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Diabetes and pregnancy
 

Diabetes and pregnancy

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    Diabetes and pregnancy Diabetes and pregnancy Presentation Transcript

    • Dr Shail Kaur Assist Prof Dept of Obs & Gynae PIMS
    • Diabetes Derived from the verb diabainein, made up of the prefix dia, "across, apart," and the word bainein, "to walk, stand." Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425. A variable disorder of carbohydrate metabolism caused by a combination of hereditary and environmental factors and usually characterized by inadequate secretion or utilization of insulin, by excessive urine production, by excessive amounts of sugar in the blood and urine, and by thirst, hunger, and loss of weight
    • American Diabetes Association (ADA) classified the disease in four categories  Type 1 diabetes: autoimmune destruction of the pancreatic β cells, resulting in an inability to produce and secrets insulin.  Type 2 diabetes: insulin resistance, a relative insulin deficiency as well, or it may be both.  Third category: gestational diabetes mellitus (GDM) is defined as the onset or first recognition of diabetes during pregnancy.  Fourth category: is associated with genetic disorders, pancreatic diseases, drug and chemical use, and infections
    • Other causes of diabetes  Genetic defects of β-cell function  Maturity onset diabetes of the young  Mitochondrial DNA mutations  Genetic defects in insulin processing or insulin action  Defects in proinsulin conversion  Insulin gene mutations  Insulin receptor mutations  Exocrine pancreatic defects  Chronic pancreatitis  Pancreatectomy  Pancreatic neoplasia  Cystic fibrosis  Hemochromatosis  Fibrocalculous pancreatopathy  Endocrinopathies  Growth hormone excess (acromegaly)  Cushing syndrome  Hyperthyroidism  Pheochromocytoma  Glucagonoma  Infections  Cytomegalovirus infection  Coxsackievirus B  Drugs  Glucocorticoids  Thyroid hormone  β-adrenergic agonists  Statins
    • Comparison of type 1 and 2 diabetes Feature Onset Type 1 diabetes Type 2 diabetes Sudden Gradual Age at onset Mostly in children Mostly in adults Body habitus Thin or normal Often obese Ketoacidosis Common Rare Usually present Absent Low or absent Normal, decreased or increased Concordance in identical twins 50% 90% Prevalence ~10% ~90% Autoantibodies Endogenous insulin
    • Gestational diabetes  Abnormal maternal glucose regulation occurs in 3-10% of pregnancies  Glucose intolerance of variable degree with onset or first recognition during pregnancy, accounts for 90% of cases of diabetes mellitus (DM) in pregnancy.  Renal glycosuria(5-50%)  diminished renal threshold due to increased glomerular filtration and impaired tubular reabsorption  Glycosuria even with blood sugar levels below 180mg/dl  No treatment required
    • Gestational diabetes mellitus (GDM)  Any degree of glucose intolerance with onset or first recognition during pregnancy  Women with gestational diabetes have a 35-60% chance of developing diabetes mellitus over 10-20 years after pregnancy.  Hyperglycemia in pregnancy results in both maternal and fetal complications.
    • Significance  GDM offers an important opportunity for the development, testing and implementation of clinical strategies for diabetes prevention.  Timely action taken now in screening all pregnant women for glucose intolerance, achieving euglycemia in them and ensuring adequate nutrition may prevent in all probability, the vicious cycle of transmitting glucose intolerance from one generation to another
    • Maternal complications        Abortions Infections Hypertension Pre-ecclampsia Polyhydramnios Preterm delivery Increased risk of prolonged labour, injuries, PPH,cesarean delivery  Puerperal sepsis, lactation failure  Development of diabetes mellitus after pregnancy.
    • Fetal complications          Macrosomia Neonatal hypoglycemia Polycythemia Increased perinatal mortality Congenital malformation Hyperbilirubinemia Respiratory distress Hypocalcaemia Long-term consequences of macrosomia include increased risk of glucose intolerance, diabetes, and obesity in childhood.
