The definition of gestational diabetes mellitus (GDM) is any degree of glucose intolerance with onset or first recognition during pregnancy. GDM can classify as A1GDM and A2GDM. Gestational diabetes managed without medication and responsive to nutritional therapy is diet-controlled gestational diabetes (GDM) or A1GDM. On the other side, gestational diabetes managed with medication to achieve adequate glycemic control is A2GDM.
Historically, the screening for gestational diabetes consisted of assessing patients history, past medical obstetric outcomes, and family history of type 2 diabetes mellitus. Even though it was useful, it was not appropriate. This screening method failed to identify approximately one-half of pregnant women with GDM. In 1973 a significant study suggested the use of the 50 g 1-hour oral glucose tolerance test as a screening for gestational diabetes; this is a very reliable method for screening, and it is used for approximately 95% of obstetricians in the united states of America as a method for screening GDM during pregnancy. In 2014, the U.S preventive service task force recommended screening all pregnant women for GDM at 24 weeks of gestation.
Gestational diabetes etiology is apparently related to 1) the pancreatic beta-cell dysfunction or the delayed response of the beta cells to the glycemic levels, and 2) the marked insulin resistance secondary to placental hormonal release. The human placental lactogen is the main hormone related to increased insulin resistance in GDM. Other hormones related to the development of this disease are growth hormone, prolactin, corticotropin-releasing hormone, and progesterone, these hormones contribute to the stimulation of insulin resistance and hyperglycemia in the pregnancy.
It has been reported some clinical risk factors for developing gestational diabetes. Those clinical factors include:
The human placental lactogen is a hormone released by the placenta during the pregnancy. It holds a comparable composition to growth hormone and induces important metabolic changes during pregnancy to support the maintenance of fetal nutritional status. This hormone is capable of provoking alterations and modifications in the insulin receptors. The following molecular variations appear to have links to diminishing glucose uptake at peripheral tissues:1) molecular alteration of the beta-subunit insulin receptor, 2) diminished phosphorylation of tyrosine kinase, 3) remodelings in the insulin receptor substrate-1 and phosphatidylinositol 3-kinase.
Maternal high glucose levels cross the placenta and produce fetal hyperglycemia. The fetal pancreas gets stimulated in response to the hyperglycemia. Insulin anabolic properties induce fetal tissues to growth at an increased rate.
There are reports that a higher body mass index and obesity can lead to low-grade inflammation. Chronic inflammation induces the synthesis of xanthurenic acid, which is associated with the development of pre-diabetes and gestational diabetes mellitus.
The past medical obstetric outcomes and family history of type 2 diabetes mellitus are important components of the history taking in GDM. The clinical features of gestational diabetes mellitus can be varied. The disproportionate weight gain, obesity, and elevated BMI can be suggestive features. The diagnosis is established by the laboratory screening method at the 24 to 28 weeks of pregnancy.
Reports exist that the gestational age when DSM develops influences pregnancy outcome.
Recommendations are for screening for gestational diabetes at 24 to 28 weeks of pregnancy with a 50-g, 1-hour oral glucose challenge test. If the values are abnormal, greater than or equal to 130 mg/dL (7.22 mmol/L), or greater than or equal to 140 mg/dL (7.77 mmol/L), a confirmatory test is necessary with a 100-g, 3-hour oral glucose tolerance test, with the following values: first hour over 180 mg/dL, second hour over 155 mg/dL, third hour more than 140 mg/dL. The presence of two or more abnormal results establishes the diagnosis of gestational diabetes.
The ADA recommends to consider screening strategy for detecting pregestational diabetes or early gestational diabetes mellitus in all women who are overweight or obese and have one or more of the following risk factors:
The American Diabetes Association (ADA) has noted that measurement of hemoglobin A1C is usable, but it may not be suitable to use alone, due to decreased sensitivity compared to oral glucose tolerance test.
The ACOG recommended levels of blood glucose in pregnancy is fasting plasma glucose under 95 mg/dL, 1 hour postprandial under 130-140 mg/dL, 2 hours postprandial below 120mg/dL.
In the postpartum period, 24 to 72 hours after the delivery, it is recommended to monitor glucose levels. After removing the placenta insulin resistance tends to improve, this can help escalate down insulin or hypoglycemic agents. Glycemic therapy will point towards achieving a euglycemic glucose level. At 4 to 12 weeks post-partum, it is recommended to perform a 75g oral glucose tolerance test to rule out the possibility of development of type 2 diabetes.
Gestational diabetes management begins with nonpharmacologic measurements like diet modifications, exercise, and glucose monitoring. The ADA recommends nutritional counseling by a registered dietitian and development of a personalized plan based on the patients BMI. In some settings, in which dietitians are not able, the physician can provide recommendations based on the three major nutritional concepts: caloric allotment, caloric distribution, and carbohydrate intake.
The amount of exercise recommended in GDM is 30 minutes of moderate-intensity aerobic exercise at least five days a week or a minimum of 150 minutes per week.
If the patient glycemic control is not adequate despite optimal adherence to diet and exercise, it is recommended to begin pharmacologic treatment. The ADA first line of treatment for GDM is insulin. The therapy with insulin has been considered the standard therapy for gestational diabetes management when adequate glucose levels are unachievable with diet and exercise.
Insulin can help achieve an appropriate metabolic control, and it is added to the management if fasting blood glucose is greater or equal to 95 mg/dL, if 1-hour glucose level is greater or equal to 140 mg/dL, or if 2-hour glucose level is greater than 120 mg/dL.
