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Dr Maryam.  Is a major cause of perinatal morbidity and mortality as well as maternal morbidity. Dr Maryam.

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Presentation on theme: "Dr Maryam.  Is a major cause of perinatal morbidity and mortality as well as maternal morbidity. Dr Maryam."— Presentation transcript:

1 Dr Maryam

2  Is a major cause of perinatal morbidity and mortality as well as maternal morbidity. Dr Maryam

3 TYPE I DIABETESTYPE 2 DM  Abrupt onset  usually young age  occasionally occurs in 30’s or 40’s  lifelong requirement for insulin replacement  Abnormalities of insulin sensitive tissues  decreased skeletal muscle and hepatic sensitivity to insulin  abnormal B cell response Dr Maryam

4  Definition  CHO intolerance of variable severity first diagnosed in Pregnancy  Prevalence 2-4%  Risk Factors  maternal age >25  Obesity  Hx of congenital anomalies in previous pregnancy  Family history of diabetes  glucosuria  prior macrosomia  previous unexplained stillbirth  ethnic group: Hispanic, Black, Native American Dr Maryam

5  A state between “ normal “ and “diabetes” in which the body is no longer using and /or secreting insulin properly.  Impaired fasting glucose : A state when fasting plasma glucose is at least 110 but under 126 mg/dl  Impaired glucose tolerance : a state when results of the oral glucose tolerance test are at least 140 but under 200 mg/dl in the 2-hour sample. Dr Maryam

6 Gestational Diabetes Dr Maryam

7 Pre-existing diabetesGestational miscarriageneonatal hypoglycaemia congenital malformationperinatal death stillbirth neonatal death increased risk of shoulder dystocia respiratory distress syndrome fetal macrosomia birth trauma (to mother and baby) induction of labour or caesarean section transient neonatal morbidity obesity and/or diabetes developing later in the baby’s life Dr Maryam

8 Neonatal Congenital Malformation  Cardiovascular anomalies: ASD, VSD  Skeletal anomalies: sacral agenesis  CNS anomalies  Genitourinary anomalies: renal agenesis, polycystic kidneys Dr Maryam

9  The precise mechanisms underlying gestational diabetes remain unknown.  The hallmark ( main mechanism ) of GDM is increased insulin resistance.  Pregnancy hormones and other factors are thought to interfere with the action of insulin as it binds to the insulin receptor.  Since insulin promotes the entry of glucose into most cells, insulin resistance prevents glucose from entering the cells properly. As a result, glucose remains in the bloodstream, where glucose levels rise. More insulin is needed to overcome this resistance; about times more insulin is produced than in a normal pregnancy. Dr Maryam

10  Insulin resistance is a normal phenomenon emerging in the second trimester of pregnancy, which progresses thereafter to levels seen in non-pregnant patients with type 2 diabetes.It is thought to secure glucose supply to the growing fetus.  Women with GDM have an insulin resistance they cannot compensate with increased production in the β-cells of the pancreas.  Placental hormones and to a lesser extent increased fat deposits during pregnancy, seem to mediate insulin resistance during pregnancy. Cortisol and progestrone are the main culprits, but human placental lactogen ( HPL), prolactin and estradiol contribute too. Dr Maryam

11  mild fasting hypoglycemia; postprandial hyperglycemia  progressive increase in tissue resistance to insulin  increase insulin secretion to maintain euglycemia  suppressed glucagon response  Increase prolactin, cortisol Normal pregnancy : Diabetogenic state Dr Maryam

12  Inform women with diabetes who are planning to become pregnant that establishing good glycaemic control before conception and continuing this throughout pregnancy will reduce the risk of miscarriage, congenital malformation, stillbirth and neonatal death.  It is important to explain that risks can be reduced but not eliminated. Dr Maryam

13  screening should be conducted at wks of gestation with use of a 50 g one hour oral glucose load  An abnormal one hour screening test with a venous plasma glucose of >140 mg/dL necessitates a full diagnostic 100 g three hours oral glucose tolerance test (GTT) Dr Maryam

14 Women at high risk for GDM have the following characteristics:  Personal past hx of GDM  A strong FH of type 2 DM  Marked obesity They should be tested as soon as possible and if initial screen is negative, be retested at wks of gestation. Dr Maryam

15 The diagnostic criteria from the National Diabetes Data Group (NDDG) have been used most often, but some centers rely on the Carpenter and Coustan criteria, which set the cutoff for normal at lower values. Compared with the NDDG criteria, the Carpenter and Coustan criteria lead to a diagnosis of gestational diabetes in 54 percent more pregnant women, with an increased cost and no compelling evidence of improved perinatal outcomes. Dr Maryam

16 2006 WHO Diabetes criteria Condition2 hour glucoseFasting glucose mmol/l(mg/dl) Normal<7.8 (<140)<6.1 (<110) Impaired fasting glycaemia<7.8 (<140)≥ 6.1(≥110) & <7.0(<126) Impaired glucose tolerance≥7.8 (≥140)<7.0 (<126) Diabetes mellitus≥11.1 (≥200)≥7.0 (≥126) Dr Maryam