    • Birth defects  CNS and skeletal  Neural tube defects  Anencephaly  Microcephaly  Caudal regression syndrome  Sacral agenesis  CVS  VSD,ASD  COA  TGA  Situs inversus  TOF  Renal  Renal agenesis  Hydronephrosis  Double ureter  Polycystic kidneys  GI  Duodenal atresia  Anorectal atresia  Omphalocele  TEF  Others  Single umbilical artery
    • Glycosylated Hb
    • Risk factors  The Western style diet of high fat, high carbohydrate,       and high sodium(a significant contributor to excessive weight gain during pregnancy and, thus, a risk factor for developing diabetes) Obesity Age greater than 25 years prior history of gestational diabetes first-degree relative with diabetes history of poor obstetrical outcome certain ethnic groups
    • Metabolism in Pregnancy  Each meal sets in motion a complex series of hormonal actions, including a rise in blood glucose and the secondary secretion of pancreatic insulin, glucagon, somatomedins, and adrenal catecholamines. These adjustments ensure that an ample, but not excessive, supply of glucose is available to the mother and fetus.  Compared with nonpregnant subjects, pregnant women tend to develop hypoglycemia between meals and during sleep. This occurs because the fetus continues to draw glucose across the placenta from the maternal bloodstream, even during periods of fasting. Interprandial hypoglycemia becomes increasingly marked as pregnancy progresses and the glucose demand of the fetus increases.  Levels of placental steroid and peptide hormones (eg, estrogens, progesterone, and chorionic somatomammotropin) rise linearly throughout the second and third trimesters. Because these hormones confer increasing tissue insulin resistance as their levels rise, the demand for increased insulin secretion with feeding escalates progressively during pregnancy. By the third trimester, 24-hour mean insulin levels are 50% higher than in the nonpregnant state.
    • Physiologic changes of late pregnancy  Human placental lactogen, which is structurally similar to growth hormone, and tumor-necrosis factor-alpha induce changes in the insulin receptor and in post-receptor signaling.  Changes in the beta-subunit of the insulin receptor, decreased phosphorylation of tyrosine kinase on the insulin receptor, and alterations in insulin receptor substrate-1 (IRS-1) and the intracytoplasmic phosphatidylinositol 3-kinase (PI3K) appear to be involved in reducing glucose uptake in skeletal muscle tissue.
    • Metabolism in Diabetes  If the maternal pancreatic insulin response is inadequate, maternal and, then, fetal hyperglycemia results. This typically manifests as recurrent postprandial hyperglycemic episodes. These postprandial episodes are the most significant source of the accelerated growth exhibited by the fetus.  During a healthy pregnancy, mean fasting blood sugar levels decline progressively to a remarkably low value of 74 ± 2.7 (standard deviations [SD]) mg/dL. However, peak postprandial blood sugar values rarely exceed 120 mg/dL.  Meticulous replication of the normal glycemic profile during pregnancy has been demonstrated to reduce the macrosomia rate.  when 2-hour postprandial glucose levels are maintained below 120 mg/dL, approximately 20% of fetuses demonstrate macrosomia.  If postprandial levels range up to 160 mg/dL, macrosomia rates rise to 35%.
    •  Surging maternal and fetal glucose levels are accompanied by episodic fetal hyperinsulinemia.  excess nutrient storage, resulting in macrosomia.  conversion of excess glucose into fat causes depletion in fetal oxygen levels.  These episodes of fetal hypoxia are accompanied by surges in adrenal catecholamines  hypertension,  cardiac remodeling and hypertrophy,  stimulation of erythropoietin, red cell hyperplasia, and increased hematocrit.  Polycythemia (hematocrit >65%) occurs in 5-10% High hematocrit values in the neonate  vascular sludging,  poor circulation, and  postnatal hyperbilirubinemia.
    • Maternal morbidity  Diabetic retinopathy  leading cause of blindness in women aged 24-64 years.  Some form of retinopathy is present in virtually 100% of women who have had type 1 diabetes for 25 years or more.  half the patients with preexisting retinopathy experienced deterioration during pregnancy,  all the patients had partial regression following delivery and returned to their prepregnant state by 6 months postpartum. Consider an ophthalmologic evaluation in the first trimester.
    •  Renal disease  patients with underlying nephropathy can expect varying degrees of deterioration of renal function during a pregnancy.  As renal blood flow and glomerular filtration rate increase 3050% during pregnancy, the degree of proteinuria will also increase.  does not measurably alter the time course of diabetic renal disease, nor does it increase the likelihood of progression to end-stage renal disease.  related to duration of diabetes and degree of glycemic control.  Perinatal complications are greatly increased    Preterm birth, intrauterine growth restriction preeclampsia
    • Elevated blood pressure  Chronic hypertension (1 in 10 diabetic pregnancies overall)  Women with gestational diabetes are at a significantly higher risk of developing hypertension after the index pregnancy.  underlying renal or retinal vascular disease are at a substantially higher risk, with 40% having chronic hypertension.  Patients with chronic hypertension and diabetes are at increased risk of intrauterine growth restriction, superimposed preeclampsia, abruptio placentae, and maternal stroke.  Preeclampsia is more frequent among women with diabetes (approximately 12%) versus the nondiabetic population (8%).  Also increases with maternal age  Increases with duration of preexisting diabetes  The rate of preeclampsia has been found to correlate with the level of glycemic control
    • Fetal Morbidity  Miscarriage  pre-existing diabetes mellitus--9-14%  Suboptimal glycemic control has been shown to double the miscarriage rate  Patients with long-standing (>10 y) and poorly controlled diabetes (glycohemoglobin exceeding 11%) have been shown to have a miscarriage rate of up to 44%.  Conversely, excellent glycemic control normalizes the miscarriage rate.
