Approximately 3 percent to 10 percent of pregnancies within studied populations are affected by gestational diabetes, a condition involving elevated blood sugar levels in women previously not diagnosed with diabetes (Metzger et al., 2007; Moore & et al, 2005; Schneider, 2014). Due to changes in diagnostic criteria, the prevalence of gestational diabetes may occur in as many as 20 percent of pregnancies (Kim, 2010).
Insulin receptors begin to dysfunction secondary to factors related to pregnancy and blood glucose levels rise. There are relatively few symptoms of gestational diabetes and screening of pregnant women is the most effective method of diagnosis. If gestational diabetes is not addressed, the baby is at risk of problems such as jaundice, inappropriately high birth weight with accompanying complications with delivery, and low blood sugars; stillbirths and seizures have also been reported. Mothers are also at increased risk of developing type 2 diabetes, cardiovascular disease, or pre-eclampsia or requiring a Caesarean section (Donovan & McIntyre, 2010; Kim, 2010). Treatment may involve dietary management, exercise recommendations, or anti-diabetic drugs such as insulin.
A study by Farrerra (2007) suggests that as women are waiting longer to have children and maternal body mass indexes increase, incidences of gestational diabetes become more prevalent; there are also higher reported cases in racially diverse populations. The complication of pregnancy has become a topic of public health concern due to the drive toward a general healthier life-style for most people as an optimum diet and regular exercise is not only a treatment after gestational diabetes develops, but may also deter the condition.
Pathophysiology
While the exact mechanism responsible for gestational diabetes has yet to be determine, researchers agree the process responsible involved resistance to insulin with pregnancy factors such as hormones thought to bind to the receptors that monitor insulin in the body. A study by Carr and Gabbe (1998) proposes that the interference happens by interfering with the pathway that signals the cell to stop allowing glucose into the structure; the sugar remains in the bloodstream and blood levels rise. A result of the higher amount of bloodstream glucose prompt approximately 1.5 to 2.5 times more insulin produced in order to encourage glucose uptake by the cells.
Hormones generated normally by the body of a pregnant woman include placental hormones, cortisol, prolactin, progesterone, estradiol, and human placental lactogen (Gabbe, Niebyl & Simpson, 2002). These work with other types of placental hormones, resistin, leptin, and tumor necrosis factor (TNF) alpha to decrease resistance to insulin in order to promote glucose intake by the fetus. Low levels or changes in TNF alpha factors have been shown to increase insulin resistance (Gabbe, Niebyl & Simpson, 2002, p. 890). Research by Buchanan & Xiang (2005) concludes that explanations why some women are not able to regulate insulin requirements may include mutations of single genes, autoimmunity, obesity, or other factors,
Literature Review
Consequences of Gestational Diabetes. The negative influence of gestational diabetes for newborns is seen after delivery as the high levels of glucose in the intrauterine environment disappears but excessive insulin production continues, resulting in hypoglycemia (Kelly, Evans & Messenger, 2005), birth weight over the 90th percentile for age of gestation and under the 10th percentile, hyperbilirubinemia, and pre-eclampsia, and admission to the neonatal intensive care unit (Moore et al, 2005). Yessoufou & Moutairou (2011) report that the primary complication for children born when mothers have gestational diabetes is macrosomia, a predisposition to obesity and diabetes.
There are indications that the same affected pathways for insulin uptake resistance are also present in the processes for hypertension. Reece (2010) reports that postpartum development of type 2 diabetes, cardiovascular disease, and metabolic syndrome is not usual for women who manifested gestational diabetes during their pregnancy. Kapoor, Sankaran, Hyer, and Shehata (2007) report that women who develop the complication may have more than seven times the risk of developing diabetes in the future than mothers without a history of gestational diabetes.
Prenatal Screening. Screening of a pregnant woman is particularly necessary when she has severe obesity, prior delivery of a baby with a large birth weight for its gestational age, a family history of diabetes mellitus (especially type 2), polycystic ovarian syndrome, or a previous history of a pregnancy accompanied by gestational diabetes (American Diabetes Association, 2003; ACOG, 2016; Metzger & Coustan, 1998). Ross (2006) suggests the mother is high risk if she is over the age of 35, has a body mass index greater than 30, or is of Arabic, south Asian, aboriginal, southeast Asian, or Pacific Islander ethnicity.
Prenatal Education. D’Ambrosio et al. (2015) conducted a study of prenatal educational materials available on the internet and found that less than 10 percent of the 1, 995, 030 search results contained information on preconception recommendations and only 42.8 percent of the pages were consistent with the recommendations of the American College of Obstetricians and Gynecologists (ACOG). Evert (2006) studied the program at the Joslin Diabetes Center in Seattle, Washington and suggests classes with presentation of approved materials for effective prenatal education; one-on-one appointments and a telephone hotline are also available at that facility.
Interview
An interview was conducted with a 37-year-old para 5, gravida 2 mother who had received laboratory findings of fasting blood glucose reading of 105 mg/dl. Kathy W. stated that she had not experienced gestational diabetes with her previous pregnancies to her knowledge, although her first live delivery was four weeks preterm with a birth weight of 6 pounds 2 ounces and the second baby was three weeks early with a birth weight of 6 pounds 4 ounces. Both children developed jaundice that was treated with light therapy. The eldest boy has been diagnosed with attention deficit disorder at age 8. Kathy had a clinical abortion when she was 17 years old and a hydatidform mole was aborted at age 30. A practicing registered nurse, she was aware of the signs of diabetes and stated that she suspected she frequently experienced hypoglycemia, but controlled the symptoms with diet. Her mother had developed senile diabetes when she was 62 following a cancer diagnosis that was the reason for her death two years later. Kathy was not aware of other relatives with diagnoses of diabetes.
