First-trimester and early second-trimester diagnosis of nuchal cystic hygroma by transvaginal sonography: diverse prognosis of the septated from the nonseptated lesion.

Fetal cystic hygroma is a congenital malformation of the lymphatic system appearing as a single or multiloculated fluid-filled cavity, most often in the nuchal region. The malformation is believed to arise from failure of the lymphatic system to communicate with the venous nuchal system. Sometimes the lesion progresses to fetal hydrops, causing fetal death. To further delineate the cause and natural history of this disorder, we have prospectively studied eight cases of cystic hygroma of the neck, detected at gestational ages of 9 to 15 weeks by transvaginal sonography. Three of the eight fetuses survived (37.5%) and were normal at birth. Either hydrops fetalis or intrauterine fetal death occurred in the other five fetuses. In one of these five, therapeutic abortion was induced because of trisomy 21. In another fetus of these five, trisomy 18 was diagnosed by amniocentesis. This pregnancy ended in intrauterine fetal death. The ultrasonic evaluation of the cystic hygromas revealed that those that were reabsorbed in the three ultimately normal viable fetuses were nonseptated cysts, whereas all the four cystic hygromas ending in fetal death or associated with aneuploidy were septated, multilocular hygromas. In another fetus with nonseptated hygroma, nonimmune hydrops developed, which resulted in premature delivery and early neonatal death.

Meconium peritonitis due to meconium ileus presenting as fetal ascites: a case report.

A case of meconium peritonitis due to meconium ileus is described. The condition was detected antenatally as fetal ascites on ultrasonography. Plain X-ray of abdomen post-natally showed specks of calcification mainly at the flanks, while on ultrasonography specks of high echogenic areas were seen throughout the abdomen which has been described as "snow-storm sign". The aetiology of meconium ileus is briefly discussed.

Atraumatic antepartum subdural hematoma causing fetal death.

A case of atraumatic antenatal fetal subdural hematoma, severe enough to cause death, is reported. Although it is often associated with traumatic delivery, its occurrence before labor suggests that assumptions of causation require some medical investigation or corroboration before trauma is accepted as the etiologic factor.

Fetal lung growth in laryngeal atresia and tracheal agenesis.

Three cases of airway obstruction in fetuses born at 21, 32 and 40 weeks gestation are reported. The first had laryngeal atresia, cystic dysplastic kidneys, oligohydramnios and immense fluid-filled lungs. The second had upper tracheal agenesis, a tracheo-oesophageal fistula, a cystic dysplastic horseshoe kidney, oligohydramnios and normal-sized lungs. The third had a pin-hole mucosal tract through an otherwise atretic larynx, normal kidneys, no oligohydramnios and normal-sized lungs. Lung weight:body weight ratios, radial alveolar or radial canalicular counts and point-counting of sections of lungs in cases 1 and 2 show that laryngeal or tracheal obstruction may prevent or reduce the pulmonary hypoplasia associated with renal dysplasia, and in cases 2 and 3, that grossly enlarged, hyperplastic lungs may not be seen unless obstruction is complete.

Fetal urine output in hydramnios.

Fetal urine output was evaluated in 12 pregnancies complicated by hydramnios. Six of these pregnancies were twin gestations with markedly elevated fetal urine output of the hyperperfused fetus. All six fetuses had urine output greater than the 95th percentile for their gestational age. These six patients were evaluated prior to and during the 29th week of pregnancy. Three singleton gestations had upper gastrointestinal obstruction and normal fetal urine output of 18.7, 18.0, and 12.3 mL/hour at 35, 35, and 31 weeks' gestation, respectively. Markedly elevated fetal urine output of 18 mL/hour (tenth to 95th percentile at 26 weeks, 4-7 mL/hour) was present in one fetus that was subsequently found to have diabetes insipidus. The remaining two singleton pregnancies with idiopathic hydramnios had upper limits of normal fetal urine output of 10 and 13 mL/hour at 31 and 32 weeks, respectively. It appears that hydramnios may be the result of polyuria of the hyperperfused twin in cases of twin-twin transfusion or diabetes insipidus. In upper gastrointestinal obstruction or idiopathic hydramnios, increased fetal urination does not appear to be present.

Fetal bradycardia during antepartum testing. Further observations.

One hundred twenty-one cases of antepartum fetal bradycardia, occurring at 36 weeks' gestation or greater, were prospectively managed by active intervention and delivery. There were no fetal deaths. Intrapartum complications were similar at all gestational ages, regardless of whether the bradycardia was associated with a reactive or nonreactive nonstress test. Only the incidence of low five-minute Apgar scores was significantly higher in the nonreactive group. The incidence of cord compression patterns (variable decelerations) in labor was higher than that of uteroplacental insufficiency patterns (late decelerations). Intervention with delivery in the presence of fetal bradycardia should be considered in all cases with evidence of fetal lung maturity.

A case of recurrent infantile polycystic kidney associated with hydrops fetalis.

Nonimmune hydrops fetalis is becoming a predominant form of fetal hydrops due to the declining incidence of immune hydrops fetalis triggered by Rh isoimmunization. Infantile polycystic kidney appeared to be related to hydrops fetalis whether it is causal or merely coincidental and may represent another entry to differential diagnoses. Infantile polycystic kidney was diagnosed by an elevated maternal serum alpha-fetoprotein (AFP) value coupled with an ultrasonographic abnormality scanned as a multicystic mass with ascites in the fetal abdomen antenatally. This study presents a case of infantile polycystic kidney that resulted in a stillborn baby with hydrops fetalis and extensive placental calcification; it was the first case in Korea in which nonimmune hydrops fetalis was associated with infantile polycystic kidney in consecutive siblings by autosomal recessive inheritance in one family. In addition, this paper comprehensively reviews the incidence, etiology, prenatal diagnosis and proper management of nonimmune hydrops fetalis.