    • Birth defects  In women with overt diabetes and suboptimal glycemic control      before conception, the likelihood of a structural anomaly is increased 4- to8-fold. Two-thirds of birth anomalies involve the cardiovascular and central nervous systems. Neural tube defects occur 13-20 times more frequently in diabetic pregnancies, genitourinary, gastrointestinal, and skeletal anomalies are also more common. the rate of anomalies was only 3.4% with glycosylated hemoglobin values (HbA1C) of less than 8.5%, versus 22.4% with poorer glycemic control in the periconceptional period (HbA1C >8.5%). Clinical trials of intensive metabolic care have demonstrated that malformation rates similar to those in the nondiabetic population can be achieved with meticulous preconceptional glycemic control.
    • Macrosomia Birth weight above the 90th percentile for gestational age or greater than 4kg. Macrosomia occurs in 15-45% of babies born to diabetic women, a 3-fold increase The priming of β-cell mass in early gestation may account for the persistent fetal hyperinsulinemia throughout pregnancy and the risk of accelerated growth, even when the mother enjoys good metabolic control in later pregnancy the most significant influences being gestational age at delivery, maternal prepregnancy body mass index (BMI), maternal height, pregnancy weight gain, the presence of hypertension, and cigarette smoking.
    • Macrosomia  Excess nutrient delivery to the fetus causes macrosomia and truncal fat deposition  Fetal birth weight correlates best with second- and thirdtrimester postprandial blood sugar levels and not with fasting or mean glucose levels.  When postprandial glucose values average 120 mg/dL or less, approximately 20% of infants can be expected to be macrosomic.  When postprandial levels range as high as 160 mg/dL, macrosomia rates can reach 35%.  Role for excessive fetal insulin levels in mediating accelerated fetal growth.
    • Macrosomia  unique pattern of overgrowth, central deposition of subcutaneous fat in the abdominal and interscapular areas. Skeletal growth is largely unaffected.  Larger shoulder and extremity circumference, a decreased head-to-shoulder ratio, significantly higher body fat, and thicker upper extremity skin folds compared with nondiabetic control infants of similar weights.  positive relationship between severity of maternal fasting hyperglycemia and risk of shoulder dystocia, with a 1 mmol increase in fasting glucose leading to a 2.09 relative risk for shoulder dystocia.
    • Growth restriction  pregnancies in women with preexisting type 1 diabetes.  The most important predictor of fetal growth restriction is underlying maternal vascular disease.  pregnant patients with diabetes-associated retinal or renal vasculopathies and/or chronic hypertension are most at risk for growth restriction.
    • Effects of growth
    • Perinatal mortality  current perinatal mortality rates among women who are diabetic remain approximately twice those observed in the nondiabetic population.  Congenital malformations, respiratory distress syndrome (RDS), and extreme prematurity account for most perinatal deaths in contemporary diabetic pregnancies
    • Birth injury  Injuries of birth, including shoulder dystocia and brachial plexus trauma, are more common among infants of diabetic mothers, and macrosomic fetuses are at the highest risk.  With strict glycemic control, the birth injury rate has been shown to be only slightly higher than controls (3.2 vs 2.5%).  Currently, clinical ability to predict shoulder dystocia is poor. Warning signs during labor (labor protraction, suspected fetal macrosomia, need for operative vaginal delivery) successfully predict only 30% of these events.
    • Polycythemia  A central venous hemoglobin concentration greater than 20 g/dL or a hematocrit value greater than 65% (polycythemia).  Hyperglycemia is a powerful stimulus to fetal erythropoietin production, mediated by decreased fetal oxygen tension.  Untreated neonatal polycythemia may promote vascular sludging, ischemia, and infarction of vital tissues, including the kidneys and central nervous system.
