Detection of intrauterine growth retardation: a new use for sonographic placental grading

Intrauterine growth retardation (IUGR) is a major source of perinatal death and long-term neurobehavioral morbidity, but its diagnosis antenatally remains difficult. Advanced placental maturity (Grade III), as determined on ultrasound examination, has previously been reported to be a marker of term gestation. In this study of 109 pregnancies which resulted in the birth of infants weighing less than or equal to 2,700 gm, the hypothesis that a Grade III placenta, according to Grannum's classification, can differentiate small-for-gestational age (SGA) infants from small non-SGA infants was tested. Of the study patients, 44 had Grade III placentas and 65 had non-Grade III (0, I, II) placentas within 1 week of delivery. The presence of a Grade III placenta was followed by the delivery of a SGA infant 59% of the time, and 62% of the SGA infants could be correctly identified (p less than 0.001). The association of a Grade III placenta and SGA birth was maintained in patients at less than or equal to 34 weeks of gestation--Grade III placenta was significantly related to the delivery of SGA infants with a true positive rate of 62% and a sensitivity of 66% (p less than 0.008). These results were consistent with the concept that for small fetuses documentation of "maturity" can be used to discriminate those with IUGR from those without this problem. Furthermore, placental "maturation," as detected sonographically, appears to be accelerated in association with IUGR, consistent with the anatomic concept of premature placental senescence. Thus, in situations in which the fetus is known to be small, sonographic grading of the placenta may be helpful in detecting IUGR.     

Apoptosis in the placenta of pregnancies complicated with IUGR.

OBJECTIVE: In this study we have investigated the presence of apoptosis in the placental tissue of pregnancies complicated with intra-uterine growth restriction (IUGR). METHOD: Placental samples were obtained from 22 normal third trimester pregnancies and 20 pregnancies complicated with IUGR. The criteria for fetal growth impairment were clinical evidence of sub-optimal growth, ultrasonographic demonstration of deviation from normal percentiles of growth and birth weight under 10th percentile. Terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labelling (TUNEL) staining was used to demonstrate the apoptotic cells in all samples. Student-t, Mann-Withney U-test, Fisher exact test and Spearman correlation were used for statistical analysis. RESULTS: We detected apoptosis in 10 placentas in the study group vs. none in the control group. Placentas from pregnancies complicated with IUGR demonstrated 0.12% (0.1%-0.4%) apoptotic cells. The rate of apoptotic cells in the placenta was significantly higher in pregnancies complicated with IUGR than normal uncomplicated pregnancy (P=0.0019). Apoptosis were more abundant in the trophoblasts, especially cytotrophoblasts, in the placenta. We could not find a correlation between the apoptosis in the placenta of pregnancies complicated with IUGR and birth weight, multi-parity, gestational age, birth weight percentile and mode of delivery (C/S vs. vaginal delivery). CONCLUSION: We believe that the increased number of apoptosis in the placenta of pregnancies complicated with IUGR may have an important compensatory role to transmit nutrition and gas exchange easily to the fetus.     

Placental pathology of idiopathic intrauterine growth retardation at term.

Placental examination was carried out in 128 consecutive cases of idiopathic intrauterine growth retardation (IUGR) at term and the findings were compared with those of 179 gestational age-matched cases with normal growth. Mean pregnancy weight and mean maternal weight gain during pregnancy of IUGR cases were both significantly lower than for non-IUGR cases. There was a higher frequency of a history of previous growth-retarded infants between IUGR cases (18 of 128, or 14%) compared with non-IUGR cases (7 of 179, or 3.9%). The studied placental lesions were placental infarction, chronic villitis, hemorrhagic endovasculitis, and placental vascular thromboses. One or more of these lesions were present in 71 of 128 (55%) of IUGR cases, and 58/179 (32%) of non-IUGR cases. Thirty-eight of 72 (53%) cases with chronic villitis were IUGR (30% of all IUGR cases). Thirty-one of 49 cases (63%) with placental infarction were IUGR cases (24% of all IUGR cases). Nineteen of 32 cases (59%) with hemorrhagic endovasculitis were IUGR cases (15% of all IUGR cases). Twelve of 17 cases (71% with placental vascular thromboses were IUGR (9% of all IUGR cases). Relationships of all placental lesions to IUGR were independent of each other. IUGR infants more frequently had multiple types of lesions in their placentas. Chronic villitis and hemorrhagic endovasculitis tended to occur in the same placentas. There were no significant relationships between maternal characteristics and placental lesions, except for an association between low pregravid weight and increased incidence of placental infarction. Decreased birth length was associated only with placental infarction (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation of placental prolactogen and E3 in the blood of pregnant women to placental grading by ultrasonography and its clinical significance

