Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with the onset or first recognition during pregnancy. Ninety percent of those diagnosed with diabetes during pregnancy will resolve after delivery (Scollan-Koliopoulos, Guadagno, & Walker, 2006). Pregnancy causes estrogen, progesterone and human placental lactogen to become elevated which provokes malfunctioning insulin, which can lead to insulin resistance and decreased cellular glucose uptake. The growing placenta causes the production of even more hormones, producing higher glucose levels and increased insulin resistance. When the pancreas can’t satisfy the demands for additional insulin, GDM results (Gattullo & Olubummo, 2009). Approximately 7%, or 200,000 pregnant women are diagnosed each year in the United States. Advanced maternal age, family history of diabetes, prior GDM, history of infant with macrosomia, and elevated BMI are all major risk factors for developing GDM. GDM is more often found in women of Asian, Hispanic or Native American descent (Cheng & Caughey, 2008). GDM can have negative effects on both the fetus and the mother. These mothers experience an increased number of Caesarian deliveries and use of forceps or vacuum extractions, resulting in severe perineal lacerations, related to fetal macrosomia. Along with the risks associated with macrosomia, the mother is also at risk for developing hypertension and preeclampsia, leading to preterm labor, as well as, developing Type 2 diabetes after the birth of her baby (Cheng & Caughey, 2008). The increased amount of glucose in the gestational diabetic is correlated with macrosomia and childhood obesity (Scollan-Koliopoulos et al., 2006). Maternal hyperglycemia can increase the risk of hypoglycemia, respiratory distress syndrome, jaundice and hypocalcemia in the neonate. The negative effects of macrosomia include shoulder dystocia, brachial plexus injuries and clavicle fractures, resulting in a traumatic birth (Cheng & Caughey, 2008). Poor glycemic control in the mother can also injure the fetus in other ways such as causing intrauterine hypoxia and placental insufficiency, leading to fetal polycythemia, which causes problems before and after birth (Fink, 2006).
The patient, R.B., of Hispanic descent, presented to the Eagle Care Clinic, on May 24, 2010, at 14 2/7 weeks. She is “sure” that her LMP was February 12, 2010. She is G4P2SAB1. She will be 35 years old at EDB (November 20, 2010) and is considered advanced maternal age. She is overweight. She has a history of two previous term vaginal deliveries, in 1995 and 2000, with both neonates weighing almost 9 pounds, which is considered macrosomia. She reports that she does not recall any complications. (The pregnancies took place in Mexico, and therefore we are not able to obtain records.) She also had a SAB in 1997, resulting in a D&C. She denies bleeding, nausea, vomiting, pain or contractions but does complain of fatigue and breast tenderness. She denies any other medical history or surgeries. She is taking prenatal vitamins and no other medication. She has no known allergies. She eats a typical Mexican diet, high in carbohydrates and fats and does not exercise. She does not use tobacco, alcohol or drugs and neither does her husband. This is an unplanned pregnancy, but her family, including two children and her husband, are very supportive and happy about the new baby. She is a stay-at-home mother, and her husband is currently working in the construction industry. They are from Mexico and only speak Spanish. They practice Catholicism. Family medical history is negative except for sister with twins. PHYSICAL EXAM
Vital signs: BP- 128/66, P- 70, RR- 16, T- 98.7 Height- 168cm, Weight- 92 kilos, BMI- 32.92
General: Pleasant, Hispanic woman, appears overweight, in no acute distress.
HEENT: WNL. Teeth intact and...