 13, 18 and 21, as well as the monosomy XO (Turner syndrome). During the last years more and more molecular genetic causes for CHD could be demonstrated. The most significant one is the microdeletion 22q11 syndrome (CATCH 22 syndrome), which is associated with different conotruncal anomalies. Also for various other congenital cardiac malformations and syndromes a genetic cause could be demonstrated. The search for genetic cofactors is important as it affects parental counselling and patient care.
Between January 1985 and November 1990, 128 pregnancies complicated by maternal red blood cell alloimmunization were referred to our Fetal Diagnosis and Treatment Unit. We examined the premise that an evaluation of fetal blood would accurately identify fetuses at risk of requiring antenatal transfusion therapy. Two hundred seventy-two diagnostic cordocenteses were performed. Criteria for the timing of repeat cordocenteses were developed retrospectively on the basis of the fetal hematocrit values, reticulocyte counts, and direct Coombs' test results of the first 84 pregnancies. These criteria were tested and confirmed prospectively on the next 44 pregnancies. On the basis of the first blood sample, four hematologic patterns (and their distributions) were identified in the 98 antigen-positive fetuses. Pattern 1: fetuses at low risk of having significant antenatal anemia (hematocrit less than 30%) (n = 11, 11%). These fetuses had normal hematocrit values and reticulocyte counts coupled with negative or trace-positive direct Coombs' test. No fetus in this group had significant antenatal anemia. Pattern 2: fetuses at intermediate risk of having anemia (n = 29, 31%). Pattern 2 fetuses had normal hematocrit values and either direct Coombs' titers of more than trace less than or equal to 2+ and normal reticulocyte counts or low reticulocyte counts (less than 2.5th percentile for gestation). Twenty-one percent (n = 6) of fetuses in pattern 2 had significant antenatal anemia. Patterns 3 and 4: fetuses at greatest risk of having severe anemia. These fetuses had normal hematocrit values associated with either reticulocyte counts greater than 97.5th percentile for gestation or a direct Coombs' test greater than or equal to 3+ (pattern 3, n = 49, 50%) or both, or a mild anemia (greater than 30% but less than 2.5th percentile for gestation) (pattern 4, n = 9, 10%). Eighty percent (n = 39) of fetuses with pattern 3 and 90% (n = 8) with pattern 4 developed a hematocrit value less than 30%. We conclude that evaluation of fetal hemolytic disease with a fetal blood specimen permits the identification of fetuses at high risk of having antenatal anemia.
Fetal blood sampling under ultrasound guidance has added a new dimension to the management of Rh hemolytic disease. Combined with the established parameters of history, antibody measurement and amniotic fluid delta OD450 readings, direct testing of the blood of the fetus completes the picture. As well as giving information that may be applied to decisions regarding management, an opportunity is provided to observe the mechanism of anti-D IgG-induced red cell destruction in vivo.
Fetal echocardiography provides an opportunity to diagnose congenital heart disease as early as the midtrimester of pregnancy, allowing for proper planning of perinatal care and counselling of the parents. This paper reviews the accuracy and outcomes of fetal cardiac ultrasound studies at The Prince Charles Hospital over the past 4 years. A total of 43 fetuses, of gestational ages 16-39 weeks, were studied. The indications for these were: previous sibling with cardiac anomaly (16 cases); abnormal heart on obstetric ultrasound scan (USS) (13 cases); abnormalities found on obstetric USS with normal appearing heart (one case); fetal bradycardia (seven cases); fetal tachycardia (four cases); irregular fetal heart beat (two cases). At birth all fetuses assessed because of a previously affected sibling were normal. Of the 13 referred because of structural heart lesions suspected on obstetric USS, eight were abnormal, four were normal and one was terminated without autopsy. Important rhythm disturbances occurred in nine of the 11 referred because of abnormal heart rates. One false positive diagnosis of a possible coarctation was made, and in four cases an abnormality was noted on USS but the diagnosis was not completely correct. Nine of the 19 infants with abnormalities detected have died. Fetal echocardiography is an accurate and useful method of diagnosing congenital heart disease in utero. Although the mortality of affected fetuses is high, antenatal diagnosis allows planning of medical care and offers the greatest chance of a successful outcome.
Fetal behaviour as an intrauterine patient is unknown. In the diagnosis of sexually transmitted diseases (STD) and in the criteria for treatment only the mother is considered leaving the fetus out. The presence of immunoglobulin M in the amniotic fluid is an indicator of fetal infection and could allow an accurate diagnosis of fetal disease or treatment, if the measurement is related to the presence or absence of organism in the amniotic fluid. In this way, the study of fetal behaviour under these conditions could be done. The objective of this research was to determine the presence of STD organism in the amniotic fluid of the STD infected pregnant women and to evaluate the prevalence and evolution of these pathologies in the fetus. No STD organism, nor immunoglobulin M were found in the 13 samples of amniotic fluid (8 pre and 5 post-treatment) of infected pregnant women. The presence of microorganisms and its relation to immunoglobulin M was not observed. More cases are needed to arrive to a conclusion regarding fetal immunology and to a better understanding of antibacterial properties of the amniotic fluid. We concluded that no contamination in the amniotic fluid or fetal infection was found in pregnant women with STD.