Serum HPL and E3 of normal pregnant women and some pathologic pregnancies were dynamically measured and the relationship between their levels and placental gradings were investigated. The peak values of HPL and E3 were found in 13.16 +/- 7.49 and 15.68 +/- 6.51 days before delivery. The serum concentrations of the two hormones in women with severe PIH syndrome, postdate pregnancy and intrauterine fetal growth retardation (IUGR) were lowered. E3 declined earlier than HPL Analysis of the HPL, E3 levels in comparison with placental grading showed that the decline of the two hormones was mainly found in patients with grade III placenta.     

The relationship of placental grade, fetal lung maturity, and neonatal outcome in normal and complicated pregnancies

Ultrasonically diagnosed maturity changes in the placenta, Grades 0 to III, have been previously shown to correlate with fetal lung maturity. In a prospective study of 230 term and preterm complicated pregnancies, we compared the relationship between sonographic placental grading, amniotic fluid phospholipids, and neonatal outcome. The frequencies of gestational age less than 38 weeks, lecithin/sphingomyelin (L/S) ratio less than 2.0, negative phosphatidylglycerol, and neonatal hyaline membrane disease were found to decrease as placental grade advanced from 0 to III. Patients were divided into subgroups on the basis of maternal complications. In patients with Grade III placentas, the frequencies of gestational age less than 38 weeks and L/S ratio less than 2.0 were significantly increased when the subgroup of patients with chronic hypertension was compared individually to both of the subgroups, repeat cesarean section deliveries, and Classes A, B, and C diabetes mellitus (both with p less than 0.05) All three infants who developed hyaline membrane disease in association with Grade III placentas were from pregnancies of less than 38 weeks complicated by chronic hypertension. These findings suggest that the presence of a Grade III placenta is affected by both gestational age and pregnancy complications. Hence, when an elective cesarean section delivery is being planned near term gestation, a Grade III placenta is a reliable predictor of lung maturity. In preterm complicated pregnancies, an ultrasound-diagnosed Grade III placenta may still be associated with hyaline membrane disease.     

Severe foetal growth retardation in a patient with uterus bicornis, velamentous insertion and partial placental abruption in the 26th week of gestation--a case report

Foetal growth retardation (IUGR) occurs in approximately 3-10 % of all pregnancies and may result from foetal, maternal or placenta-related conditions. In IUGR, the placental weight is often reduced and the placental capacity, reflected by the organ's weight, is impaired. Uterine malformations have an incidence of 3-4 % and may be the cause of placental abruptions occurring in 0.4-1.3 % of all pregnancies. We report on a patient in the 26 (th) week of pregnancy who was admitted with vaginal bleeding. A uterus bicornis had been found previously. Sonography showed severe foetal growth retardation and a pathological foetal Doppler signal. A haematoma located cranial of the os uteri was sonographically diagnosed, and a partial placental abruption was suspected. Due to a pathological cardiotocography, a primary Caesarean section was performed. Intraoperative evaluation confirmed the presence of a uterus bicornis. In addition, the placenta showed an insertio velamentosa. The growth retarded foetus - 490 g birth weight - was anaemic. Respiratory therapy and surfactant substitution were performed because of a respiratory distress syndrome. At a corrected age of 8 weeks the boy was sent home without neurological sequelae. In the case reported, a malformation of the uterus was the cause of a pathologically altered placenta. The multiple factors responsible for the described severe intrauterine growth retardation were a low placental weight and thus a reduced placental capacity, an impaired foetal circulation caused by the velamentous insertion, as well as a partial placental abruption. In normotensive pregnancies with IUGR, macroscopic and histopathological examinations of the placenta are therefore strongly recommended. Prior to getting pregnant, the therapeutic options should be explained to women with uterine malformations.     

