Congenital malignant neoplasms are very rare with neuroblastomas, accounting for the majority of such tumors and frequently producing extensive metastases before birth.' The case presented here represents the first known sonographic demonstration of a metastatic neoplasm in utero. Important features of this case, which support the diagnosis of congenital neuroblastoma, include the presence of a solid neck mass, hydramnios, fetal hydrops, fetal tachycardia, and intractible maternal vomiting in the third trimester. CASE REPORTA 30-year-old white female, gravida 3 para 2 was admitted with a 3-week history of nausea and vomiting. Her early pregnancy and past medical history were unremarkable. By dates, her gestation was approximately 32 weeks. Total weight gain during her pregnancy was 22 pounds (10 kg) with an increase of 3 pounds since the previous monthly clinic visit. Physical examination revealed a blood pressure of 102432 mm Hg, pulse 140 with a regular rhythm, and no fever. Her tongue and skin were dry, suggesting mild dehydration. Fundal height measured 37 cm consistent with polyhydramnios. Hematocrit and blood chemistries, including blood urea nitrogen, were normal. Fetal heart rate was 180 beatdminute.Gray-scale ultrasonography revealed polyhydramnios, edema of the fetal scalp and body, and a solid mass in the region of the neck (Fig. 1). There were no dilated bowel loops, and the neural axis appeared intact and separate from the mass (Fig. 2). Fetal heart rate was recorded at 180-200 beatdminute, indicative of fetal tachycardia. The placenta was large and posterior in position. 512The patient was followed conservatively and given intravenous fluids. The next day a 2000-g stillborn female was spontaneously delivered. The symptoms of nausea and vomiting disappeared in the postpartum period.Postmortem examination revealed a severely macerated infant with marked edema and desquamation of the skin, especially of the face and scalp. A 7 x 7 x 6 cm firm mass extended across the entire neck, more prominent on the right side, and compatible with cervical lymphadenopathy (Fig. 3). The mass was solid, fleshy, and relatively avascular. Examination of the internal organs showed white tumor nodules studding the surface of the liver and kidneys. Necrotic tumor masses were present in the myocardium, right lung, kidneys, adrenals, and abdominal lymph nodes. The placenta was edematous but free of tumor. Sectioning of the umbilical cord demonstrated three vessels.Microscopic examination of the tumor nodules revealed sheets of small cells with scanty cytoplasm and pleomorphic nuclei demonstrating indentation of the nuclear membrane, clumping of chromatin, and multiple prominent nucleoli. The pathological diagnosis was congenital metastatic neuroblastoma. DISCUSSIONNumerous causes of fetal neck masses have been demonstrated by ultrasound. These include meningocele, encephalocele, cystic hygroma, cervical teratoma, epignathus, and "pseudo" mass due to an abnormal twin gestational sac. Sabbagha stresses the value of first asses...

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Sonographic examination of the gallbladder in two patients with preeclampsia and right upper quadrant pain demonstrated notable thickening of the gallbladder wall. The sonographic abnormality and clinical symptoms completely resolved after delivery and/or medical management of the preeclampsia. This finding is probably secondary to the hypoalbuminemia characteristic of preeclampsia and should not be mistaken for intrinsic gallbladder disease.

The nephrogram is a sensitive indicator of renovascular compromise. An infrequently reported but characteristic nephrographic abnormality is the cortical rim nephrogram. This "rim sign" refers to a thin nephrographic rim outlining a kidney with an otherwise faint nephrogram. We report 2 patients with this nephrographic appearance due to acute renal artery insult. The rim nephrogram is a reliable sign of underperfusion of the kidney. It is dependent on collateral capsular vessels supplying the outer renal cortex. Underperfusion can be due to a primary renal artery problem or secondary to compromise of renal artery perfusion because of elevated interstitial or tubular pressure in the kidney. The sign has not been described with systemic circulatory problems.