Longitudinal observation of deterioration of Doppler parameters, computerized cardiotocogram and clinical course in a fetus with growth restriction

Abstract

We report on a fetus with intrauterine growth restriction detected at 27 weeks' gestation, who was longitudinally followed up until delivery by cesarean section 33 days later (31 + 5 weeks) due to severe decelerations in CTG. Longitudinal Doppler assessment of the umbilical artery (UA), the middle cerebral artery (MCA) and the main branch of the right pulmonary artery (RPA), the ductus venosus (DV) and the left coronary artery was compared to clinical course and computerized CTG. At first presentation (day--33) increased resistance in both the UA and uterine arteries with bilateral notches was found. Absent enddiastolic flow (AED) in the UA was found at day--19 and reverse flow (RED) at day--11. The MCA showed a decreased pulsatility first at day--19 and again at day--11 together with RED in the UA. The RPA initially (day--33) showed increased PI which returned to normal values at day--19 but increased again at day--1, when the DV showed RED and the coronary arteries became visible. The DV was normal until day--11, then its PI began to increase together with occurence of RED in the UA, but reverse flow in the DV occurred only on the eve (day--1) of severe decelerations in CTG. Short-term variability in computerized CTG was stable at 6 to 7 ms, except for an intermediate drop to 4 ms at day--10. Maternal hypertension was found at day--19 and mild preeclampsia developed at day--12. A reduction of fetal movements was noticed at day--5. This report shows that at 29 weeks gestation despite detection of AED resp. RED in the UA a prolongation of pregnancy for 19 resp. 11 days is possible. In addition to abnormal CTG, late signs of fetal deterioration are reverse flow in the DV and visibility of the coronary arteries. The role of increased resistance in the main branches of the pulmonary arteries should be examined in the future.

Arterial and Ductus venosus Doppler in Fetuses with Absent or Reverse End-Diastolic Flow in the Umbilical Artery: Longitudinal Analysis

“…Thus, whenever possible, sequential determinations as well as additional parameters such as the fetal heart rate curve should be considered. This is in alignment with a case report by Machlitt and co-workers [32] who described deterioration of a fetus over 33 days until delivery at 31 + 5 gestational weeks. In this case DV showed a transient normalisation after increased pulsatility was measured 10 and 7 days before reversed end-diastolic flow and fetal heart rate pathology required delivery.…”

Assessment of fetal pulmonary artery flow by Doppler echocardiography after antenatal corticoid therapy

“…Despite the elevation of the resistance in PA in cases with IUGR already reported [4], the indexes variation would not be significantly influenced by the presence of IUGR because in this data each subject is its own control on the evaluation of the drug on PA blood flow. The findings suggest that vasodilation might be associated to the mechanism of action for corticosteroid to accelerate fetal lung maturation.…”

Aquaporins in development – a review

“…There is evidence in the literature suggesting that fetuses suffering from severe intrauterine growth retardation (IUGR) show a progressive impairment of cardiac function, as demonstrated by reduced peak velocities at outflow tracts, decreased cardiac output and abnormal venous flow patterns [95-98]. Furthermore, in growth-retarded human fetuses the ventricular ejection force was equally decreased in both ventricles [95].…”

“…As it is a pure water channel one would suspect that it could regulate the rate at which cells might swell in osmotic stress, such as encountered in myocardial ischemia [98]. Such osmotic swelling is predicted to shorten the action potential, thus modulating the excitability of the heart.…”

“…Such osmotic swelling is predicted to shorten the action potential, thus modulating the excitability of the heart. It is known that cell swelling inhibits the action of some antiarrhythmic drugs [98]. AQP 4 is well established as a component of skeletal fast-twitch fibres [99] and the level of AQP4 is decreased by muscle denervation [100].…”