1. High Risk Pregnancy - 2010

2. High Risk Pregnancies Disordered Eating Obesity Hypertensive Disorders Gestational Diabetes

3. Disordered Eating & Pregnancy: Prevalence 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 Some published numbers for disordered eating in the population ( (Mitchell et al. J midwifery & women’s health, 2006) –Prevalence of binge eating disorder ~ 1.2%-4.5% –Prevalence of anorexia nervosa in young females is 0.03% –About 25% of individuals with anorexia nervosa develop a chronic course.

4. 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 weigh 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)

5. 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.

6. 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

7. 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.

8. Pregnancy and Eating Disorders: A review and clinical Implications (Franko and Walton, Int.J. Eating Disorders, 1993) British report on 6 of 327 women who had attended eating disorder clinic and got pregnant  Median BMI was 16.8 (range 14.9-18.1)  Median length of time with AN was 15 years (range 11-17)  Average weight gain was 8 kg (range 5-14) - recommendations for low BMI are 13-18  Poor third trimester fetal growth was found in all 5 babies who were monitored  Babies had some catch up in infancy

9. Pregnancy Outcome and Disordered Eating (Abraham et al J Psychosom Obstet Gynecol, 1994) 24 women reported previous problems with disordered eating. These women had higher rates of antenatal complications such as IUGR, PIH, edema, GDM, vaginal bleeding (p<0.05) These women also were more likely to have infants with birthweights < 25th % ile (p<0.02)

10. Bulimia Symptoms and other risk behaviors during pregnancy in women with Bulimia Nervosa (Crow et al, Int J Eat Disord, 2004) 129 participants in a long-term follow up study of women who had been treated for BN at the University of Minnesota 322 pregnancies

11. Crow et al., 2004

12. 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.

13. Kouba, 2005

15. 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

16. Recent EDPast EDNon-obese controls Laxative use in pg 8.20.80.2 Pregnancy SIV26.53.90.7 High exercise in pregnancy 32.731.221.2 Strong desire to loose weight 63.531.422.2 Loss of control over eating 72.542.836.1

17. Postpartum eating and Body Image for all Women It is of note that in a general population of postpartum women, eating disorder behaviors increase markedly in the first 3 months post-partum and remain high for the next 9 months. Some women actually first experience clinical eating disorders during this time. (Stein et al Eating Habits and Attitudes in the Post Partum Period. Psychosomatic Med., 1996)

18. 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.

19. 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

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

21. 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

22. 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.

23. 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

24. 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

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

26. 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

27. 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

28. 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.

29. Maternal Obesity Rates of obesity are increasing world- wide Obesity before pregnancy is associated with risk of several adverse outcomes

30. 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 Pregnancy Concerns Associated with Maternal Obesity

31. 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

32. 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

33. 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

34. 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

35. 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%

36. Concerns with surgical births –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

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

38. 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

39. 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

40. 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

41. Cost Costs were 3.2 times higher for women with BMI > 35 Longer hospitalizations

42. 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.”

43. Emerging Issues: Bariatric Surgery Outcomes Challenges of studies: –Appropriate control groups? –Outcomes to measure? –Selection bias –Changes in procedures over time Clinical recommendations

44. 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

45. Pregnancy Outcomes after Gastric-Bypass Surgery Dao, et al. Am J Surg, 2006 N= 21 pregnant within first year post- surgery; 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.”

46. Pregnancy following gastric-bypass (Dao, 2006) < 1 year (21)> 1 year (13) Mean BMI: At surgery At pregnancy 49 35 46 28 Mean weight gain4 #34# Mean birthweight2868 g (2 sets twins) 2727 g (3 sets twins) “Major” pregnancy complications 51 “Minor” pregnancy complications 53

47. 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.

48. 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.”

49. Pregnancy after Bariatric Surgery: A comprehensive review. Sheiner. Arch Gynecology Obstet. 2008. Post surgery women at increased risk for poor perinatal outcomes. “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.”

50. 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

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

52. 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 morbitity and mortality

53. 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

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

55. Use of “PIH” Public Health Population-based prevention vs. Medical Clinical Treatment New WIC risk criteria to be implemented in 2011: “The term pregnancy induced hypertension includes gestational hypertension, preeclampsia and eclampsia.” OG of Canada, 2008 Clinical treatment guidelines: “The term PIH (pregnancy induced hypertension) should be abandoned as its meaning in clinical practice is unclear.”

56. WORKING GROUP REPORT ON HIGH BLOOD PRESSURE IN PREGNANCY N A T I O N A L I N S T I T U T E S O F H E A L T H N A T I O N A L H E A R T, L U N G, A N D B L O O D I N S T I T U T E July 2000

57. 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

58. 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

59. Gestational Hypertension 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

60. 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/dL (“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

61. 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.

