High Risk Pregnancy 2012 High Risk Pregnancies Disordered

High Risk Pregnancy - 2012

High Risk Pregnancies • Disordered Eating • Obesity • Hypertensive Disorders • Gestational Diabetes

Disordered Eating & Pregnancy: Prevalence • Prevalence in general population (Swanson et al. Arch Gen Psychiatry. 2011): – Lifetime prevalence estimates of anorexia nervosa, bulimia nervosa, and binge-eating disorder were 0. 3%, 0. 9%, and 1. 6%, respectively. • Few data on prevalence of disordered eating in pregnancy • Difficult to adequately capture this information from women. Women may have needs for secrecy and denial so information about history of eating disorders is often not given to health care providers during pregnancy

Diagnostic Criteria: Anorexia Nervosa (American Psychiatric Association) • Refusal to maintain body weigh at or above normal weight for age and height • Intense fear of gaining weight or becoming fat, even through underweight • Disturbance in the way in which one’s body weight or shape is experienced, • Undue influence of body weigh or self-evaluation or denial of the seriousness of current low body weight • In postmenarcheal females, amenorrhea (absence of at least three consecutive menstrual cycles)

Diagnostic Criteria: Bulimia Nervosa (American Psychiatric Association) • Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: – In a discrete period of time, eating an amount of food definitely larger than most people would eat – A sense of lack of control over eating during the episode • Recurrent inappropriate compensatory behavior such as self-induced vomiting, misuse of laxatives, diuretics, enemas or other medications. • Binge eating and inappropriate compensatory behaviors occur at least twice a week for 3 months • Self-evaluation is unduly influenced by body shape and weight • The disturbance does not occur exclusively during anorexia nervosa.

Diagnostic Criteria: Not otherwise specified (American Psychiatric Association) • For females, all the criteria for AN are met, except that the individual has regular menstrual cycles. • All criteria for AN is met, except the weight is WNL, despite significant weight loss • Regular use of inappropriate compensatory behaviors in an individual of normal weight after eating small amounts of food • Repeated chewing and spitting out food, but not swallowing • Binge-eating disorder: recurrent episodes of binge eating in the absence of regular use of compensatory behaviors characteristic of BN

Disordered Eating & Pregnancy · Results of published studies are inconsistent · Developmental tasks of pregnancy are often about the same issues that arise in some women with eating disorders · Body changes · Alterations in roles · Concerns about a woman’s own mothering and needs for psychological separation.

Fertility and prenatal attitudes towards pregnancy in women with eating disorders: results from the Avon Longitudinal Study of Parents and Children (Easter et al. BJOG. 2011) • Women with hx of AN, BN more likely to have seen a doctor fertility problems • Women with hx of AN less likely to have intentional pregnancies (OR 0. 5, 95% CI 0. 4– 0. 7; P < 0. 001) • AN + BN group the odds of negative feelings towards pregnancy at 18 weeks of gestation was 2. 3 compared with the general population (OR 2. 3, 95% CI 1. 3– 4. 1; P < 0. 01;

Pregnancy and neonatal outcomes in women with eating disorders (Kouba et al. Obstet Gynecol, 2005) • Recruited women from 13 Swedish prenatal clinics & screened and diagnosed eating disorders. • 68 controls & 49 nulliparous, nonsmoking women diagnosed with: • 24 AN • 20 BN • 5 NOS • Mean duration of eating disorders was 9 years (range 3 -15) • 16 (33%) of women with hx of eating disorders had received TX • 11 (22%) of women with eating disorders had a relapse during pregnancy that led to contact with a psychologist or psychiatrist.

Kouba, 2005

Kouba, 2005

Recency of ED (Micali et al. J Psychosom. Research, 2007) • N=12, 252 – 57 reported recent episode of ED (6 AN, 51 BN) – 395 reported past history of ED • Note: “recent” not defined in paper. • Asked about behaviors at 18 weeks and 36 weeks via mailed questionnaire

Recent ED Past ED Non-obese controls Laxative use in pg 8. 2 0. 8 0. 2 Pregnancy SIV 26. 5 3. 9 0. 7 High exercise in pregnancy 32. 7 31. 2 21. 2 Strong desire to loose weight 63. 5 31. 4 22. 2 Loss of control over eating 72. 5 42. 8 36. 1

Eating Habits and Attitudes in the Post Partum Period (Stein et al. Psychosomatic Med. , 1996) • N=97, prospective cohort study of primip. women followed during pregnancy and at 3 and 6 mos pp. • Eating Disorder Examination (EDE): restraint, eating concern, shape concern, weight concern and global scores about state over last 28 days • Repeated measures ANOVA indicated that changes in eating disorder pathology pp were largely due to changes in body weight.