Fetal and maternal thyroid function are working independently under physiologic conditions. In case of maternal autoimmune hyperthyroidism during pregnancy there is an up to 12% chance for the fetus to develop thyroid dysfunction, mediated by the transplacental passage of maternal immunoglobulins directed against TSH receptors in the fetal thyroid gland. This may lead to intrauterine growth retardation, craniosynostosis, preterm delivery, perinatal death, etc. Sonography and fetal blood sampling provide important information to detect fetuses at risk and allow intrauterine therapy. Furthermore prenatal diagnosis is important in case of maternal antithyroid drug ingestion possibly leading to fetal hypothyroidism and goitre. The cooperation of specialists for internal and fetal medicine is required for the management of maternal thyroid disease in pregnancy.
Fetal echocardiography allows for early detection of congenital heart disease, and pregnancy termination may be an option in cases of complex defects. In the current study, the most important factors contributing to the diagnosis and termination of affected pregnancies are reviewed and their combined effect on the future prevalence of liveborn congenital heart disease is evaluated. The relative reduction of the prevalence of the most severe forms of congenital heart disease is estimated as the product of the probability that (1) a fetal cardiac screening is performed (p (evaluation)), (2) an affected pregnancy is detected (P (detection)), (3) pregnancy termination is decided following antenatal diagnosis (P (decision)). In areas where termination of pregnancy is a realistic and supported option, a universal sonographic screening of all pregnancies (P (evaluation) = 1), with an average reported sensitivity of 35% and a termination rate of 43% following antenatal diagnosis, would result in a 15% overall reduction of the prevalence of the most severe forms of congenital heart disease. However, wide variability exists regarding the defect-specific estimates (2-50% prevalence relative reduction) due to considerable differences in the reported diagnostic sensitivity and termination rates associated with each heart defect. If an earlier diagnosis could be achieved, which is reported to be associated with an average 1.4-fold increased probability of termination, the overall reduction of the prevalence of congenital heart disease could approach 21%. As the skills of obstetric and pediatric cardiology sonographers improve, fetal echocardiography is expected to have a substantial impact on the future epidemiology of liveborn congenital heart disease.
We report out experience in the perinatal management of a complex case of fetal hemolytic disease primarily due to Rhesus incompatibility combined with fetal alloimmune thrombocytopenia. The lowest fetal hemoglobin and platelet levels were 2.6 g/dl and 13,000/microliter, respectively. Intrauterine treatment consisted of six transfusions of packed red cells into the umbilical vein and one transfusion of platelets. The neonate required four transfusions of packed red cells to correct her hyporegenerative erythropoiesis. Postnatal management also included one platelet transfusion, intravenous immunoglobulins and erythropoietin. Although some degree of fetal thrombocytopenia may invariably be found in fetal red cell incompatibility, other rare causes need to be excluded.
Fetal hemoglobin (HbF, alpha2gamma2) decreases polymerization of sickle hemoglobin, and high levels correlate with decreased morbidity and mortality in sickle cell disease (SCD). Therefore, a therapeutic goal for patients with SCD is pharmacologic reactivation of HbF. Decreased HbF production is associated with DNA methylation (by DNA methyltransferase [DNMT]) at the gamma-globin (HbF) gene promoter. The cytosine analogs 5-azacytidine and 5-aza-2'-deoxycytidine (decitabine) hypomethylate DNA by inhibiting DNMT. In early studies, 5-azacytidine produced significant HbF elevations in patients with thalassemia and SCD, but clinical development of this class of agent was halted after a poorly controlled animal study suggested that 5-azacytidine might be carcinogenic. However, the majority of preclinical studies with decitabine have suggested a chemopreventive rather than carcinogenic effect. Furthermore, decitabine, unlike 5-azacytidine, does not incorporate into RNA and is a more directed DNA-hypomethylating agent. Therefore, we have pursued studies of decitabine to pharmacologically reactivate HbF in patients with SCD. In phase I/II studies, decitabine at DNA-hypomethylating, but noncytotoxic, doses was well tolerated and effective at increasing HbF and total hemoglobin levels both in patients who had and had not responded to prior hydroxyurea therapy. In treated patients, there were marked improvements in a range of surrogate clinical endpoints measuring red blood cell adhesion, endothelial damage, and coagulation pathway activity. Pharmacologic reactivation of HbF through DNA hypomethylation holds promise as an effective disease-modifying intervention for patients with SCD. Larger studies are required to confirm the safety and effectiveness of decitabine with chronic use, and to more clearly establish its role in patients with SCD.
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