    • Postnatal hyperbilirubinemia  Twice that in a healthy population  Prematurity and polycythemia are the primary contributing factors
    •  Neonatal Hypocalcemia  Up to 50% of infants of diabetic mothers have low levels of serum calcium (< 7 mg/100 mL).  functional hypoparathyroidism  Hypoglycemia  Approximately 15-25% of neonates delivered from women with diabetes during gestation develop hypoglycemia during the immediate newborn period.  Neonatal hypoglycemia is less frequent when tight glycemic control is maintained during pregnancy and in labor.  Unrecognized postnatal hypoglycemia may lead to neonatal seizures, coma, and brain damage.
    • Respiratory problems  The nondiabetic fetus achieves pulmonary maturity at a mean gestational age of 34-35 weeks. By 37 weeks' gestation, more than 99% of healthy newborn infants have mature lung profiles as assessed by phospholipid assays.  However, in a diabetic pregnancy, the risk of respiratory distress may not pass until after 38.5 gestational weeks.  Until recently, neonatal respiratory distress syndrome was the most common and serious morbidity in infants of diabetic mothers
    • Obesity  Excessive body fat stores, stimulated by excessive glucose      delivery Maternal obesity, common in type 2 diabetes, appears to significantly accelerate the risk of infants being LGA. Approximately 30% of fetuses of women with diabetes mellitus in pregnancy are large for gestational age (LGA). In preexisting diabetes mellitus, this incidence appears to be slightly higher (38%). growth velocity of the abdominal circumference is often well above the growth percentiles seen in nondiabetic fetuses, and it is higher than the fetal head and femur percentiles. The growth of the abdominal circumference begins to rise significantly above normal after 24 weeks.
    • Metabolic syndrome  By age 10-16 years, offspring of diabetic pregnancy have a 19.3% rate of impaired glucose intolerance  The childhood metabolic syndrome  childhood obesity,  hypertension,  dyslipidemia, and  glucose intolerance.
    •  Cardiovascular risk factors  higher levels of biomarkers for endothelial damage and inflammation, higher leptin levels, BMI, waist circumference, and systolic blood pressure and decreased adiponectin levels. The association remained significant when controlling for maternal prepregnancy BMI.  Neurocognitive development  maternal GDM and low socioeconomic status were associated with an increased risk for attentiondeficit/hyperactivity disorder (ADHD) at age 6  children exposed to both GDM and low socioeconomic status were at even greater risk for ADHD and also at increased risk for compromised neurobehavioral functioning
    • Preconceptional counselling  Provide information, advice and support that will help to reduce the risks of adverse pregnancy outcomes for mother and baby.  It is important to explain that risks can be reduced but not eliminated.  The importance of avoiding unplanned pregnancy should be an essential component of diabetes education from adolescence for women with diabetes.  Lifestyle modification  Diet  Strict glycemic control  Folic acid
    • Pre-conceptional counselling NICE Guidelines Women with diabetes who are planning to become pregnant and their families should be offered information about how diabetes affects pregnancy and how pregnancy affects diabetes.  The information should cover: • the role of diet, body weight and exercise • the risks of hypoglycaemia and hypoglycaemia unawareness during pregnancy • how nausea and vomiting in pregnancy can affect glycaemic control • the increased risk of having a baby who is large for gestational age, which increases the likelihood of birth trauma, induction of labour and caesarean section
    • Pre-conceptional counselling • the need for assessment of diabetic retinopathy before and during pregnancy • the need for assessment of diabetic nephropathy before pregnancy • the importance of maternal glycaemic control during labour and birth and early feeding of the baby in order to reduce the risk of neonatal hypoglycaemia • the possibility of transient morbidity in the baby during the neonatal period, which may require admission to the neonatal unit • the risk of the baby developing obesity and/or diabetes in later life.
    • Safety of medications for diabetes before and during pregnancy  Women with diabetes may be advised to use metformin as an adjunct or alternative to insulin in the pre-conception period and during pregnancy, when the likely benefits from improved glycaemic control outweigh the potential for harm.  All other oral hypoglycaemic agents should be discontinued before pregnancy and insulin substituted.  Rapid-acting insulin analogues (aspart and lispro) are safe to use during pregnancy.  insufficient evidence about the use of long-acting insulin analogues during pregnancy. Therefore isophane insulin (NPH insulin) remains the first choice for long-acting insulin during pregnancy.
    • First-Trimester Laboratory Testing  more intensive use of studies that are part of normal prenatal care (eg, ultrasonography).  HbA1C,  blood urea nitrogen, serum creatinine,  thyroid-stimulating hormone, and free thyroxine levels  spot urine protein-to-creatinine ratio  capillary blood sugar levels 4-7 times daily.