Stereological study of the placentae in intrauterine growth retardation with different ponderal index]

10 placentae each from the cases of IUGR with normal ponderal index (NPI) and low ponderal index (LPI) and 10 from normal pregnancy as control were analysed quantitatively with stereological principles. This study showed the placental weight, volume, surface area of villi and villous fetal capillary in IUGR were significantly reduced than that in control group. The percentage ratio of the fetal capillary volume was increased significantly in IUGR group but the ratio of vasculo-syncytial membrane/villous fetal capillary decreased. It suggested that compensation to anoxemia in placenta of IUGR was incomplete. The data also found that all the parameters in NPI group were decreased significantly than that in LPI group, which implied NPI group had a more severe growth deficiency of the placental functional structure. When placental growth deficiency occurs in the first or second trimester, both the fetal length and weight will be severely affected.     

Ultrasonographically observed preterm grade III placenta and perinatal outcome

Ultrasound studies of placenta were conducted in 270 singleton normal pregnancies. Women were enrolled between 31 and 34 weeks of gestation and were followed up for the outcome of pregnancy. Women with grade III placental maturity comprised the study group (n = 64) and those with grade I placenta were enrolled as control group (n = 206). Another 100 normal women were enrolled to note the prevalence of grade III placenta at term. There was an increased incidence of intrauterine growth retardation (6.20%) and fetal distress (7.8%) in the study group compared with the control group (nil), which was statistically significant. The incidence of low birth weight was also higher (34.37%) in the study group compared with the control group (22.33%). Three women in the study group developed preeclampsia at subsequent follow up visit but none in control group (P less than 0.01). Prevalence rate of grade III placenta at term was 28%. In view of these findings preterm grade III placenta is found to be a sensitive predictor of poor perinatal outcome.     

Histomorphology of the placenta and the placental bed of growth restricted foetuses and correlation with the Doppler velocimetries of the uterine and umbilical arteries

The aim of the present study was to evaluate the histomorphology of the placenta and the placental bed and to correlate this with the Doppler study of the uterine and umbilical arteries of intrauterine growth restricted pregnancies. The study group consisted of 47 women with intrauterine growth restricted foetuses. Twenty-five uneventful pregnancies with appropriate for gestational age foetuses were selected as controls. Doppler studies of umbilical and uterine arteries were performed within the last week before delivery. Placental bed biopsies were obtained at Caesarean section with direct visualization of the placental site. The incidence of pathologic bed biopsies in control, IUGR with normal uterine artery Doppler velocimetry and IUGR with abnormal uterine artery Doppler velocimetry was 0 per cent, 16.6 per cent and 79.3 per cent respectively (P< 0.001). Placentae from IUGR cases with abnormal umbilical artery Doppler velocimetries had a significantly increased number of villous infarcts, cytotrophoblast proliferation and thickening of the villous trophoblastic basal membrane (P=0.001, P=0.038 and P=0.02 respectively). Abnormal placental bed biopsy pathology was significantly associated with abnormal uterine artery velocimetry (OR 33.7, 6.5-173.6; P< 0.001). Abnormal placental pathology was significantly associated with abnormal umbilical artery Doppler velocimetry (OR 21.04, 3.8-115.9;P< 0.001). Women with both abnormal uterine and umbilical artery Doppler velocimetries were delivered earlier and their babies had lower mean birth and placental weight (P< 0.001). In conclusion, placental bed biopsy and placental pathologies are best reflected by abnormal uterine and umbilical artery velocity waveforms, respectively. The most severe clinical outcomes and perinatal mortality are present when both uterine and umbilical districts are altered.     