An observational study of mothers with eating disorders and their infants ( Stein et al. , J Child Psychol Psychiat, 1994) • 2 groups of primips: • Index group, women who had met EDE criteria for disordered eating during pp period, n=34 • Control group, balanced for SES, age, and child’s gender, n=24 • At one year: • EDE • Child’s growth • Structured observation of child and mother at task and mealtime

Mealtime Behaviors ( Stein et al. , J Child Psychol Psychiat, 1994)

Discussion ( Stein et al. , J Child Psychol Psychiat, 1994) • Index mothers were more intrusive than control mothers • About 1/3 of the index infants and one of the control infants had growth faltering • Regression analysis models to predict infant weights were best fit when included: – – maternal height, infant birthweight conflict during meals mothers concern about own body shape

• Also, eating disordered women make poor role models. Your influence could lead your daughters to their own eating disorders and your sons to believe that the most important thing about women is their weight.

Clinical Implications • Careful screening and monitoring • Possible use of self administered, computer assisted screening tool • Psychotherapy may be indicated • Interventions are not evidence based at this time, but based on case studies & individual counselor’s experiences

Clinical Interventions: Nutrition • “Frequent weigh-ins, lectures about weight gain, and even well-meaning comments by clinical staff can be triggers for increasing the frequency of eating disordered behaviors. ” (Mitchell et al. J midwifery & women’s health, 2006) • If appropriate: – Discuss and provide materials about nutrients and food in pregnancy – Design individual food plan – Determine optimal range of weight gain – Discuss hydration shifts in pregnancy and need for fluid

Clinical Interventions: Exercise • Assess exercise level • Suggest joining exercise groups and new mothers groups to normalize experience of weight concerns

Clinical Interventions: Psychosocial • Making the fetus as real as possible to the patient very early – Focus on fundal measurements? • Empathetically addressing fears of weight gain and feelings of being out of control • Assurance about normal weight gain and patterns of pp weight loss • Education of significant others

Clinical Intervention: Infant Feeding • Offer assistance with parenting concerns • Offer information about infant feeding: – infant’s ability to self regulate – attention to infant cues & signals – use of food as reward or control mechanism

Bulik Hypothesis (Int J Eat Disord, 2005) • Preterm birth is associated with threefold increase in risk of AN • Neurodevelopmental insults in premature infants could contribute to delayed oral-motor growth and onset of early eating problems. • Women with low prepreg BMI & inadequate nutrition during gestation have increased risk for preterm delivery – cycle of risk is established.

Maternal Obesity • Rates of obesity are increasing worldwide • Obesity before pregnancy is associated with risk of several adverse outcomes

Pregnancy Concerns Associated with Maternal Obesity • Nutrition and Pregnancy Outcome. Henriksen, Nutrition Reviews, 2006 • Management of Obesity in Pregnancy. Catalono. Obstetrics and Gynacology, 2007 • Position of the American Dietetic Association and American Society for Nutrition: Obesity, Reproduction, and Pregnancy Outcomes. J Am Diet Assoc. 2009; 109: 918 -927

Fertility • Obesity associated with increased time to conception • 25% of ovulatory infertility attributed to obesity • Less success with assisted reproductive technologies • Potential mechanisms – Adipose tissue impact on hormone availability – Insulin resistance associated with lowered fertility

Diagnosis of Pregnancy • Menses tend to be irregular and pelvic exams and ultrasound exams may be difficult • AFP values are lower in obese women due to increased plasma volume • Blood pressure monitoring may be difficult

Antepartum Outcomes • Higher rates of NTD even with folic acid supplementation (RR = 3. 0 in one study) • Increased risk for both chronic and pregnancy induced hypertension • Increased risk for severe preeclampsia (BMI < 32. 3, risk was 3. 5 times that of controls) • Increased risk of GDM, IDD and NIDD • Increased twining • Increased UTI

