A series of 15 monochorionic twins with a great variety of cerebral lesions is reported. Seven cases illustrate the classical situation: the recipient twin was affected and his co-twin, the donor was macerated. In 5 cases, the lesions were described in the donor twin as well and once, as early as 22 weeks. The lesions were usually hypoxic-ischemic, in 2 they were hemorrhagic. In 1 case there was a malformation. Fetal US were performed in 11 cases and the diagnosis of either IUGR, death of a fetus and/or brain lesions in the survivor could be made in 10 cases and once as early as 21 weeks. In fetuses born alive, transfontanellar US or CT scan have confirmed the diagnosis made on fetal US. The pathogenesis of the lesions is not fully understood. Lesions in the recipient twin may result from emboli or thromboplastic material originating from the macerated co-twin. We suggest that blood pressure instability or episodes of severe hypotension might as well lead to brain and/or visceral lesions in the recipient twin. In the donor, the lesions result from hypotension and/or anemia. With improvement and generalization of imaging techniques, the vitality of the fetuses as well as biometric parameters and anatomical structures will be better controlled. However, in case of a fetal death, occurrence of lesions in the survivor is unpredictable and no uniform policy has been proposed yet. Studies with Doppler and continuous monitoring of funicular circulation should improve our knowledge on feto-fetal transfusion and permit to detect hemodynamic fluctuation or impairment.

Umbilicoportosystemic shunts encompass different congenital vascular abnormalities that should be recognized because they may interfere with fetal growth and circulation.

Mesoblastic nephroma (Bolande's tumour) is a rare renal tumour, but, overall, is the most frequent benign renal tumour in childhood and the most frequent renal tumour during the first year of life. It is increasingly diagnosed with US during the fetal period. We report the findings of two patients who showed the "ring" sign, an anechoic ring surrounding the tumour and typical of mesoblastic nephroma. We identified a Doppler signal in the ring in both cases, and pathology confirmed the vascular origin of this sign.

Mosaic tetrasomy 12p is a dysmorphic syndrome which has been described under the name of Pallister mosaic syndrome and Teschler‐Nicola/Killian syndrome and has sometimes been incorrectly interpreted as tetrasomy 21. Here we report the first case to be diagnosed prenatally and confirmed by enzyme assays, and we summarize the clinical and biological characteristics of all the cases reported so far under various names.

The aim of this study was to specify the sonographic, anatomical and morphological aspects of the fetal anal sphincter and to compare them with pathological and physiological findings. The sphincter was examined by serial sectioning and staining of embryo and fetal tissue and by real-time ultrasound. Its function was analysed using amniotic fluid digestive enzyme assays in cases of anorectal atresia and cystic fibrosis. Morphological findings indicate that the functional components of the anal sphincter do not differentiate before 30 weeks and therefore do not account for the observed anal continence at 22 weeks. Ultrasound measurements of the sphincter indicate three developmental phases: 1) slow growth from 14 to 19 weeks; 2) rapid growth from 19 to 30 weeks; 3) subsequently, no further increase, but contractions indicative of peristaltism. Amniotic fluid digestive enzyme assays indicate that anal sphincter maturation begins with perforation of the anal membrane at 12 weeks. Comparison of pathological cases (anorectal atresia and cystic fibrosis) suggests two possible explanations of fetal anal obstruction: increasing viscosity of digestive secretion or the presence of the three anal sphincter muscles, even if still immature. Our results clarify the evacuation and retention of meconium during fetal life and the role of the terminal part of the digestive tract, notably the anal sphincter. Prenatal diagnosis of anorectal atresia is therefore possible before 20 weeks of gestation by measurement of amniotic fluid digestive enzymes and ultrasonography, thus enabling better neonatal management.