The individual fetal weight/estimated placental weight ratios in monochorionic twins with selective intrauterine growth restriction

OBJECTIVES: To evaluate the individual fetal weight/estimated placental weight ratios (F/P ratio) of the two fetuses in monochorionic (MC) twins with selective intrauterine growth restriction (IUGR). MATERIAL AND METHODS: MC twin with selective IUGR was defined as an estimated fetal weight below the 10th percentile in one twin of MC pregnancy. The estimated individual placental weight was obtained by cutting the placenta along the vascular equator into two territories. A total of 15 MC twins with selective IUGR and 18 MC twins without selective IUGR were included in this study. RESULTS: The individual F/P ratio in the IUGR twin is significantly higher than that in the appropriate for gestational age (AGA) one in MC twin with selective IUGR (6.4 vs 4.0 respectively, p < 0.001). In MC twin without IUGR, the F/P ratios are not significantly different between the two fetuses (5.4 vs 5.1, respectively). CONCLUSION: The high F/P ratio in the IUGR twin in MC with selective IUGR may be due to the placental reserve phenomenon, so that a smaller placental territory may suffice to perfuse the IUGR twin. In other words, in MC twin gestations with an IUGR twin, the fetal weights are not proportional to the placental masses.     

Effects of aspirin on placenta and perinatal outcomes in patients with poor obstetric history

Objective: The aim of this study was to compare a low-dose aspirin treatment on placental and perinatal effects in the patients with poor obstetric history such as preeclampsia, intrauterine growth retardation (IUGR) in previous pregnancy. Study design: This retrospective study of 86 pregnant women was conducted between April 2002 and June 2005. In this study period 364 placentas were examined and the patients with poor obstetric history such as IUGR and preeclampsia were selected. Then the patients were assigned to three groups; group 1 (n = 30) was composed of women with no risk in previous pregnancy; group 2 (n = 27) was composed of patients with poor obstetric history (e.g., preeclampsia, IUGR) who were treated with aspirin and patients in group 3 (n = 29) had poor obstetric history without any treatment (patients who were started to follow-up after 14 weeks of gestation). Patients in group 2 were treated with a low-dose aspirin (80 mg/day) as soon as a urinary pregnancy test was positive. Treatment was usually stopped at 34 completed weeks of gestation. On histopathologic examination of the placenta, uteroplacental vascular pathologic features and secondary villous damage (such as fibrinoid necrosis of desidual vessels, villous infarct, severely increased villous fibrosis, severely increased syncytiotrophoblast knotting, obliteration of the vessel lumen, severely increased villous hypervascularity) and also lesions involving coagulation (such as excessive perivillous fibrin deposition, multiple occlusive thrombi in uteroplacental vessels, avascular villi ) were examined. Results: There were no significant differences between the groups with respect to maternal age, body mass index at the first trimester and delivery. Also there were no significant differences among groups with respect to placental weight, fetal height, weight, gestational week, umbilical artery pH, pO2, pCO2 and base excess status. The incidences of preeclampsia were 3.3, 7.4, 6.8% and the incidences of IUGR were 6.7, 11.1, 6.8% in the groups, respectively (P > 0.05 for both). Although the percentages of all pathologic findings were higher in groups 2 and 3, these differences were not statistically important. Conclusion: When low-dose aspirin is taken, starting at the beginning of pregnancy in patients with poor obstetric history, there are still high frequencies of uteroplacental vascular and related villous lesions persisted on placental bed. Also it has no beneficial effects on perinatal outcomes in these patients.     

Are placental lakes of any clinical significance?

