Background—The goal of this statement is to review available literature and to put forth a scientific statement on the current practice of fetal cardiac medicine, including the diagnosis and manage...

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Diagnosis and Treatment of Fetal Cardiac Disease A Scientific Statement From the American Heart Association

Objective: To monitor pregnancies in women with pre-existent insulin dependent diabetes for pregnancy loss, congenital malformations, and fetal growth in a geographically defined area of north west England. Design: Population cohort study. Setting: 10 maternity units in Cheshire, Lancashire, and Merseyside which had no regional guidelines for the management of pregnancy in diabetic women. Subjects: 462 pregnancies in 355 women with insulin dependent diabetes from the 10 centres over five years (1990-4 inclusive). Main outcome measures: Numbers and rates of miscarriages, stillbirths, and neonatal and postneonatal deaths; prevalence of congenital malformations; birth weight in relation to gestational age. Results: Among 462 pregnancies, 351 (76%) resulted in a liveborn infant, 78 (17%) aborted spontaneously, nine (2%) resulted in stillbirth, and 24 (5%) were terminated. Of the terminations, nine were for congenital malformation. The stillbirth rate was 25.0/1000 total births (95% confidence interval 8.9 to 41.1) compared with a population rate of 5.0/1000, and infant mortality was 19.9/1000 live births (5.3 to 34.6) compared with 6.8/1000. The prevalence of congenital malformations was 94.0/1000 live births (63.5 to 124.5) compared with 9.7/1000 in the general population. When corrected for gestational age, mean birth weight in the sample was 1.3 standard deviations greater than that of infants of non-diabetic mothers. Infants with congenital malformations weighed less than those without. Conclusion: In an unselected population the infants of women with pre-existent insulin dependent diabetes mellitus have a 10-fold greater risk of a congenital malformation and a fivefold greater risk of being stillborn than infants in the general population. Further improvements in the management of pregnancy in diabetic women are needed if target of the St Vincent declaration of 1989 is to be met. Key messages Infants of women with established insulin dependent diabetes mellitus have 10 times the population risk of congenital malformations and five times the stillbirth rate Excess mortality among infants of women with pre-existent insulin dependent diabetes mellitus is predominantly due to congenital malformations The birth prevalence of congenital malformations can be reduced by good periconceptional glycaemic control, but the challenge remains to implement this on a population basis Macrosomia remains a problem among infants of women with established insulin dependent diabetes mellitus

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Outcomes of pregnancy in insulin dependent diabetic women: results of a five year population cohort study

Gestational diabetes and obesity are the common metabolic abnormalities occurring during pregnancy. Decreased maternal pregravid insulin sensitivity (insulin resistance) coupled with an inadequate insulin response are the pathophysiological mechanisms underlying the development of gestational diabetes. Insulin-regulated carbohydrate, lipid and protein metabolism are all affected to a variable degree. Decreased maternal insulin sensitivity in women with gestational diabetes may increase nutrient availability to the fetus, possibly accounting for an increased risk of fetal overgrowth and adiposity. Epidemiological studies from Europe show an increased risk of the insulin resistance syndrome in adults who were low birth weight at delivery. However, in the United States over the past 20 y there has been a significant 33% increase in the incidence of type 2 diabetes, which has been associated with a parallel increase in obesity. All age groups have been affected but the most dramatic increases have occurred in adolescents. The relationship between decreased maternal insulin sensitivity and fetal overgrowth particularly in obese women and women with gestational diabetes may help explain the increased incidence of adolescent obesity and related glucose intolerance in the offspring of these women. In this review, we address 1) the pathophysiology of gestational diabetes, 2) the changes in maternal insulin sensitivity during pregnancy that effect maternal accretion of adipose tissue and energy expenditure, 3) the influence of maternal metabolic environment on fetal growth, 4) the life-long effect of being born at either extreme of the birth weight continuum and 5) micronutrients and decreased insulin sensitivity during pregnancy.

Gestational Diabetes and Insulin Resistance: Role in Short- and Long-Term Implications for Mother and Fetus

Effects of diabetic pregnancy on the fetus and newborn.

Maternal insulin-dependent diabetes has long been associated with congenital malformations. As other causes of mortality and morbidity have been eliminated or reduced, malformations have become increasingly prominent. Although there is not universal agreement, the great majority of investigators find a two- to threefold increase in malformations in infants of insulin-dependent diabetic mothers. This increase is not seen in infants of gestational diabetics. It probably is not present in women whose diabetes can be controlled by diet or oral hypoglycemic agents. The risk does not appear to be primarily genetic since diabetic fathers do not have an increased number of malformed offspring. Most studies show a generalized increase in malformations involving multiple organ systems. Multiple malformations seem to be more common in diabetic than non-diabetic infants. Caudal regression has the strongest association with diabetes, occurring roughly 200 times more frequently in infants of diabetic mothers than in other infants. The teratogenic mechanism in diabetes is not known. Hyperglycemia may be important but human studies focusing on the period of organogenesis are lacking. Hypoglycemia has also been suggested based mainly on animal experiments. Insulin appears unlikely. Numerous other factors including vascular disease, hypoxia, ketone and amino acid abnormalities, glycosylation of proteins, or hormone imbalances could be teratogenic. None has been studied in sufficient detail to make a judgment. A large-scale prospective study is required to determine early fetal loss rates, correlate metabolic status during organogenesis with outcome, and assess the effect of diabetic control on malformation rates.

Malformations in Infants of Diabetic Mothers

PERINATAL mortality has decreased in pregnancies complicated by diabetes mellitus.1 As losses from stillbirths, intrapartum asphyxia, and hyaline-membrane disease diminish, major congenital anomalies emerge as the most important causes of mortality in infants of diabetic mothers.1 , 2 The overall incidence of major anomalies was 6 to 9 per cent in several large studies of such infants1 2 3 — three to four times that found in a general neonatal population.4 Fetal malformations occur before eight weeks of gestation (postmenstrual dates), when most diabetic pregnant women have not yet come to medical attention.5 Until recently, there has been no objective method to assess control . . .

Elevated maternal hemoglobin A1c in early pregnancy and major congenital anomalies in infants of diabetic mothers.

Diabetes Care suggests that negative reinforcement on the part of the caregiver is less likely to discourage pregnancy than it is to discourage prepregnancy planning.

P J Dunn

Papers

Elevated maternal hemoglobin A1c in early pregnancy and major congenital anomalies in infants of diabetic mothers.

Diabetes Care suggests that negative reinforcement on the part of the caregiver is less likely to discourage pregnancy than it is to discourage prepregnancy planning.