Fetal Outcomes • Morbidly obese women have increased risk of preterm delivery – 25% of preterm births are indicated because of maternal medical/ob problems • Neonatal death - stillbirth – Increase in overweight women twice that of normal weight women – Increase in morbidly obese women is 240% greater

Labor and Birth Outcomes • Increased incidence of cesarean births in nulliparous women • BMI < 30: 21% • BMI 30 -35: 34% • BMI 35 -40: 48% • VBAC success rates: – Normal weight women = 71% – Overweight women = 66% – Obese women = 55%

Concerns with Surgical Births for Obese Mothers – Operative times are longer – Increased incidence of blood loss during surgery – Differences in responses to anesthesia (greater spread/higher levels) – Increased risk of post-op complications • Wound infections • Deep venous thrombophlebitis • endometritis

Postpartum Outcomes • Increased risk for endometrial infection • Increased prevalence of urinary incontinence • Decreased rates of lactation success – Initiation – Duration – Amount of milk produced

Infant Outcomes • Large infants - effect is independent of maternal diabetes- rates of macrosomia (>4000 g): – Normal weight women: 8 % – Obese women: 13% – Morbidly obese women: 15% • Increased infant mortality - RR for infants born to obese women was 4. 0 compared to women with BMI < 20

Long Term Risks to Infant • Children born to obese mothers twice as likely to be above 95 th percentile BMI at age 2 • Metabolic syndrome in at age 11: – Hazard ratio = 2. 19 (1. 25 -3. 82) if LGA – Hazard ratio = 1. 81 (1. 03 -3. 19) if maternal obesity

Swedish population-based study (Cedergren, 2004) • n=805, 275 • Morbid obesity (BMI>40) compared to “normal” weight – 5 fold risk of preeclampsia – 3 fold risk of still birth after 28 weeks – 4 fold risk of LGA • BMI >35, <40, associations remain, but not as strong

Cost • Costs were 3. 2 times higher for women with BMI > 35 • Longer hospitalizations

ADA Position Statement, 2009 “Given the detrimental influence of maternal overweight and obesity on reproductive and pregnancy outcomes for the mother and child, it is the position of the ADA and the American Society for Nutrition that all overweight and obese women of reproductive age should receive counseling prior to pregnancy, during pregnancy, and in the interconceptional period on the roles of diet and physical activity in reproductive health, in order to ameliorate these adverse outcomes. ”

Lifestyle interventions for overweight and obese women to improve pregnancy outcome: systematic review & meta-analysis (BMC Med. 2012) • 13 RCT and 6 non-randomized clinical trials • Antenatal dietary and lifestyle intervention (combinations of individual and group counseling & classes provided in multiple sessions over time) in obese women reduces pregnancy weight gain with trend to reduced GDM (OR. 80, . 058 -1. 10). • No clear differences in caesarean delivery, LGA, several other pregnancy-related outcomes.

Bariatric Surgery Challenges of studies: – Appropriate control groups? – Outcomes to measure? – Selection bias – Changes in procedures over time – “Clinicians should be aware that data collected on this subject are often gathered from post-op pregnant women provided with good prenatal care and screening for nutritional deficiencies. ” Pregnancy after Bariatric Surgery: A comprehensive review. Sheiner. Arch Gynecology Obstet. 2008.

Outcomes After Malabsorptive Procedures such as Roux-en-Y(Bernert et al. Diabetes Metab. 2007; Catalono. Obstet Gynecol, 2007) • • • Associated Complications: Small bowel ischemia Nutrient deficiencies (iron, folate, B 12) Fetal abnormalities SGA & preterm birth Cesarean delivery

Pregnancy Outcomes after Gastric-Bypass Surgery • Dao, et al. Am J Surg, 2006 • N= 21 pregnant within first year postsurgery; 13 pregnant after first year (Texas) • Author's conclusions: “Pregnancy outcomes within the first year after weight-loss surgery revealed no significant episodes of malnutrition, adverse fetal outcomes or pregnancy complications. ”

Pregnancy following gastric-bypass (Dao, 2006) < 1 year (21) > 1 year (13) Mean BMI: At surgery At pregnancy Mean weight gain Mean birthweight “Major” pregnancy complications “Minor” pregnancy complications 49 35 4 # 46 28 34# 2868 g (2 sets twins) 5 2727 g (3 sets twins) 1 5 3

Birth Outcomes in Obese Women After Laparoscopic Adjustable Gastric Banding • Dixon et al. Obstet Gynecology. 2005 • N=79 (Australia) • Mean maternal weight gain= 9. 6 +/- 9. 0 kg • Mean birthweight = 3, 397 • Incidence of PIH, GDM, stillbirth, preterm delivery low and high birth weights more similar to population than obese women.