The aim of this study was to determine prospectively whether an association exists between the finding of placental lakes at the 20 week scan and an increased risk of uteroplacental complications or a poor pregnancy outcome. We studied the placental appearances in 1,198 consecutive second trimester ultrasound scans performed for routine foetal abnormality screening at our institution. The placental thickness was measured at its widest diameter in the sagittal plane and the presence or absence of placental lakes was recorded. The birth weight in each case was plotted against the centile charts in use at the hospital and recorded. Specific outcome measures included foetal growth restriction (IUGR) with a birth weight below the 5th centile, pre-eclampsia, placental abruption, and perinatal deaths. Placental lakes were seen in 17.8 per cent of the scans. There was no significant association with either maternal socio-demographic factors or perinatal mortality (OR 0.94, 95 per cent CI 0.35-2.51). No association was seen with maternal cigarette smoking (OR 1.07, 95 per cent CI 0.75-1.52), a birth weight below the 5th centile (OR 0.68, 95 per cent CI 0.39-1.18), the development of pregnancy induced hypertension (OR 0.68, 95 per cent CI 0.35-1.32), severe pre-eclampsia (OR 0.72, 95 per cent CI 0.21-2.50), or placental abruption (OR 1.79, 95 per cent CI 0.46-6.99). A finding of placental lakes was six times more likely with a thick placenta >3 cm at 20 weeks gestation (OR 6.30, 95 per cent CI 4.39 to 9.05). A finding of placental lakes during the second trimester ultrasound scan does not appear to be associated with uteroplacental complications or an adverse pregnancy outcome. The lesions are more prevalent with increasing placental thickness.     

Perinatal outcome in women with severe pregnancy complications and multiple thrombophilias

Hypercoagulability leading to placental thrombosis has been implicated in severe pregnancy complications. We compared the perinatal outcome in women with severe preeclampsia, intrauterine growth retardation (IUGR) and severe abruptio placentae and multiple acquired and inherited thrombophilias (study group, n=22) to matched women with similar complications and single thrombophilia (control group, n=22). Gestational age at delivery and birth weight were significantly lower in the study group compared to the control group (p<0.01) and among the study women with severe preeclampsia and IUGR. Severe pregnancy complications may occur earlier during pregnancy and more seriously affect perinatal outcome in women with multiple thrombophilias.     

Caffeine-cigarette interaction on fetal growth

The influence of caffeine and cigarette consumption on fetal growth during pregnancy was studied retrospectively in 913 newborn infants. Analysis of variance was adjusted for length of gestation and sex. A significant caffeine-cigarette interaction was found on birth weight (F = 85.4, p less than 0.01). Among women smoking 15 cigarettes or more per day, birth weight was 206 gm (+/- 57.7 gm) lighter for babies whose mothers consumed 300 mg or more of caffeine per day. Head circumference and length of the newborns were affected only by cigarette smoking. Another caffeine-cigarette interaction was observed on placental weight (F = 15.0, p less than 0.01). Among women who consumed less than 300 mg of caffeine daily, placental weight increased with cigarette consumption. However, it diminished (p less than 0.05) among women smoking 15 cigarettes or more per day if they consumed 300 mg or more of caffeine daily. This is the first time that such interactions were found to influence birth and placental weights, indicating that the concomitant consumption of caffeine and cigarette constitutes a higher risk for the developing fetus.     

Early preterm delivery due to placenta previa is an independent risk factor for a subsequent spontaneous preterm birth