    • Second-Trimester Laboratory Testing  A repeat spot urine protein-to-creatinine study in women with elevated value in first trimester, a repeat HbA1C, and capillary blood sugar levels 4-7 times daily.  If preeclampsia is suggested, order the following tests:      24-hour urine collection Blood urea nitrogen and serum creatinine Liver function tests Uric acid Complete blood cell count  Assessment of fetal well-being  nonstress test,  amniotic fluid index,  fetal growth and  Doppler ultrasonographic examination of the umbilical cord and middle cerebral artery
    • Screening  All pregnant women need to be screened for gestational diabetes.  Pregnant women with no known history of diabetes are screened at 24-28 weeks gestation.  Women at high risk for GDM are screened at the first prenatal visit.  oGTT is the test of choice in both groups.
    • Risk factors for GDM            Increased weight (ie, BMI greater than or equal to 25) Decreased physical activity First degree relative with diabetes Member of ethnic group with high prevalence of diabetes (African American, Latino, Native American, Asian American, Pacific Islander) Prior history of GDM or delivery of a baby greater than 4kg Metabolic abnormalities - Hypertension, HDL less than 35 mg/dL, triglyceride level greater than 250 mg/dL Polycystic ovarian syndrome HbA1C 5.7% or higher Impaired glucose tolerance or impaired fasting glucose testing in the past Evidence of insulin resistance (acanthosis nigricans or severe obesity) History of cardiovascular disease
    • Effect of race  Prevalence rates are higher in black, Hispanic, Native American, and Asian women than in white women.  In these high-risk populations,  the recurrence risk with future pregnancies -68%.  one-third will develop overt diabetes mellitus within 5 years of delivery, with higher-risk ethnicities having risks nearing 50%.  Race also influences many complications of diabetes mellitus in pregnancy
    • Patient Education & Consent  Reasons for screening  Process of the OGTT test.  Discussion of the ramifications of an abnormal test  Aware that in the event of an abnormal test, treatment needs to begin immediately, whether that entails dietary modifications, oral hypoglycemic agents, or insulin.
    • 100-g OGTT  carbohydrate loading for 3 days preceding the test (>150 g carbohydrates)  overnight fast of 8–14 hours the night before. remain seated during the test, and should not smoke.  fasting plasma glucose >95mg/dL  1-hr plasma glucose >180 mg/dL  2-hr plasma glucose >155 mg/dL  3-hr plasma glucose >140 mg/dL
    • Diabetes  The standard criteria for the diagnosis of diabetes is as follows:  HbA1c of 6.5% or higher  Fasting plasma glucose of 126 mg/dL or higher  2-h plasma glucose of 200 mg/dL or higher during an 75- g OGTT  A symptomatic patient with random plasma glucose of 200 or higher (all plasma glucose values are recorded as mg/dL).  The pregnant women who meet the above criteria are considered to have overt type 2 diabetes mellitus.
    • ACOG recommendation  Screening for GDM at initial prenatal visit  History  Risk factors  50 gram/1-hour OGTT. (> 140 mg/dl)  The diagnosis of GDM continues to be based on the 100 gram/3-hour tolerance test  Fasting less than 95mg/dL,  1-hr less than 180 mg/dl,  2-hr less than 155 mg/dL, and  3-hr less than 140 mg/dL,  with 2 or more abnormal values to confirm diagnosis.
    • Monitoring and Follow up  In the event of an abnormal OGTT  counselled on gestational diabetes mellitus  nutritional counselling.  Glycaemic control is less than ideal, medication should be initiated.  Following delivery,  screened for persistent diabetes 6-12 weeks postpartum  lifelong screening for prediabetes or diabetes development every 3 years.
    • Ultrasonography  In the first trimester,  pregnancy dating and viability  nuchal translucency if the fetus is at high risk for cardiac defects (eg, because of high maternal glycohemoglobin)  In the second trimester,  detailed anatomy ultrasonogram at 18-20 weeks,  fetal echocardiogram if the maternal glycohemoglobin value was elevated in the first trimester.  In the third trimester,  growth ultrasonogram to assess fetal size every 4-6 weeks from 26 to 36 weeks in women with overt preexisting diabetes.  growth ultrasonogram for fetal size at least once at 36-37 weeks for women with gestational diabetes mellitus.  more frequently if macrosomia is suggested.
