Presentation on theme: "DIABETES MELLITUS WITH PREGNANCY BY: DR. MALAK AL-HAKEEM Assistant Professor and Consultant Obstetrics and Gynaecology."— Presentation transcript:
DIABETES MELLITUS WITH PREGNANCY BY: DR. MALAK AL-HAKEEM Assistant Professor and Consultant Obstetrics and Gynaecology
Carbohydrate Metabolism Before Pregnancy Glucose is the energy source for all tissues and cells. Insulin acts on its receptors causing glucose to enter the cells for : 1- Oxidation (glycolysis) to form ATP. 2- Storage as glycogen.
Postprandial phase Elevated glucose level induces insulin release. Insulin induces glycogen formation in liver and muscles, also decreases glycogenolysis and glyconeogenesis. Insulin stimulates amino acids uptake by muscle cells. Insulin inhibits lipolysis in adipocytes.
Post absorptive phase Six hours after meal, blood glucose level falls to base line with secondary decrease in insulin production. The liver changes its function from net glucose disposal to net glucose production.
Fasting phase The liver glycogen is converted to glucose by glycogenolysis. As glycogen storage is depleted, glucose is produced by glyconeogenesis from protein and fat break down. Lypolysis occurs producing glycerol ( used to form glucose in liver ) and free fatty acids ( ketone bodies ).
CARBOHYDRATE METABOLISM DURING PREGNANCY POST PRANDIAL Increased resistance to insulin action mainly on muscle cells and to less extent on liver cells by: Increased maternal corticosteroids concentration.
CARBOHYDRATE METABOLISM DURING PREGNANCY Production of hpL and PGH. Increased estrogen and progesterone. Increased body weight and decrease physical activity. As a result of diminished maternal sensitivity to insulin action, insulin production is increased to keep pregnant women euglycaemic.
CARBOHYDRATE METABOLISM DURING PREGNANCY FASTING Fall in glucose level (used by the fetus) Enhancement of fat catabolism and production of free fatty acids (decreased insulin second to fasting hypoglycemia)
Diabetes mellitus and pregnancy In USA 4% of pregnant women have diabetes, 88% of them have GDM. The rest ( 12% ) have pregestational diabetes. From the pregestational group 35% are type 1 and 65% are type 2.
Types Of Diabetes TYPE 1 DIABETES. Also known as IDDM. Usually occurs below the age of 30,with abrupt onset. Patients are usually lean. Sever hyperglycemia with tendency of Ketoacidosis. Absent or sever def. In insulin( autoimmune).
TYPE 2 DIABETES. Also known as NIDDM. Relative pancreatic insuf. is present in all patients. The primary disorder is peripheral insulin resistance, mainly at skeletal muscle.
TYPE 2 DIABETES. In the beginning there will be increased insulin production then insuf. Occurs usually in older ( > 40 ) and obese patients. Ketoacidosis is rare.
GESTATION DIABETES Diabetes first recognize during pregnancy. Is consider a form of type 2 DM.
MATERNAL COMPLICATIONS Hypertensive disorders Risks of PET and eclampsia are 3-4 folds that of normal pregnancy (15%). Hypertensive disorders are also more frequent with poor glycemic control. Possible explanation in pre-gestation diabetes are: Vasculopathy Decreased glomerular filtration rate Na retentive properties of insulin
Preterm Labour The relative risk in one study was 1.6 over a control population. Women with pregestational diabetes have increase risk of both indicated and spontaneous preterm labour. Tocolytics and corticosteroids cause elevation of the blood glucose level.
Hydraminose Overall incidence of 16% in all diabetic pregnancy with higher rate in pregestational diabetes. Cause? Fetal urination. Altered osmolality of AF
Pyelonephritis 4% incidence. Increase incidence of CS.
MANAGEMENT OF PRE- GESTATION DIABETES DURING PREGNANCY Insulin is the main drug used, few centers use oral hypoglycemic agents. Team work by obst, endocrino, diabetic educator and neonatologist. Patients cooperation is essential by diet control – regular monitoring – physical exercise.
Rapid acting Onset minutes.Peak 1-2h. Duration 3-4h. Most cases can be controlled on a mixture of regular + NPH insulin twice daily before breakfast and before supper. Insulin infusion pump for best control
Oral Hypoglycemic Agents (OHA) Glyburide ( sulphoneurea group) is the most commonly used. Increases endogenous pancreatic insuline secretion. Mild peripheral improvement of insulin action.
OHA was contraindicated during pregnancy for its teratogenic effect and not providing good glycemic control. Several studies have not found harmful effects from glyburide in either early or late pregnancy and have reported good glycemic control. OHA are not recommended during pregnancy by the ACOG and the ADA.
COMPLICATIONS OF DIABETES Diabetic nephropathy. Occurs in long standing diabetes. Sig. Protienuria is always present. Followed by loss of function. Hypertension is common.