ABSTRACT: BACKGROUND: To determine whether patients with placenta previa who delivered preterm have an increased risk for recurrent spontaneous preterm birth. METHODS: This retrospective population based cohort study included patients who delivered after a primary cesarean section (n = 9983). The rate of placenta previa, its recurrence, and the risk for recurrent preterm birth were determined. RESULTS: Patients who had a placenta previa at the primary CS pregnancy had an increased risk for its recurrence [crude OR of 2.65 (95 % CI 1.3-5.5)]. The rate of preterm birth in patients with placenta previa in the primary CS pregnancy was 55.9 %; and these patients had a higher rate of recurrent preterm delivery than the rest of the study population (p < .001). Among patients with placenta previa in the primary CS pregnancy, those who delivered preterm had a higher rate of recurrent spontaneous preterm birth regardless of the location of their placenta in the subsequent delivery [OR 3.09 (95 % CI 2.1-4.6)]. In comparison to all patients with who had a primary cesarean section, patients who had placenta previa and delivered preterm had an independent increased risk for recurrent preterm birth [OR of 3.6 (95 % CI 1.52-8.51)]. CONCLUSIONS: Women with placenta previa, who deliver preterm, especially before 34 weeks of gestation, are at increased risk for recurrent spontaneous preterm birth regardless to the site of placental implantation in the subsequent pregnancy. Thus, strict follow up by high risk pregnancies specialist is recommended.     

Low midpregnancy placental volume in rural Indian women: A cause for low birth weight?

OBJECTIVE: We sought to study midpregnancy placental volume in rural Indian women, its maternal determinants, and its relationship to neonatal size. STUDY DESIGN: We performed a prospective community-based study of maternal nutrition and fetal growth in 6 villages near the city of Pune. Measurements included midpregnancy placental volume determined by means of ultrasonography at 15 to 18 weeks' gestation, maternal anthropometric measurements before and during pregnancy, and maternal blood pressure and biochemical parameters during pregnancy. Neonatal size and placental weight were measured at birth. RESULTS: The mothers were short and underweight (mean height, 1.52 m; weight, 42 kg; body mass index, 18 kg/m(2)) and produced small babies (mean birth weight, 2648 g). Midpregnancy placental volume (median, 144 mL) was related to the mother's prepregnancy weight (r = 0.15; P <.001) but not to weight gain during pregnancy, blood pressure, or circulating hemoglobin, ferritin, red blood cell folate, or glucose concentrations. Midpregnancy placental volume was related to placental weight at birth (r = 0.29; P <.001) and birth weight (r = 0.25; P <.001) independent of maternal size. CONCLUSION: In Indian mothers midpregnancy placental volume is significantly associated with prepregnant maternal weight and is an independent predictor of birth weight. Our findings may provide clues to the high prevalence of low-birth-weight infants in India.     

The Effect of Intrauterine Growth Retardation on the Expression of Developmental Factors in Porcine Placenta Subsequent to the Initiation of Placentation

Intrauterine growth retardation (IUGR) hinders fetal growth and postnatal development in swine; however the etiology of IUGR is essentially unknown. Expression of fourteen candidate genes associated with placental development or IUGR was examined in gestational day 50 (gd50) control and IUGR fetus whole placental tissue or areolae by real-time PCR. Endothelial nitric oxide synthase (ENOS) mRNA expression was elevated in gd50 IUGR placenta and areola compared to gd50 control. Since ENOS could modulate vascular tone and angiogenesis via nitric oxide production, data suggest that the increase in IUGR may be an adaptive response to poor perfusion to maintain pregnancy.     

Doppler sonography of the uterine and the cubital arteries in normal pregnancies, preeclampsia and intrauterine growth restriction: evidence for a systemic vessel involvement