Dixon Conclusions: • “Pregnancy outcomes after LAGB are consistent with general community outcomes rather than outcomes from severely obese women. The adjustability of the LABG assists in achieving these outcomes. ”

Clinical Management of Pregnancy Following Bariatric Sugary (ACOG Committee and Catalano, Obstet Gynecology, 2007) 1. Advise women about risk of unexpected pregnancy following LAGB & need for contraception 2. Delay pregnancy for 12 -18 months – avoid rapid weight loss phase and catabolic state 3. Close monitoring during pregnancy by both ob and surgeon to allow for adjustments of gastric bands 4. Supplement with folate, calcium, B 12

Hypertensive Disorders During Pregnancy • • Incidence Definitions Etiology/pathophysiology Role of Nutrition

Incidence • Second leading cause of maternal mortality in US – 15% of maternal deaths (eclampsia: disseminated intravascular coagulation, cerebral hemorrhgae, hepatic failure, acute renal failure) • Hypertensive disorders occur in 6 to 8% of pregnancies • Contribute to neonatal morbidity and mortality

High Risk Women · · · Under age 20 or over 40 Poor nutritional status Smoking Overweight Other health problems such as renal disease, endocrine disorders (diabetes), autoimmune diseases (lupus) · Multiple gestation · Some fetal anomalies · History of preeclampsia · Risk 10% with mild preeclampsia late in pregnancy · Risk 40% with severe preeclampsia started early in pregnancy

Risk Also Associated with: • Primigravidity • Genetic disease factors • Familial predisposition – family history of hypertension

American Society of Hypertension Position Paper: Hypertension in Pregnancy The Journal of Clinical Hypertension Volume 11, Issue 4, pages 214– 225, April 2009. • Definitions from working group report • Paper includes: – Clinical spectrum – Pathogenic mechanisms – Management

Chronic Hypertension • Known hypertension before pregnancy or rise in blood pressure to > 140/90 mm Hg before 20 weeks • Hypertension that is diagnosed for the first time during pregnancy and that does not resolve postpartum is also classified as chronic hypertension. • ~ 25% risk of superimposed preeclampsia

Risks to Women with Chronic Hypertension • 22% developed preeclampsia; of those: – 48% had SGA baby – 51% delivered before 37 weeks • Risk of preeclampsia higher with: • High BMI • Smoking • Black ethnic origin Adverse Perinatal Outcomes and Risk Factors for Preeclampsia in Women With Chronic Hypertension: A Prospective Study. Chappell, Lucy C. ; Enye, Stephen; Seed, Paul; Briley, Annette L. ; Poston, Lucilla; Shennan, Andrew H. Hypertension. 2008; 51: 1002 -1009

Gestational Hypertension detected for the first time in pregnancy with systolic BP 140 or greater & diastolic BP 90 or greater; no proteinuria • 25 -40% of women with gestational hypertension advance to preeclampsia

Proteinuria • Proteinuria is defined as the urinary excretion of 0. 3 g protein or greater in a 24 -hour specimen. – This will usually correlate with 30 mg/d. L (“ 1+ dipstick”) or greater in a random urine determination with no evidence of urinary tract infection. • Because of the discrepancy between random protein determinations and 24 -hour urine protein in preeclampsia it is recommended that the diagnosis be based on a 24 -hour urine if at all possible

Preeclampsia The presence of hypertension accompanied by proteinuria in pregnancy, usually after 20 weeks • Symptoms may include renal failure & HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) • 4% of women with preeclampsia advance to eclampsia • Treatment: close monitoring & delivery before mother’s health is at excess risk.