COMPLICATIONS OF DIABETES Diabetic retinopathy. Occurs in long standing diabetes. Micro vascular impairment of retinal vessels. Diabetic neuropathy. Mainly peripheral nerves
DIABETES IN PREGNANCY Before the discovery of insulin (1922) most patients were infertile, maternal mortality was 20% and perinatal mortality was more than 50%. After insulin maternal mortality is rare. PNM decreased over the years, aiming to reach that of nondiabetic pregnancy.
Classifications Of Diabetes White classification. Depends on the duration in years since the diagnosis. Assesses individual risks. Does not make attempt for the degree of glycemia before or during pregnancy.
Classifications Of Diabetes New classification. Pregestation diabetes. 1) type 1 diabetes. - with retinopathy - with nephropathy 2) type 2 diabetes. - with retinopathy - with nephropathy
PREGESTATION DIABETES 2 per 1000 pregnancy. Type 1 is common ( age of patient ). Type 2 is increasing especially in certain ethnic groups like SA. Fetal risks are similar in both type 1 & 2. Maternal risks are more linked to type 1 (duration of the disease).
FETAL COMPLICATIONS Congenital anomalies 2 – 4 times the expected frequency. Significant relation with the degree of glycemia at conception and / or during the early days of the first trimester. The incidence congenital anomalies is related to the level of HbA 1c in the 1 st trimester ( n =< 6 ).
Types of anomalies Cardiac as VSD, ASD, transposition of the great vessels. NTD and renal agenesis. Anal and rectal atresia. Caudal regression syndrome ( sacral agenesis ). Cong. Anomalies account for 50% of the perinatal death in IDDM.
Early pregnancy loss. - related to the degree of preconception glycemic control. Fetal macrosomia. - poor glycemic control stimulates fetal growth during the 2 nd. And 3 rd. Trimester ( start to occur from 24 weeks ). - fetal hyper glycemia causes excess insulin production ( anabolic hormone ).
Fetal macrosomia. - mild maternal hyperglycemia may still cause fetal macrosomia. - postprandial glucose levels in 3 rd trimester are the best predictor of fetal size.
Late fetal demise. - occurs usually in last six weeks. - still in the range of o% to 4%. - cause ? May be due to maternal Ketoacidosis or fetal acidosis.
Birth asphyxia and injuries ( big size ). Respiratory distress syndrome - caused by fetal hyperglycemia or fetal hyperinsulinemia which delay lung maturity.
Neonatal hypoglycemia. - occurs in 30 – to 50% of infants of diabetic mother during the 1 st three hours postpartum. - occurs 2 nd to fetal beta cell hyperplasia.
Polycythemia. - caused by fetal anoxia secondary to increased metabolic activity and oxygen consumption. -fetal hyperinsulinemia stimulates fetal erythropoietin. - in sever cases it may lead to right side heart failure or renal vein thrombosis.
Neonatal Hyperbilirubinaemia. - polycythemia and immaturity of hepatic bilirubin conjugation enzymes. Hypocalcemia caused by low parathyroid hormone in the infant.
Heredity. -more common in type 2 than type 1. -in type 2, 15% with one affected parents and 60% if both are. - in type 1 it is 1.3 and 1.6% respectively.
Management of pregestational diabetes Medical management A]Insulin B]Diet C]Exercise
INSULIN For patient taking two injections /day –2/3 of the total dose of insulin is given am in a ratio of 2 NPH to 1 regular. –1/3 of the total dose is given PM with NPH to regular. ratio 1:1. –The aim of the treatment is to keep the fasting level in the 1st trimester below 5.8 mmol/l and postprandial below 7.8mmol/l. –In the 2nd and 3rd trimester the previous values should be < 5 fasting and <6.7 post prandial.
–Post prandial glucose level is the most difficult to control. –For intensive control the insulin pump is used. It delivered continuous basal supply of insulin which is augmented by a pre-feeding dose. –All effort should made to avoid Ketoacidosis which occurs more frequent and at a lower glucose level in pregnancy. –Ketone bodes are freely diffuse to the baby and can kill it.
Diet 30 – 35 kcal / kg % carbohydrates, 20% proteins and < 30% fats divided into 3 meals + two snacks. Regular exercise to improve glucose sensitivity and take up by muscles.
Follow up Patients should be seen every 1-2 weeks. They are advised to do three to four times daily glucose monitoring at home.
LABOUR AND DELIVERY As the patient is kept fasting, the insulin requirements are usually stable during lab. So continuous insulin infusion is the best way to control maternal glycemia at this time. Capillary glucose monitoring should be performed every 1-2hr. Blood glucose should be < 7.8 during lab.
POSTPARTUM CARE Insulin resistance of pregnancy reverses within hours of delivery. In patient with type 1 diabetes, the insulin should be reduced to the pre pregnancy dosage
POSTPARTUM CARE Patient with type 2, no insulin should be given and her glucose level should be monitored. Breast feeding should be encouraged TFT should be assessed after delivery in patient with type 1 (25% are affected with thyroiditis)
OBSTETRIC MANAG EMENT First Trimester Accurate dating by LMP and USS. Vomiting of early pregnancy may make control difficult. Total insulin dose is 0.6 u /kg.