AIMS: The decrease in uterine resistance during normal pregnancy is known to be related to invading trophoblast cells which derive from placental tissue. Uterine and peripheral resistance is elevated in preeclampsia. The aim of the present study was to prospectively examine uterine and peripheral resistance in pregnancies complicated by preeclampsia (PE), fetal intrauterine growth restriction (IUGR) and pregnancy induced hypertension (PIH). METHODS: Sixty-seven women with normal pregnancies, 17 with PE, 12 with IUGR underwent Doppler sonographic investigation of the uterine and the cubital arteries. The Pulsatility Index (PI) was calculated for each vessel. Statistical analysis was performed and a P-value <0.05 was considered significant. RESULTS: Patients with preeclampsia and IUGR showed a significant higher resistance at the placental (mean PI 1.267 and 1.063), nonplacental (mean PI 1.631 and 1.124) and cubital artery (mean PI 3,777 and 3.995) compared to the normal pregnancy group (mean PI 0.678; 0.859 and 2.95 respectively). Mean birth weight in the PE group was 1409 g, in the IUGR group 1649 g and 3419 g in the normal pregnancy group. CONCLUSIONS: Pregnancies with IUGR are associated with elevated peripheral resistance in the maternal arterial system as seen in pregnancies with preeclampsia. Our findings encourage to further investigate the maternal vascular system in high risk pregnancies.     

Heat shock proteins and heat shock protein-antibody complexes in placental tissues.

OBJECTIVE: The relationship between pregnancy outcome and expression of the heat shock proteins (hsps) or hsp-antibody complexes of 60kD (hsp60), 70kD (hsp70), and 90kD (hsp90) in placental tissue and circulating antibodies to hsps was evaluated. METHOD: Expression of hsp60, hsp70, and hsp90 in placentae from 12 women with preterm birth, eight with intrauterine growth restriction (IUGR), and 10 with term birth, as well as the presence of the corresponding antibodies, was investigated by a new carbocyanine double fluorescence technique. Results were compared with microbiological findings and circulating antibodies to hsps in sera. RESULTS: In each placental specimen examined, hsp60, hsp70, and hsp90 were identified. However, hsp70-antibody complexes were detected in only four of the preterm labor cases. Similarly, hsp60-antibody complexes were detected in only five preterm labor patients and in one patient with IUGR. None of the placentae contained hsp90-antibody complexes. In the preterm birth group, all patients with hsp60-antibody complexes were also positive for circulating antibodies to hsp60. The presence of hsp70-antibody complexes also correlated with hsp70 antibody in sera. CONCLUSIONS: Formation of hsp60- and hsp70-antibody complexes in the placenta may contribute to the induction of preterm birth. Women sensitized to these antibodies may be at increased risk for adverse pregnancy outcome.     

Sonographic Maturation of the Placenta at 30 to 34 Weeks Is Not Associated With Second Trimester Markers of Placental Insufficiency in Low-risk Pregnancies

ObjectiveAdvanced placental maturation (Grannum [G] grade 3) before term is associated with adverse perinatal outcomes associated with placental insufficiency. The nature and timing of the underlying pathology of this process is presently unclear. We hypothesized that advanced placental maturation at 30 to 34 weeks’ gestation is not associated with established second trimester markers of severe placental dysfunction.MethodsIn a cohort study of 1238 low-risk Caucasian women with singleton pregnancies who had sonographic assessment of placental maturation and fetal growth at 34 weeks, the results of maternal serum screening (MSS) and uterine artery Doppler (UtAD) flow studies at 16 weeks were related to adverse perinatal outcomes associated with placental insufficiency: antepartum hemorrhage, preeclampsia, preterm birth < 37 weeks, small for gestational age (< 10th percentile), or postnatal evidence of intrauterine growth restriction (IUGR; ponderal index < 5th percentile).ResultsG1 was found in 127 women (10.3%), G2 was found in 18 women (1.5%), and no cases of G3 were observed. Advanced Grannum grading was significantly associated with IUGR (48 [4.4%] in G0, 9 [7.1%] in G1, 5 [27.8%] in G2; P < 0.001), but was dependent on smoking status. IUGR was not predicted by abnormal MSS or abnormal UtAD findings at either the second or third trimester ultrasounds.ConclusionG2 maturation at 30 to 34 weeks’ gestation is associated with mild IUGR at delivery in low-risk women and with smoking. IUGR was not predicted by either second or third trimester markers of severe placental dysfunction. Future studies directly observing the placenta in the late third trimester may aid the elusive diagnosis of “late-onset” mild IUGR.