Preelampsia Severity (ASH Position statement, 2009) Less Severe More Severe Presentation ≥Gestational week 34 ≥Gestational week 35 Diastolic BP <100 mm Hg >110 mm Hg Headache Absent Present Visual disturbances Absent Present Abdominal pain Absent Present Oliguria Absent Present Creatinine (GFR) Normal Elevated (decreasing) LDH and AST proteinuria Normal mild to moderate Elevated nephrotic range (>3 g/24 h)b Nonreassuring fetal testingc Absent Present

Eclampsia • Occurrence in a woman with preeclampsia, of seizures that can not be attributed to other causes

Pathophysiology • Appears to be strongly related to placenta – When placenta is delivered begins to abate • Initiating Scenario- Stage 1: – Abnormal placental implementation & failed remodeling of maternal spiral arteries – Reduced blood flow to placenta & reduced placental perfusion Roberts & Gammill, Preeclampsia, recent Insights. Hypertension, 2005

Normal Pregnancy: vascular luminal diameter increased 4 fold & vessel wall modified by loss of smooth muscle so becomes flaccid

Figure 1. Two-stage model of the pathophysiology of preeclampsia. The model indicates preeclampsia as occurring in 2 stages. The initiating abnormality (stage 1) is failed vascular remodeling of the vessels that supply the placental bed. This is linked to the maternal syndrome of preeclampsia (stage 2). Preeclampsia: Recent Insights. Roberts, James; Gammill, Hilary. Hypertension. 46(6): 1243 -1249, December 2005. © 2005 American Heart Association, Inc. Published by American Heart Association. 2

Stage 2 • Reduced placental blood flow leads to – Oxidative stress – Production of cytokines, antiangiogenic factors, other products… • Abnormal function of maternal vascular endothelium: – – Liver Kidney Brain Other organs • Additional Characteristics: – alterations in immune response at the maternal interface – increase in inflammatory cytokines in placenta and maternal circulation, “natural killer” cells, and neutrophil activation

Emerging Understandings • Early preeclampsia: appears to be more related to the evolution of an extremely altered cardiovascular response probably triggered by a placental disorder. • Late preeclampsia: seems to be more linked to maternal constitutional factors. – Predisposing cardiovascular or metabolic risks Herbert Valensise, Barbara Vasapollo, Giulia Gagliardi, Gian Paolo Novelli. Early and Late Preeclampsia Two Different Maternal Hemodynamic States in the Latent Phase of the Disease. Hypertension. 2008; 52: 873 -880

Fetal Impacts · Decreased blood volume · Decreased placental blood flow may occur 3 -4 weeks before increased BP · Hypoxia · Decreased nutrient delivery

Maternal fetal/placental interactions in preeclampsia. The development of the maternal syndrome of preeclampsia (stage 2) requires that reduced placental perfusion interact with maternal factors. These constitutional factors are the maternal characteristics that increase the risk of cardiovascular disease in later life. They are modified by the physiological changes of pregnancy. Preeclampsia: Recent Insights. Roberts, James; Gammill, Hilary. Hypertension. 46(6): 1243 -1249, December 2005. © 2005 American Heart Association, Inc. Published by American Heart Association. 2

Long Term Outcomes Associated with Hypertensive Disorders in Pregnancy

Women with Preeclampsia are at Higher Risk of CVD later in Life Morgana L. Mongraw-Chaffin, Piera M. Cirillo, Barbara A. Cohn. Preeclampsia and Cardiovascular Disease Death Prospective Evidence From the Child Health and Development Study Cohort. Hypertension. 2010; 56: 166 -171

Geelhoed, J. J. M. et al. Preeclampsia and Gestational Hypertension Are Associated With Childhood Blood Pressure Independently of Family Adiposity Measures Circulation. 2010; 122: 1192 -1199 Copyright © 2010 American Heart Association

State of Nutritional Science • Stage 1 – very little known about the impact of nutrition early in placental development • Stage 2 – many nutrition studies attempting to intervene on maternal responses · Smooth muscle contraction · Prostaglandin synthesis

Cochrane, 2010: Ca supplementation during pregnancy for preventing hypertensive disorders and related problems • 13 studies • “Ca supplementation appears to almost halve the risk of pre-eclampsia and to reduce the rare occurrence of the composite outcome death or serious morbidity. There were not other clear benefits or harms. ” • Effect greatest for high risk women and those with low Ca intake.