17  HbA1c is a form of hemoglobin used primarily to identify the average plasma glucose concentration over prolonged periods of time.  The 2010 American Diabetes Association Standards of Medical Care in Diabetes added the A1c ≥ 6.5% as another criterion for the diagnosis of diabetes, but this is controversial and has not been universally adopted. Dr Maryam

18  The goal is to prevent adverse pregnancy outcomes.  Counseling before pregnancy (for example, about preventive folic acid supplements) and multidisciplinary approach (a dietitian, a nurse, a diabetic educator, a social worker and a physician ) are important for good pregnancy outcomes.  Patient is seen every 1-2 wks until 36 wks gestation and then weekly.  Patient is asked to keep an accurate diary of their blood glucose concentration. Dr Maryam

19  Refer to a dietitian  Any diet needs to provide sufficient calories for pregnancy, typically 2, ,500 kcal with the exclusion of simple carbohydrates.  Recommend a complex, high fiber CHO diet  Avoid concentrated sweets  Caloric composition includes: 40-50% from complex, high fiber CHO, 20% from protein, and 30-40% from primarily unsaturated fat.  The calories are distributed 10-20% at breakfast, 20-30% at lunch, % at dinner, and 30% as snacks.  The main goal of dietary modifications is to avoid peaks in blood sugar levels.  Since insulin resistance is highest in mornings, breakfast carbohydrates need to be restricted more. Dr Maryam

20  With exercise the blood glucose level decreases because the muscles increase their need for glucose.  This effect lasts for at least 12 hours after exercise. Dr Maryam

21  Insulin: If monitoring reveals failing control of glucose levels with these measures, or if there is evidence of complications like excessive fetal growth, treatment with insulin might become necessary.  The most common therapeutic regime involves premeal fast-acting insulin to blunt sharp glucose rises after meals. Care needs to be taken to avoid low blood sugar levels ( hypoglycemia ) due to excessive insulin injections.  Oral Hypoglycemic Agents: There is some evidence that certain oral glycemic agents might be safe in pregnancy, or at least, are significantly less dangerous to the developing fetus than poorly controlled diabetes. Glyburide (Glibenclamide ) a second generation sulfonylurea has been shown to be an effective alternative to insulin therapy  Metformin: has shown promising results, with its oral format being much more popular than insulin injections Dr Maryam

22  Pt should check their fasting glucose and a 1 hour or 2 hour postprandial glucose level after each meal, for a total of four determinations each day.  If the fasting value is > 95 mg/dL, or 1 hr value > mg/dL or 2 hr value > 120 mg/dL, insulin therapy needs to be initiated.  The goal of insulin therapy is to maintain glucose levels below mg/dl and 2 hr PP below 120 mg/dl. Dr Maryam

23  Is used as a tx for infertility in PCOS.  Is a category B drug  Hasn’t been well studied for use in pregnancy.  Both the ACOG and ADA do not endorse the use of metformin in the tx of GDM until additional RCTs support its safety and effectiveness. Dr Maryam

24  First trimester u/s and a fetal echo to assess congenital cardiac anomalies.  Second trimester u/s to assess fetal growth.  Twice weekly testing NSTs and amniotic fluid volume determination beginning at 32 wks gestation to assess fetal well-being. Dr Maryam

25 Early delivery may be indicated for:  women with poor glycemic control  pregnancies complicated by fetal abnormalities Otherwise, pregnancies are allowed to go to term.  If delivery is scheduled before 39 wks gestation, an amniocentesis to assess for fetal lung maturity is performed.  If corticosteroids are used to accelerate lung maturity, insulin requirement needs to be increased in the next 5 days. Dr Maryam

26 The goal is to maintain normoglycemia in order to prevent neonatal hypoglycemia.  Check patient’s glucose q1-2 hours.  Start insulin drip to maintain a glucose level of between mg/dL.  Observe infant closely for hypoglycemia, hypocalcemia, and hyperbilirubinemia after birth. Dr Maryam

27 Insulin requirements decrease rapidly after delivery, because insulin resistance quickly resolves.  After delivery measure blood glucose. -fasting blood glucose concentrations should be <105 mg/dL and one hour postprandial concentrations should be < 140 mg/dL. Dr Maryam

28 Follow up:  If the pt’s postpartum GTT is normal, she should be re- evaluated at a minimum of 3 years interval with a fasting glucose.  All pts should be encouraged to exercise and lose wt.  All pts should be evaluated for glucose intolerance or DM before a subsequent pregnancy. Dr Maryam

29  Keep babies of women with diabetes with their mothers unless there is a clinical complication.  Admit the baby to a neonatal unit if he or she: is hypoglycaemic with abnormal signs has respiratory distress or jaundice that requires monitoring or treatment has signs of cardiac decompensation, neonatal encephalopathy or polycythaemia needs intravenous fluids or tube feeding (unless adequate support is available on the postnatal ward) is born before 34 weeks (or between 34 and 36 weeks if dictated clinically). Dr Maryam


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