Gestational diabetes is defined as any degree of glucose intolerance that has its onset or is first diagnosed during pregnancy. Kuhl, Hornnes, and Andersen (1985) state that gestational diabetes occurs when the pancreas of a pregnant woman fails to increase insulin production to compensate for the natural decrease in cells’ sensitivity to insulin. The cardinal signs of diabetes are polyuria (related to decreased reabsorption at the renal tubules because of the osmotic activity of glucose), polydipsia (related to polyuria), polyphagia (related to starved cells as a result of inability to transport glucose into cells), and weight loss (related to the use of fat and muscle tissues for energy). If left untreated, the extra glucose in the blood can pass to the baby through the placenta, causing the baby to boost insulin production. All that excess glucose is stored in the baby as fat leading to a large for gestational age size, which can complicate delivery. Also, the baby’s overproduction of insulin may increase his or her risk of obesity and type two diabetes later in life (Joslin Diabetes Center, 2008). This phenomenon occurs in about four percent of all pregnancies and is more common in women with one or more of the following risk factors: overweight, over 30 years of age, strong family history of diabetes, previously had a baby weighing more than nine pounds at birth, polycystic ovary syndrome, glycosuria, impaired fasting glucose or impaired glucose tolerance, and African-American, Hispanic, Asian, American Indian, or a Pacific Islander descent (Ladewig, London, and Davidson, 2009). According to the text, the prognosis of gestational diabetes without significant vascular damage is positive (Ladewig et al. 2009). However, there are still more risks associated with the diagnosis compared to a normal pregnancy. One of the maternal risks of gestational diabetes is hydramnios, or increased amniotic fluid, can occur in 10-20% of diabetic pregnancies. This is thought to occur as a result of fetal polyuria and occasionally results in premature rupture of membranes and onset of labor (Ladewig et al. 2009). Preeclampsia also occurs more often in diabetic pregnancies, especially when vascular change has already occurred. Hyperglycemia can slowly lead to ketoacidosis, which if left untreated can result in coma and death for the mother and the fetus. Women with GDM are also more susceptible to monilial vaginitis and urinary tract infections related to increased glycosuria (Ladewig et al. 2009). One fetal-neonatal risk is death from maternal ketoacidosis; however the major cause of death among infants of diabetic mothers is congenital anomalies. Most anomalies involve the central nervous system, heart, and skeletal system. Sacral agenesis occurs almost exclusively in diabetic pregnancies (Ladewig et al. 2009). A large for gestational age baby or macrosomic baby is at increased risk for shoulder dystocia and traumatic birth injuries if delivered vaginally (Ladewig et al. 2009). After the umbilical cord is severed, the baby is cut off from the mother’s hyperglycemic blood supply but will continue to make excess insulin, resulting in hypoglycemia two to four hours after birth (Ladewig et al. 2009). Also, if a pregnant woman has vascular damage from diabetes, intrauterine growth restriction may occur as a result of decreased placental perfusion (Ladewig et al. 2009). Respiratory distress syndrome, polycythemia, and hyperbilirubinemia are also linked with diabetic pregnancies (Ladewig et al. 2009).
Screening for Gestational Diabetes
While a universal recommendation for an approach to screening and diagnosis of GDM does not exist, the Committee on Obstetric Practice continues to recommend a two-step approach. They state “All pregnant women should be screened for GDM, whether by patient history, clinical risk factors, or a 50-g, 1-hour glucose challenge test at 24–28 weeks of gestation. The diagnosis of GDM...
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