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

63. 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

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

65. © 2005 American Heart Association, Inc. Published by American Heart Association.2 Preeclampsia: Recent Insights. Roberts, James; Gammill, Hilary. Hypertension. 46(6):1243-1249, December 2005. 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).

66. 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

67. 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

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

69. © 2005 American Heart Association, Inc. Published by American Heart Association.2 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.

70. Long Term Outcomes Associated with Hypertensive Disorders in Pregnancy

71. 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

72. Copyright ©2010 American Heart Association 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

73. 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

74. Calcium  Epi studies suggest inverse relation between dietary calcium and PIH  Recent meta-analysis found Ca intake of 1.5-2 g associated with reductions in systolic and diastolic BP without adverse effects.  Does lowering BP have effect on pathophysiology of PIH?

75. Effect of routine calcium supplementation during pregnancy on relative risk (RR) of preeclampsia SubgroupTypical RR (95% CI) Low-risk (n = 6 trials)0.79 (0.65, 0.94) High-risk 2 (n = 4 trials)0.22 (0.11, 0.43) Adequate-calcium diet 0.86 (0.71, 1.05) (900 mg/d)(n = 4 trials) Low-calcium diet (<900 mg/d) (n = 6 trials)0.32 (0.21, 0.49) Those at high risk: teenagers, had had preeclampsia previously, had increased sensitivity to angiotension II, or had preexisting hypertension. Ritchie LD, King, JC. Am J Clin Nutr. 2000:71(suppl):1371S-4S

76. 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.

77. Omega-3 Fatty Acids In Maternal Erythrocytes and Risk of Preeclampsia (Williams et al, Epidemiology, 1995) Theory: –Ratio of omega 6 and omega 3 fa may modify processes related to PIH such as platelet and leukocyte reactivity, vasodilation, and inflammatory processes. Study design: –small case control, n=22 cases, 40 controls –adjusted for parity and pre-pregnancy BMI

78. Omega-3 Fatty Acids In Maternal Erythrocytes and Risk of Preeclampsia (Williams et al, Epidemiology, 1995) Results: –Women with the lowest tertile of n-3 in erythrocytes had odds ratio of 7.6 (95% CI=1.4-40.6) for developing preeclampsia.

79. 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

80. 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

81. Cochrane: Exercise or other physical activity for preventing pre-eclampsia and its complications (2006) Data from two trials (2006) –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

82. Antioxidants and Preeclampsia: Possible Mechanisms Placental underperfusion may mediate a state of oxidative stress. Oxidative stress, coupled with an exaggerated inflammatory response, may result in the release of maternal factors that result in inappropriate endothelial cell activation and endothelial cell damage Supplementing women with antioxidants may increase their resistance to oxidative stress, and hence could limit the systemic and uteroplacental endothelial damage seen in pre-eclampsia Cochrane, 2008

83. Cochrane: Antioxidants for preventing pre-eclampsia (2008) Ten trials, 6533 women –5 were rated high quality Most trials used combined vitamin C and E

84. Cochrane: Antioxidants for preventing pre-eclampsia (2008) Outcome # trialsRR95% CI preeclampsia 90.730.51-1.06 Severe preeclampsia 21.250.89-1.76 Preterm birth 51.100.99-1.22 SGA 50.830.62-1.11 Any baby death 41.120.81-1.53 Maternal abdominal pain 11.611.11-2.34

85. Cochrane: Antioxidants for preventing pre-eclampsia (2008) “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.”

86. Vitamin D Very active field of research Vitamin D could be associated via: –Immunomodulatory properties –Functions with vascular structure/BP regulation –Inflammatory responses Some RCTs find protective effects

87. Cochrane: Antioxidants for preventing pre-eclampsia (2008) “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.”

88. 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

89. 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

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

91. 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

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

93. 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.

94. 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.

95. 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.”

96. 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

97. 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

98. 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

99. 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).

100. 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

101. Table 1— Diagnosis of GDM with a 100-g oral glucose load 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. mg/dlmmol/l Fasting955.3 1-h18010.0 2-h1558.6 3-h1407.8

102. 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

103. 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

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

105. 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

106. 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.

107. 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

108. Nutrition Management All women with GDM should receive nutritional counseling, by a registered dietitian when possible For obese women (BMI >30 kg/m2), 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

109. 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

110. Exercise Programs of moderate physical exercise have been shown to lower maternal glucose concentrations in women with GDM

111. 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.”

112. 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

113. 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.”

114. Offspring Newborns of women with GDM have increased adiposity and reduced fat free mass even if not macrosomic Breastfeeding may be protective against childhood overweight in children born to GDM