A 28-year-old woman, gravida 7, para 6, was referred at 21 weeks' gestation to our ultrasound unit because of bilateral fetal lower limb edema diagnosed previously. Ultrasonography showed a constriction ring around both legs, and, with the aid of color Doppler, arterial flow was demonstrated in both legs beneath the constriction ring. Subsequent examinations during the 24th and 28th weeks revealed absence of flow below the constriction ring of the right leg and decreased flow in the left leg. This was followed by the gradual bending, breaking and resorption of the tibia and fibula of the right leg. Between weeks 30 and 34, gradual shrinkage of the remains of the right leg beneath the knee was recorded by serial ultrasonic observations. At the 38th week of gestation, a male infant was born by normal vaginal delivery. Examination at birth revealed amputation of the right leg below the knee, with a denuded end of the stump. There was a partial amputation of the left leg below the knee, with tissue continuity being maintained by the posterior neurovascular bundle, and a posterior strip of skin. The left foot was extremely edematous, with an area of necrosis dorsally. This case afforded us the opportunity of in utero following of natural limb amputation in the amniotic band syndrome.

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Objectives Fetal gallbladder non-visualization on prenatal ultrasound in the second trimester is uncommon and in most cases

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The clinical significance of sonographically detected fetal hepatic hyperechogenicities has not been fully established. The aim of this study was to assess various aspects of fetal hepatic hyperechogenicities detected in utero, including natural history, prenatal investigation and pregnancy outcome. In a retrospective survey of pregnant women presenting to the ultrasonographic unit, five fetuses with a mean gestational age of 20 weeks (range 14-24 weeks) were antenatally diagnosed as having hepatic hyperechogenicities. All cases underwent extensive investigation to establish the etiology and to determine the spectrum of ultrasonographic presentation. In three fetuses, only parenchymal lesions were found, while two had combined lesions: parenchymal and peritoneal. The earliest prenatal ultrasonographic diagnosis was made at 14 weeks' gestation in a fetus with combined hyperechogenic lesions, which, at 12 weeks' gestation, demonstrated unexplained fetal ascites. Associated abnormalities were found in only one fetus in which a solitary parenchymal lesion was associated with direct communication of the intrahepatic portion of the umbilical vein with the right atrium, and high output cardiac failure. In this case, termination of pregnancy confirmed ischemic hepatic necrosis. In the other four cases, no direct etiology could be determined, and all four pregnancies continued to term with normal neonatal follow up until 12 months of age. The present data suggest that in cases of fetal hepatic hyperechogenicities, where apparent intrauterine infection or neoplasia can be ruled out, a vascular disruption phenomenon is a putative etiology. If there are no associated morphological abnormalities or abnormal karyotypes, the prognosis may be favorable.