Cochrane: Marine oil, and other prostaglandin precursor, supplementation for pregnancy uncomplicated by preeclampsia or intrauterine growth restriction (2006) • 6 trials • No “clear difference” in the RR of preeclampsia between groups

Physical Activity to Prevent Preeclampsia? • “Regular physical activity, particularly when performed during the year before pregnancy and during early pregnancy, is associated with a reduced risk of preeclampsia. ” – Any regular activity – 35% reduction of risk – Vigorous activities – 54% reduction of risk Sorensen, Tanya K. ; Williams, Michelle A. ; Lee, I-Min; Dashow, Edward E. ; Thompson, Mary Lou; Luthy, David A. . Recreational Physical Activity During Pregnancy and Risk of Preeclampsia, Hypertension. 2003; 41: 1273 -1280

Cochrane: Exercise or other physical activity for preventing pre-eclampsia and its complications • Data from two trials – Appeared to protect, but samples too small – There is insufficient evidence for reliable conclusions about the effects of exercise on prevention of pre-eclampsia and its complications. • Update 2010 – adding results of 4 additional trials ? ? ?

Cochrane: Antioxidants for preventing pre-eclampsia (2008) • Ten trials, 6533 women; 5 were rated high quality • Most trials used combined vitamin C and E • “Evidence from this review does not support routine antioxidant supplementation during pregnancy to reduce the risk of pre-eclampsia and other serious complications in pregnancy. ”

Other Nutrition Related Factors · Na: Pregnant women with proteinuric hypertension have lower plasma volume Na. restriction is associated with accelerated volume depletion – not recommended · Energy and Protein intake: increases not found to be useful · Weight reduction or limited gain in pregnancy: not found to be useful · Garlic & Chinese Herbs: Cochrane - no good quality studies

Pregnant Women with Chronic Hypertension: • Take prenatal vitamin mineral supplement • Follow a diet that meets Dietary Guidelines • Moderate physical activity • Follow recommended weight gain patterns for BMI

Women Diagnosed with Preeclampsia • No real dietary treatment • Recommended levels of energy, protein, sodium • Physical activity restrictions as medically recommended

Postpartum Women who Had Preeclampsia While Pregnant • At higher risk for CVD and subsequent hypertension in pregnancy: • Follow healthy lifestyle • Specifically – – Plenty of fruits & vegetables – Adequate calcium status – Healthy weight

Position Statement Gestational Diabetes Mellitus American Diabetes Association 2004 & 5 th International Workshop-Conference on Gestational Diabetes Mellitus (Diabetes Care. Supplement July 2007)

Definition • Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. The definition applies whether insulin or only diet modification is used for treatment and whether or not the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancy.

Prevalence • 7% of all pregnancies are complicated by GDM in US • more than 200, 000 cases annually in US • prevalence may range from 1 to 14% of all pregnancies, depending on the population studied and the diagnostic tests employed.

Infant Concerns in GDM • Higher risk of: • • neural tube defects birth trauma hypocalcemia hypomagnsemia hyperbilirubinemia prematurity syndromes subsequent childhood and adolescent obesity and risk of diabetes

Infant Concerns, cont. – Macrosomia in infant due to high glucose levels from mother and fetal insulin response leading to increased fat deposition, associated with complications at delivery. – Hypoglycemia of infant following delivery due to high fetal insulin levels at delivery and sudden withdrawal of maternal glucose transfer

Maternal Concerns • Higher risk of: – hypertension – preeclampsia – urinary tract infections – cesarean section – future diabetes

Diagnosis • Assess risk at first visit • If high risk (marked obesity, personal history of GDM, glycosuria, or a strong family history of diabetes) GTT ASAP • Women of average risk should have testing undertaken at 24– 28 weeks of gestation • Low-risk status requires no glucose testing

Low Risk Criteria • Age <25 years • Weight normal before pregnancy • Member of an ethnic group with a low prevalence of GDM • No known diabetes in first-degree relatives • No history of abnormal glucose tolerance • No history of poor obstetric outcome

Non GTT dx • A fasting plasma glucose level >126 mg/dl (7. 0 mmol/l) or a casual plasma glucose >200 mg/dl (11. 1 mmol/l) meets the threshold for the diagnosis of diabetes, if confirmed on a subsequent day, and precludes the need for any glucose challenge

One-step Approach • Perform a diagnostic oral glucose tolerance test (OGTT) without prior plasma or serum glucose screening • May be cost-effective in high-risk patients or populations (e. g. , some Native-American groups).