Fetal atrial septal aneurysm: a cause of fetal atrial arrhythmias.

Atrial arrhythmias are commonly found during fetal echocardiography performed during pregnancy to evaluate fetal arrhythmias. An association between atrial arrhythmias and an atrial septal aneurysm has been noted in children and adults. In this study, 105 fetuses were evaluated by fetal echocardiography, 39 (37%) referred to evaluate fetal arrhythmia and 66 (63%) to rule out congenital heart disease. An atrial septal aneurysm was found in 42 (40%) of the fetuses and an atrial arrhythmia in 37 (35%). An atrial septal aneurysm was found in 25 (64%) of the 39 fetuses referred to evaluate a fetal arrhythmia compared with only 17 (26%) of the 66 fetuses referred to rule out congenital heart disease. In this study, the association of an atrial septal aneurysm with an atrial arrhythmia was highly significant (p less than 0.001).

Prenatal gastric dilatation and infantile hypertrophic pyloric stenosis.

Fetal sonography showed persistent gastric dilatation with no other abnormalities. Following uneventful pregnancy and delivery, the patient presented with typical clinical and radiologic features of infantile hypertrophic pyloric stenosis. Literature review indicates that this association was never reported.

Erythroblastosis and reticulocytosis in anemic fetuses.

The fetal blood erythroblast and reticulocyte counts were determined in umbilical cord samples obtained at 17 to 36 weeks' gestation from 127 pregnancies complicated by red blood cell isoimmunization. The reticulocyte count increased linearly with fetal anemia, and the erythroblast count increased exponentially. Significant erythroblastosis was observed only when the hemoglobin concentration deficit was greater than 7 gm/dl. Of the 52 fetuses with a hemoglobin concentration deficit greater than 7 gm/dl, 35 had ultrasonographic evidence of hydrops. These data suggest that medullary hematopoiesis is stimulated by mild anemia and that recruitment of extramedullary sites occurs when anemia is severe. Extensive hepatic erythropoiesis may be the cause of fetal hydrops in red blood cell isoimmunization.

Fetal renal failure associated with intrauterine growth retardation.

Four preterm infants with severe intrauterine growth retardation had renal failure from birth. The amount of asphyxia associated with the birth process did not fully explain the renal failure. Before delivery all for fetuses had severe oligohydramnios and an empty urinary bladder. These observations strengthen the view that severe intrauterine growth retardation may be accompanied by oligohydramnios caused by fetal renal failure.

Congenital hydrocephalus secondary to prenatal intracranial haemorrhage.

A high incidence of intracranial haemorrhage in utero of uncertain aetiology has been previously identified as an important cause of stillbirth in infants of immigrant Pacific Islanders in New Zealand. Congenital hydrocephalus is now described as a consequence of intracranial haemorrhage in 2 stillborn Pacific Islander infants. A large intracerebral haemorrhage, hydrocephalus and hydrops in one infant was first recognized prenatally by ultrasonography and caused intrauterine death at 26 weeks' gestation. Severe hydrocephalus in the other infant was first identified just before labour at term but the pathological findings were of old intraventricular haemorrhage with narrowing of the aqueduct of Sylvius as a reaction to the haemorrhage. Prior intracranial haemorrhage may be the cause of an increased incidence of hydrocephalus in Pacific Islander stillbirths and of some otherwise unexplained cases of congenital hydrocephalus in other races.

Changes in the long bones due to fetal immobility caused by neuromuscular disease. A radiographic and histological study.

The long bones in eleven newborn infants who had neuromuscular disease were studied and were found to be thin, hypomineralized, and elongated. In most of the bones, there were multiple diaphyseal or metaphyseal fractures, or both. By light microscopy, the outstanding findings were fractures through the growth plate and diaphysis and thinning of the cortices. The etiology of the fractures and the insufficient substance of the bone is the reduction in the intrauterine motion of the fetus, which leads to fragility of the bones and contractures of the joints. The severity of the alterations may have been related to the time of the onset of the abnormalities and to the duration and degree of the intrauterine akinesia.

Antenatal origin of neurologic damage in newborn infants. I. Preterm infants.

Currently, the diagnosis of white matter necrosis may be performed with echoencephalography when cysts are observed in the white matter adjacent to the lateral ventricles. One hundred twenty-seven infants with a gestational age less than 36 weeks (mean [+/- SE] gestational age = 31 +/- 3.2 weeks) were studied in the neonatal period with echoencephalography to determine the incidence of white matter necrosis and the perinatal variables associated with this complication. Twenty-three infants (18.3%) had white matter necrosis. Thirteen (10.3%) had cysts by day 3 (11 on day 1), indicating that the onset of white matter necrosis occurred antenatally. The incidence of antenatal white matter necrosis was inversely related to birth weight and was more frequent in infants weighing less than 1000 gm (19%). Stepwise logistic regression analysis of 31 antenatal variables showed that placental vascular anastomoses in multiple pregnancies, funisitis, and purulent amniotic fluid were the only complications associated with antenatal white matter necrosis. Follow-up neurologic evaluations were abnormal in four of six patients with antenatal white matter necrosis. The findings in this study focus attention on prenatal, rather than intrapartum and postnatal, factors as causative agents of neurologic morbidity and emphasize the importance of early and sequential evaluation of neonatal brain structures.