    • White classification  Gestational diabetes (type A)  Class A1: gestational diabetes; diet controlled  Class A2: gestational diabetes; medication controlled  Pregestational diabetes  Class B: onset at age 20 or older or with duration of less than 10 years  Class C: onset at age 10-19 or duration of 10–19 years  Class D: onset before age 10 or duration greater than 20 years  Class E: overt diabetes mellitus with calcified pelvic vessels  Class F: diabetic nephropathy  Class R: proliferative retinopathy  Class RF: retinopathy and nephropathy  Class H: ischemic heart disease  Class T: prior kidney transplant
    • Diet recommendations  3 small meals and 2-3      small snacks Less carbs at breakfast Choose foods high in fiber Choose foods with less sugar and fat Drink 8 cups of liquid per day Get enough vitamins and minerals
    • Recommendations  Calorie restriction according to BMI  6 servings  Not more than 50% carbohydrate  Complex carbohydrate and cellulose  Remaining equal portions protein and fat
    • Precautions to be taken if on insulin  Be aware of the risk of hypoglycemia, and take a high-sugar snack  It may be necessary to eat small snacks between meals.  If exercise right after a meal, have a snack after the exercise.  If exercise two hours or more after a meal, eat the snack before the     exercise. One serving of fruit will maintain blood sugar for most shortterm activities (about 30 minutes). One serving of fruit plus a serving of starch will be enough for activities that last longer (an hour or more). Don't reduce insulin intake before exercising. Don't inject insulin into a part of the body that will be exercised; for example, if walking, avoid injecting into the leg.
    • SINGS AND SYMPTOMS OF GDM Hypoglycemia (Low Blood Sugar) CAUSES: ONSET: Too little food, too much insulin or diabetes medicine, or extra exercise. Sudden, may progress to insulin shock. BLOOD SUGAR: Below 70 mg/dL. Normal range: 70-115 mg/dL WHAT TO DO? Drink a cup of orange juice or milk or eat several hard candies Test Blood sugar Within 30 minutes after symptoms go away, eat a snack e.g. sandwich, and a glass of milk Contact doctor if symptoms don’t stop
    • Care of feet  Check feet every day. for red spots, cuts, swelling, and blisters.  coverage for special shoes.  Wash feet every day. Dry them carefully, especially between the toes.  Keep skin soft and smooth. Rub a thin coat of skin lotion over the tops     and bottoms of feet, but not between toes. Trim toenails straight across and file the edges with an emery board or nail file. Wear shoes and socks at all times. Never walk barefoot. Protect feet from hot and cold. Keeps the blood flowing to feet. Put feet up when sitting. Wiggle your toes and move ankles up and down for 5 minutes, two (2) or three (3) times a day. Don't cross legs for long periods of time. Don't smoke.
    • Indications for hospitalization  Persistant nausea and vomiting  Significant maternal infection  DKA  Poor control/compliance  Preterm labour
    • Intra-partum management  Absolute requirements  Dextrose containing iv fluids  Insulin  Hourly glucose monitoring  Continuous fetal heart rate monitoring  Continuous tocodynametry  Manage labour as normal
    • APA Insulin drip protocol  Iv fluid mainline:d5w@125cc/hr  Insulin drip  Check RBS every hour  Mix 100U regular insulin in 500cc NS(0.2U/cc) RBS Drip rate cc/hr U/hour <80 Off 0 80-100 2.5 0.5 101-140 5.0 1.0 141-180 7.5 1.5 181-220 10 2.0 >220 12.5 2.5
    • Care of the neonate      Hypoglycemia in the newborn less than 35 mg/dL in the term infant. it is more common in infants of women with pregestational diabetes The newborn must be carefully monitored for at least the first 2 hours after birth. Early feeding and intravenous glucose are therapies commonly used, depending on blood glucose level and symptoms. Infant must monitored for hypocalcaemia, hypomagnesaemia, polycythemia and hyperbilirubinemia, polycythemia, and more common in women with pregestational diabetes, and a team approach to monitoring and caring for these infants should be in place. The most common newborn complication after birth is hypoglycemia which, if uncorrected, may result in seizures.
    • Post-partum health education     Women with pregestational diabetes should continue to be managed by a physician goal of continued glycemic control, determination of postpartum recovery status, and recommendation of family planning methods. Because of evidence that the incidence of childhood diabetes is lower among those who were breastfed, breastfeeding should be encouraged and supported Breastfeeding may also promote improved glycemic and lipid profiles in women with diabetes Provision of an appropriate and effective contraceptive is the first step in preconception care for a next