OBSTETRIC MANAGEMENT Second & Third Trimester Patient is seen every 2/52 till 28/52 then weekly to assess glycemic control. Total insulin dose is 0.7 u and 0.8 u in 2 nd and 3 rd trimester respectively. FP at 16-20/52 for NTD
OBSTETRIC MANAGEMENT USS for cong. Anomalies by 20 weeks. Antenatal fetal monitoring for assessing fetal well being. CTG BPP Doppler from 34/ 52 weeks, and earlier in uncontrolled cases. Check for hydraminose and hypertension.
Ante partum Fetal surveillance In Diabetic Patients No data from large or randomized studies to demonstrate the efficacy of any surveillance approach. A reactive CTG is predictive of fetal wellbeing. BPP is as good as CTG, it does not improve fetal out come if CTG is reactive.
BPP was the principle technique of antenatal fetal surveillance in a group of 238 well controlled diabetic patients with no SB but 3 neonatal deaths with congenital anomalies. Others found BPP is not as reliable in pregnancy complicated by diabetes compared to non diabetic pregnancy.
Doppler umbilical artery studies show increase resistance in diabetic women with Vasculopathy. However acute fetal distress may not be expressed by abnormal Doppler studies.
GESTATION DIABETES Diabetes first diagnosed during pregnancy Includes diabetes that is first appears and that first recognize during pregnancy. Incidence of 2% to 8% of all pregnancy and is increasing. GDM is 10 times more common than pregestational diabetes.
GESTATION DIABETES The majority of patients are treated by diet and exercise and few will need insulin. There is increase risk of recurrent GDM in future pregnancy.
GESTATION DIABETES There is increase risk of developing type 2 diabetes later in life. Up to 50% within 5 years of delivery. Carries the same risks to the fetus as pregestational diabetes except for congenital anomalies.
GESTATION DIABETES The offspring of patients with GDM are at future risks for type 2 diabetes and obesity as adults.
Risk factors for GDM Maternal age > 30 years. Maternal obesity. Family history of type 2 diabetes. GDM in previous pregnancy. Recurrent rate of 20% to 50% (23 folds higher than the normal population).
Risk factors for GDM Large for date babies increase the risk of future diabetes by 6 folds. Polycystic ovarian syndrome. Ethnicity as native American and SA.
PATHOGENESIS Like type 2, GDM is characterized by a variable combination of increase insulin resistance and relatively decrease secretion.
PATHOGENESIS Like type2, GDM starts first by increase insulin production to compensate for the increase resistance. With increase insulin resistance with pregnancy, further augmentation of insulin production may not be possible.
SCREENIG FOR GDM All pregnant women at 24 to 28 weeks. Earlier screening for: 1.Family history of type 2 diabetes. 2.Maternal obesity 3.Previous gestational diabetes 4.Previous macrosomic baby or IUFD.
SCREENIG FOR GDM Testing of urine for sugar has no role as screening test. Random blood sugar has poor sensitivity and specificity HbA 1c is a poorly sensitive test for diagnosis Fasting blood sugar is a good screening test 50 gms GCT is the best screening test.
Diagnosis Three hours 100 gms OGTT after 8 hours fasting and regular diet for 3-4 days. Four readings are measured, 0, 1, 2, 3 hours. If 2 readings are abnormal it is diagnostic. One abnormal reading indicate impaired GTT Patient with impaired GTT has an incidence of 20% to get a macrosomic baby.
WHO 75g. OGTT Fasting = or < 7.8 1hour = or < 11
COMPLICATIONS OF GDM Increase risk of hypertension and cs. No increase risk of fetal malformation and early pregnancy loss( hyperglycemia not present until late 2 nd trimester) Other fetal and neonatal complications (seen in pregestational) diabetes are present.
Management Of GDM Most women can be managed by diet control and exercise alone. About 20% will require insulin therapy. Aim of treatment is to keep fasting levels < 5.3 and postprandial < 6.8
Management Of GDM Diet control should be tried. The diet consists of 30 to 35 kcal/ kg /day in non obese and 25 kcal/kg/day in obese. Daily caloric intake is divided among 3 meals and 1 or 2 snacks.
Management Of GDM Insulin therapy. Is recommended if despite diet control blood sugar series are abnormal. Most authors start insulin for those who are unable to maintain their fasting glucose < 5.8 and 2 hours pp. < 6.8
LABOUR & DELIVERY GDM on insulin patient are delivered between 38 weeks and term depending on the glycemic control. During labour insulin is given by IV. Infusion drip as in pregestational diabetes.
Postpartum Care After delivery, insulin requirement remain low, and most women normalize their plasma glucose levels. Capillary glucose should be performed 2- 4 times /day. If persistent hyperglycemia is noted, undiagnosed pregestational diabetes may have been actually present.
Postpartum Care In those whose blood glucose normalizes after delivery, OGTT is recommended 6 weeks later. As 50% of these patients are at increase risk for type 2 diabetes long term follow up is essential.