In fetuses with idiopathic growth restriction, 1) low birth weight, 2) umbilical artery reversed flow, and 3) ductus venosus absent or reversed flow are associated with an increased perinatal morbidity and mortality.

The summary of data regarding diagnostic specificity and sensitivity of TVS in women undergoing surgery for deep endometriosis may allow us to conclude that TVS should remain the first-line method in the evaluation of patients with suspicion of DPE. When TVS is insufficient, second-line "modified-techniques" should be considered. Choosing the most effective technique is a challenge and should be based on patient history and clinical signs/symptoms.

Intrauterine growth retardation is a pathology which is found in 3–10% of all pregnancies and it is associated with around 20–25% of all fetal intrauterine deaths and with long-term neurologic sequelae. It presents an increased risk of distress during labor and delivery and a greater risk of perinatal mortality. The causes of IUGR and the cardiac and venous Doppler in normal fetuses are analyzed, and the hemodynamic cardiac modifications in IUGR fetus are discussed. The fetal cardiac function in intrauterine growth retardation shows a redistribution of the fetal cardiac output, which tends to favor the left ventricle as the mechanism to compensate for the uteroplacental insufficiency. The Doppler velocity indices are modified as the fetal condition progressively deteriorates and they represent an important tool for the management of the complicated pregnancy.

Activin A levels are elevated in maternal serum of pregnant women with hypertensive disturbances. Because follistatin is a circulating binding protein for activin A, the present study was designed to evaluate whether serum follistatin and activin A levels also change in patients with hypertensive disorders in the last gestational trimester. The study design was a controlled survey performed in the setting of an academic prenatal care unit. Healthy pregnant women (controls, n=38) were compared with patients suffering from pregnancy-induced hypertension (PIH, n=18) or pre-eclampsia (n=16). In addition, the study included a subset of patients with pre-eclampsia associated with intrauterine growth restriction (IUGR, n=5). Maternal blood samples were withdrawn at the time of diagnosis (patients) or in a random prenatal visit (controls), and serum was assayed for follistatin and activin A levels using specific enzyme immunoassays. Hormone concentrations were corrected for gestational age by conversion to multiples of median (MoM) of the healthy controls of the same gestational age. Follistatin levels were not different between controls and patients, while activin A levels were significantly increased in patients with PIH (1·8 MoM), pre-eclampsia (4·6 MoM), and pre-eclampsia+IUGR (3·2 MoM, P<0·01, ANOVA). The ratio between activin A and follistatin was significantly increased in patients with PIH (1·5 MoM) and was further increased in patients with pre-eclampsia (4·5 MoM) and in the group with preeclampsia+IUGR (2·6 MoM). Follistatin levels were positively correlated with gestational age in control subjects (r=0·36, P<0·05) and in patients with PIH (r=0·46, P<0·05) or pre-eclampsia (r=0·61, P<0·01), while activin A correlated with gestational age only in the healthy control group (r=0·69, P<0·0001). The finding of apparently normal follistatin and high activin A levels in patients with PIH and pre-eclampsia suggests that unbound, biologically active, activin A is increased in women with these gestational diseases.

Prophylactic oxytocics should be offered routinely in the third stage of labor in all women. The prophylactic use of uterotonics should be individualized.