Two-step approach • Initial screening by measuring the plasma or serum glucose concentration 1 h after a 50 -g oral glucose load • Diagnostic OGTT on that subset of women exceeding the glucose threshold value on the GCT

Table 1— Diagnosis of GDM with a 100 -g oral glucose load mg/dl mmol/l Fasting 1 -h 95 180 5. 3 10. 0 2 -h 3 -h 155 140 8. 6 7. 8 Two or more of the venous plasma concentrations must be met or exceeded for a positive diagnosis. The test should be done in the morning after an overnight fast of between 8 and 14 h and after at least 3 days of unrestricted diet ( 150 g carbohydrate per day) and unlimited physical activity. The subject should remain seated and should not smoke throughout the test.

Nutritional Therapy in GDM • Treatment started before 30 weeks reduces likelihood of serious neonatal morbidity – Individualize MNT – Daily self monitoring of blood glucose (SMBG) – Insulin when needed (20% needed) • Goals: – prevent perinatal morbidity and mortality by normalizing the level of glycemia – prevent ketosis – provide adequate energy and nutrients for maternal and fetal health • dependent on maternal body composition

Monitoring • Daily self-monitoring of blood glucose (SMBG) • Urine glucose monitoring is not useful in GDM. Urine ketone monitoring may be useful in detecting insufficient caloric or carbohydrate intake in women treated with calorie restriction.

Monitoring • Blood pressure and urine protein monitoring to detect hypertensive disorders. • Increased surveillance for pregnancies at risk for fetal demise is appropriate • Assessment for asymmetric fetal growth by ultrasonography to assess need for insulin

Nutrition Management • All women with GDM should receive nutritional counseling, by a registered dietitian when possible • For obese women (BMI >30 kg/m 2), a 30– 33% calorie restriction (to 25 kcal/kg actual weight per day) has been shown to reduce hyperglycemia and plasma triglycerides with no increase in ketonuria • Restriction of carbohydrates to 35– 40% of calories has been shown to decrease maternal glucose levels and improve maternal and fetal outcomes

Insulin • Insulin therapy is recommended when MNT fails to maintain self-monitored glucose at the following levels: – – – Fasting whole blood glucose 95 mg/dl (5. 3 mmol/l) Fasting plasma glucose 105 mg/dl (5. 8 mmol/l) 1 -h postprandial whole blood glucose 140 mg/dl (7. 8 mmol/l) 1 -h postprandial plasma glucose 155 mg/dl (8. 6 mmol/l) 2 -h postprandial whole blood glucose 120 mg/dl (6. 7 mmol/l) 2 -h postprandial plasma glucose 130 mg/dl (7. 2 mmol/l) • Oral agents (not recommended in 2004), in 2007: – Glyburide (glibenclamide): studies indicate may be useful adjunct to MNT/PA; may be less successful with obese patients – Metformin: crosses placenta, insufficient evidence that prevents GDM – Acarbose: safety not fully evaluated

Exercise for Diabetic Pregnant Women: Cochrane, 2009 • 4 trials, 114 women with GDM • Trials conducted in third trimester for about 6 weeks; exercising three times a week for 20 -45 minutes • “There is insufficient evidence to recommend, or advise against diabetic pregnancy women to enroll in exercise programs…. . further trials needed. ”

Treatments for Gestational Diabetes: Cochran, 2009 • 8 RCTS, 1418 women • Reduced risk of pre-eclampsia with intensive tx (dietary advice & insulin) compared to usual care • Reduced perinatal morbidity (death, shoulder dystocia, bone fracture, nerve palsy) with intensive TX compare to usual care • Reduction in proportion of infants weighing more than 4000 g; no sig diff when mothers received oral drugs compared to insulin. • “Specific treatment including dietary advice and insulin for mild GDM reduces the risk of maternal and perinatal morbidity. ”

Follow-up Care • Reclassification of maternal glycemic status should be performed at least 6 weeks after delivery – If glucose levels are normal post-partum, reassessment of glycemia should be undertaken at a minimum of 3 -year intervals – Avoid medications that worsen insulin resistance (e. g. , glucocorticoids, nicotinic acid) – Seek medical attention if develop symptoms suggestive of hyperglycemia. • Increased risk of congenital anomalies in subsequent pregnancies – Use family planning to assure optimal glycemic regulation from the start of any subsequent pregnancy

Long Term • Majority will eventually develop diabetes- – 35 -60 percent within 10 years – risk continues at least 1 -2 decades after GDM pregnancy • “There is substantial research evidence that lifestyle change and use of metformin or thazolidinediones can prevent or delay the progression of IGT to type 2 diabetes after GDM. ”