The oral hypoglycemic agents, metformin and glyburide, are increasingly being used among women with gestational diabetes, despite the lack of FDA approval. Glyburide can initiate at a dose of 2.5 mg, and the maximum dose is 20mg. Metformin therapy should start at a dose of 500 mg, and the maximum dose is 2500 mg.
Basal insulin dose can be calculated using the patient’s weight formula, 0.2 units/kg/day. If the blood glucose level becomes elevated following a meal, rapid-acting insulin, or regular insulin can be prescribed before the meal, starting the dose with 2 to 4 units.
In the first trimester, the total daily insulin requirement is 0.7 units/kg/day, in the second trimester it is 0.8 units/kg/day, and in the third trimester, it is 0.9 to 1.0 units/kg/day.
The patient should divide the total daily dose of insulin into two halves; one half given as basal insulin at bedtime, and the other half divided between three meals and given as rapid-acting, or regular insulin before meals.
Lispro and aspart have approval for usage in pregnancy. The short-acting insulin is associated with less hypoglycemia.
At 4 to 12 weeks post-partum, the recommendation is to perform a 75g oral glucose tolerance test to rule out the possibility of the development of type 2 diabetes, impaired fasting glucose or impaired glucose tolerance test.
The complications of developing gestational diabetes categorize as maternal and fetal. The fetal complications include macrosomia, neonatal hypoglycemia, polycythemia, shoulder dystocia, hyperbilirubinemia, neonatal respiratory distress syndrome, increased perinatal mortality, and hypocalcemia. Maternal complications include hypertension, preeclampsia, increased risk of developing diabetes mellitus, and increased risk of cesarean delivery.
The management and treatment of women with gestational diabetes is an emerging challenge for health care providers and teams. Thus, today, gestational diabetes requires an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results and prevent further complications. Efforts and strategies are necessary to recognize them effectively. The development of prevention strategies would facilitate the treatment of gestational diabetes and would help improve health outcomes. Women with gestational diabetes have an increased risk of developing type 2 diabetes over 10 to 20 years after pregnancy.
Many pregnant women who develop diabetes are not diagnosed until very late, which significantly increases the morbidity of the disease.
Many healthcare institutions are now operating pharmacy or nurse practitioner diabetic clinics that offer diabetic education to pregnant females. These clinics regularly monitor blood glucose and refer patients to an endocrinologist. This practice reduces the burden of the obstetrician, lowers healthcare costs, and helps the delivery of optimal care for those who need it.
All members of the interprofessional healthcare team need to collaborate and work together to manage gestational diabetes. Nursing stands at the forefront of patient encounters to determine adherence to therapeutic choices, and monitor for therapy efficacy as well as being alert for potential adverse effects, which they will communicate to other team members. Pharmacists need to perform medication reconciliation, verify the dosing of insulin or other antihyperglycemic drugs, and assist with patient counseling about medication and lifestyle adherence. In this cooperative paradigm, the interprofessional team can guide outcomes most successfully. [Level 5]
|||Coustan DR, Gestational diabetes mellitus. Clinical chemistry. 2013 Sep; [PubMed PMID: 23536513]|
|||Jawad F,Ejaz K, Gestational diabetes mellitus in South Asia: Epidemiology. JPMA. The Journal of the Pakistan Medical Association. 2016 Sep; [PubMed PMID: 27582153]|
|||Spaight C,Gross J,Horsch A,Puder JJ, Gestational Diabetes Mellitus. Endocrine development. 2016; [PubMed PMID: 26824237]|
|||ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstetrics and gynecology. 2018 Feb [PubMed PMID: 29370047]|
|||Law KP,Zhang H, The pathogenesis and pathophysiology of gestational diabetes mellitus: Deductions from a three-part longitudinal metabolomics study in China. Clinica chimica acta; international journal of clinical chemistry. 2017 May; [PubMed PMID: 28213010]|
|||Mack LR,Tomich PG, Gestational Diabetes: Diagnosis, Classification, and Clinical Care. Obstetrics and gynecology clinics of North America. 2017 Jun; [PubMed PMID: 28499531]|
|||Chiefari E,Arcidiacono B,Foti D,Brunetti A, Gestational diabetes mellitus: an updated overview. Journal of endocrinological investigation. 2017 Sep; [PubMed PMID: 28283913]|
|||Brzozowska M,Bieniek E,Szosland K,Lewinski A, Gestational diabetes - is diet and insulin the only solution? Neuro endocrinology letters. 2017 Oct; [PubMed PMID: 29106783]|
|||Zheng J,Wang H,Ren M, Influence of exercise intervention on gestational diabetes mellitus: a systematic review and meta-analysis. Journal of endocrinological investigation. 2017 Oct; [PubMed PMID: 28401529]|
|||Alfadhli EM, Gestational diabetes mellitus. Saudi medical journal. 2015 Apr; [PubMed PMID: 25828275]|
|||Zhu Y,Zhang C, Prevalence of Gestational Diabetes and Risk of Progression to Type 2 Diabetes: a Global Perspective. Current diabetes reports. 2016 Jan; [PubMed PMID: 26742932]|
|||Senat MV,Deruelle P, [Gestational diabetes mellitus]. Gynecologie, obstetrique [PubMed PMID: 26948827]|
|||Lindsay RS,Mackin ST,Nelson SM, Gestational diabetes mellitus-right person, right treatment, right time? BMC medicine. 2017 Aug 28; [PubMed PMID: 28844206]|
|||Ashwal E,Hod M, Gestational diabetes mellitus: Where are we now? Clinica chimica acta; international journal of clinical chemistry. 2015 Dec 7; [PubMed PMID: 25655741]|