Kathy had undergone diabetic dietetic instructions and was told to test her blood glucose levels with fingersticks three times daily and increase her intake to 2000 calories. Her height is 5 foot, 7 inches and pre-pregnancy weight was 130. Kathy is very athletic, exercising to capacity at least four times a week with weight training, lessons in martial arts, and stationary biking. She stated that she gained only five pounds with her first delivery and 10 pounds with her second. At 22 weeks gestation, she has gained 8 pounds with this pregnancy.
Kathy stated that the recommended food intake was much higher than her usual and she was finding it difficult to keep her blood sugars stable. After a review of her usual diet, it appeared the proper balance of nutrients was in place without excessive sugars and carbohydrates. It is possible Kathy’s high level of exercise was an influence. She expressed a desire to stop trying to adhere to the recommended diet and return to her previous intake. Although it was advised that she return to the dietician for counseling, followup three weeks later showed that Kathy had indeed stopped the recommended guidelines for a mother with gestational diabetes and her blood sugars had returned to normal. It is unclear what may have caused the fluctuations in blood test results previously.
Conclusion
If current trends continue, gestational diabetes mellitus may become one of the most common complications of pregnancy. Rising obesity in women, sedentary lifestyles, and poor diet contribute to the effects on mother and child, particularly if not recognized and treated. Negative outcomes appear to decrease when healthcare professional monitor maternal blood glucose levels, weight gain, and the impact on fetal stress and growth in utero.
There is a consensus among researchers that additional studies are needed to determine the optimum targets for glucose levels and weight gain in addition to dosage and timing of pharmaceuticals. Research into postpartum developments in mothers and children are required to evaluate the effectiveness of screening measure and intervention. The information gathered has the potential to significantly impact the increasing number of women seeking prenatal care around the world.
References
ACOG. (2016). Search - ACOG. Acog.org. Retrieved 9 March 2016, from ‘
http://www.acog.org/Search?Keyword=screening+for+gestational+diabetes
American Diabetes Association. (2003). Gestational Diabetes Mellitus. Diabetes Care,
27(Supplement 1), S88-S90. http://dx.doi.org/10.2337/diacare.27.2007.s88
Buchanan, T., & Xiang, A. (2005). Gestational diabetes mellitus. Journal of Clinical
Investigation, 115(3), 485-491. http://dx.doi.org/10.1172/jci24531
D’Ambrosio, A., Agricola, E., Russo, L., Gesualdo, F., Pandolfi, E., & Bortolus, R. et al. (2015).
Web-Based Surveillance of Public Information Needs for Informing Preconception
Interventions. PLOS ONE, 10(4), e0122551.
http://dx.doi.org/10.1371/journal.pone.0122551
Donovan, P., & McIntyre, H. (2010). Drugs for gestational diabetes. Australian Prescriber,
33(5), 141-144. http://dx.doi.org/10.18773/austprescr.2010.066
Ferrara, A. (2007). Increasing Prevalence of Gestational Diabetes Mellitus: A public health
perspective. Diabetes Care, 30(Supplement 2), S141-S146.
http://dx.doi.org/10.2337/dc07-s206
Kapoor, N., Sankaran, S., Hyer, S., & Shehata, H. (2007). Diabetes in pregnancy: a review of
current evidence. Current Opinion in Obstetrics And Gynecology, 19(6), 586-590.
http://dx.doi.org/10.1097/gco.0b013e3282f20aad
Kelly, L., Evans, L., & Messenger, D. (2005). Controversies around gestational diabetes.
Practical information for family doctors. Canadian Family Physician Medecin De
Famille Canadien, 51(5), 688–695.
Kim, C. (2010). Gestational diabetes: risks, management, and treatment options. International
Metzger, B., Buchanan, T., Coustan, D., de Leiva, A., Dunger, D., & Hadden, D. et al. (2007).
Summary and Recommendations of the Fifth International Workshop-Conference on
Gestational Diabetes Mellitus. Diabetes Care, 30(Supplement 2), S251-S260.
http://dx.doi.org/10.2337/dc07-s225
Moore, T.,et al. (2005). Diabetes Mellitus and Pregnancy: Practice Essentials,
Gestational Diabetes, Maternal-Fetal Metabolism in Normal Pregnancy.
Emedicine.medscape.com. Retrieved 9 March 2016, from
http://emedicine.medscape.com/article/127547-overview
Reece, E. (2010). The fetal and maternal consequences of gestational diabetes mellitus. The
http://dx.doi.org/10.3109/14767050903550659
Ross, G. (2006). Gestational Diabetes. Australian Family Physician, 35(6), 392-396. Retrieved
Schneider, C. (2014). Diabetes and the Risk to Your Family Tree. DiabetesCare.net. Retrieved 9
March 2016, from http://www.diabetescare.net/authors/clara-schneider/diabetes-and-the risk-to-your-family-tree#ixzz3L3ZMFUrS
Yessoufou, A., & Moutairou, K. (2011). Maternal Diabetes in Pregnancy: Early and Long-Term
Outcomes on the Offspring and the Concept of “Metabolic Memory”. Experimental
Diabetes Research, 2011, 1-12. http://dx.doi.org/10.1155/2011/218598
