Perinatal mortality and morbidity is markedly increased in intrauterine growth restricted (IUGR) fetuses. Prenatal identification of IUGR is the first step in clinical management. For that purpose a uniform definition and criteria are required. The etiology of IUGR is multifactorial and whenever possible it should be assessed. When the cause is of placental origin, it is possible to identify the affected fetuses. The major complication is chronic fetal hypoxemia. By monitoring the changes of fetal vital functions it is thus possible to improve both management and outcome. The timing of delivery is crucial but the optimal management scheme has not yet been identified. When IUGR is identified at very early gestational ages, serial assessments of the risk of continuing the in utero fetal life under adverse conditions versus the risks of the prematurity should be performed. Delivery of IUGR fetuses should take place in centers where appropriate neonatal *This paper was produced under the auspices of the WAPM for a consensus on issues in perinatal practice, coordinated by Giampaolo Mandruzzato, MD. **Corresponding author: Giampaolo Mandruzzato, MD Via del Lazzaretto vecchio 9 34132 Trieste Italy E-mail: mandruzzatogiampaolo@tin.it assistance can be provided. Careful monitoring of the IUGR fetus during labor is crucial as the IUGR fetus can quickly decompensate once uterine contractions have started.
Objective: The terms early- and late-onset fetal growth restriction (FGR) are commonly used to distinguish two phenotypes characterized by differences in onset, fetoplacental Doppler, association with preeclampsia (PE) and severity. We evaluated the optimal gestational age (GA) cut-off maximizing differences among these two forms. Patients and Methods: A cohort of 656 consecutive singleton pregnancies with FGR was created. We used the decision tree analysis to evaluate the GA cut-off that best discriminated perinatal mortality, association with PE and adverse perinatal outcome (fetal demise, early neonatal death, neonatal acidosis at birth, and 5-min Apgar score <7). Results: We identified 32 weeks at diagnosis as the optimal cut-off, resulting in two groups with 7.1 and 0%, p < 0.001 perinatal mortality, 35.1 and 12.1%, p < 0.001 association with PE, and 13.4 and 4.6%, p < 0.001 composite adverse perinatal outcome. Abnormal versus normal umbilical artery (UA) Doppler classified two groups with 10.6 and 0.2%, p < 0.001 perinatal mortality, 50.0 and 11.8%, p < 0.001 association with PE, and 18.2 and 4.2%, p < 0.001 composite adverse perinatal outcome. Conclusions: UA Doppler discriminated better the two forms of FGR with average early- and late-onset presentation, higher association with PE and poorer outcome. In the absence of UA information, a GA cut-off of 32 weeks at diagnosis maximizes differences between early- and late-onset FGR.
Prematurity is associated with cerebral abnormalities that might account for poorer cognitive performance. The aim of our study was to investigate the correlations between corpus callosum reductions and neuropsychologic performance in adolescents who were born preterm. Twenty-five subjects born before 33 weeks' gestation were compared with 25 subjects born at term and of similar age, gender, and sociocultural status. All subjects underwent magnetic resonance imaging and neuropsychologic examinations. Premature subjects performed worse than controls in global cognitive functioning, verbal memory, and verbal fluency. Corpus callosum measurements showed a global reduction owing mainly to thinning in the splenium, posterior midbody, and genu. Corpus callosum size significantly correlated with gestational age, Wechsler Performance IQ, and memory performance. These results suggest that cerebral growth during infancy does not compensate for corpus callosum reduction and that this reduction reflects neuropsychologic deficit. The cognitive impairment can arise from the paucity of the complex interneuronal connections owing to fiber damage, particularly myelinated fibers.
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