Lactacidemia in Intrauterine Growth Restricted (IUGR) Pregnancies: Relationship to Clinical Severity, Oxygenation and Placental Weight

Abstract

ABSTRACT:The aim of the study was to evaluate the impact of clinical severity and placental weight upon fetal lactacidemia in intrauterine growth restricted (IUGR) pregnancies. Seventy pregnancies complicated by IUGR were compared with 70 normal (appropriate for gestational age, AGA) pregnancies at the time of elective cesarean section. IUGR pregnancies were divided according to clinical severity in three groups: Group 1 had normal fetal heart rate (FHR) and normal pulsatility index of the umbilical artery (PI); Group 2 had normal FHR and abnormal PI; and Group 3 had abnormal FHR and PI. No cases with severe lactacidemia had placental weights Ն250 g. Forty-four fetuses had placental weight Ͻ250 g: Twenty-four had severe lactacidemia and all were Group 2 and 3, whereas 20 had normal umbilical artery lac (lactate) (and small placentas) regardless of the clinical severity. Gestational age, fetal and placental weights, F/P ratios, uv (umbilical vein) and ua lac and ua oxygen content and pH were significantly decreased in fetuses with small placentas and high lactate. There was a significant relationship between fetal and placental weight in AGA and IUGR. However, IUGR fetuses with placental weight Ն250 g exhibited an F/P ratio significantly lower than that in AGA fetuses suggesting that IUGR may be due to a reduction of placental function per gram of tissue. (Pediatr Res 59: 570-574, 2006) L actate represents the end product of anaerobic metabolism of glucose. However, many experimental as well as studies in human pregnancies both in vivo (1-3) and in vitro (4,5) have shown that lactate is produced within the placenta and delivered into both the maternal and umbilical circulation where it serves as source of carbon for fetal growth. This has been clearly demonstrated by studies in pregnant sheep where fetal utilization of lactate at term is three times higher than the umbilical uptake (approximately 4 mg/kg/min) in the welloxygenated fetus (6). The fetal liver is the organ with the highest lactate consumption and liver lactate uptake almost equals umbilical uptake: lactate is then used for oxidation and synthesis of fatty acid and glycogen (7). In human pregnancies, fetal lactate concentration is higher than maternal (2,3). Many clinical studies at the time of delivery (i.e. under non-steady stressed conditions) have shown that umbilical venous and arterial lactate concentrations as well as the umbilical venoarterial concentration difference correlate with Apgar scores both at 1= and 5= (8,9). In clinical studies performed at the time of spontaneous delivery, lactate concentrations have been shown to represent a much more reliable marker of fetal acidosis compared with pH measurements (10,11). However, difficulties in sample management have limited its widespread clinical application. Recently the characteristics of L-lactic acid transport across the human placental syncytiotrophoblast have been described (12,13) as has been done for human erythrocytes (14), hepatocytes (15), intestinal brush border membrane (16,17)...

Hypoglycemia and the Origin of Hypoxia-Induced Reduction in Human Fetal Growth

“…While the net lactate flux data ostensibly demonstrates a switch from fetal consumption at low altitude to fetal production at high altitude, the wide range of plasma lactate values means that neither flux is significantly different from zero. Interestingly however, the inverse correlation between umbilical arterial lactate and O 2 content reflects the same relationship observed by Marconi et al in IUGR pregnancies [63].…”

Umbilical uptakes and transplacental concentration ratios of amino acids in severe fetal growth restriction

“…This study of AA uptake and utilization by growth-restricted fetal lamb helps in interpreting data related to human FGR. Clinical studies of FGR pregnancies have shown relationships between placental weight and fetal weight similar to those shown in Figure 1 (18). A significant relationship of placental weight and fetal oxygenation in human FGR has also been demonstrated (8).…”

A Decrease in DKK1, a WNT Inhibitor, Contributes to Placental Lipid Accumulation in an Obesity-Prone Rat Model1

“…Additionally, studies have suggested that the ratio of fetal to placental weight is a better marker of placental efficiency, because it represents the amount of fetus produced for each gram of placenta. The ratio MATERNAL OBESITY AND PLACENTAL WNT SIGNALING has been evaluated by several studies, in which the researchers have concluded that a large placenta, when accompanied by a smaller fetus, is associated with IUGR as well as SGA offspring, gestational diabetes, and possible risks of late-onset diseases [7,[62][63][64]. In the present study, we found that placental weight was not affected by maternal weight but that the fetal weight:placental weight ratio was decreased in obese dams, indicating that despite being the same size as those of lean dams, the placentas of these obese dams were not able to support proper fetal development.…”