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Title: High%20Risk%20Pregnancy%20-%202007


1
High Risk Pregnancy - 2007
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
    womens 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 ones 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 womans 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 (plt0.05)
  • These women also were more likely to have infants
    with birthweights lt 25th ile (plt0.02)

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
2 Studies from Sweden.
13
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.

14
Kouba, 2005
15
Kouba, 2005
16
Birth outcomes and pregnancy complications in
women with a history of AN (Ekeus et al, BJOG,
2006)
  • Birth register study
  • 1000 primiparous women who were discharged from
    hospital with dx of AN from 1973-1996 who gave
    birth 1983-2002
  • All non AN births (827,582)
  • Birthweights lower (p0.005) in AN group
  • Mean AN, 3387
  • General population mean, 3431
  • Longer hospital say for AN (gt 6 months) not
    associated with different outcomes
  • No difference in SGA and any other negative birth
    outcomes for mother or baby

17
Birth outcomes and pregnancy complications in
women with a history of AN (Ekeus et al, BJOG,
2006)
  • Authors explanation of findings
  • Our findings may be a result of gradual
    improvement in the care process, both AN and
    maternity care.
  • A country with a satisfactory maternity
    surveillance, outcome of pregnancy and delivery
    may be just as good for women with a hx of AN as
    for the general population.
  • OR..the fertility problems associated with AN
    mean that pregnancy will only occur in less
    severe cases

18
Avon Longitudinal Study of Parents and Children
  • N14,472
  • Representative of women in the UK
  • 8590 of women who were expected to deliver
    babies in Avon geographical area between April
    1991 and December 1992

19
Associated Risks Percents(Micali et al. Br J
Psych., 2007)
AN (n171) BM (n191) AN BN (n82) Other Pysch. Disord (n1166) General Population (n10,636)
Smoking T1 28 26 40 40 21
Smoking T2 20 21 24 33 16
Alcohol T1 12 19 25 19 15
20
Recency of ED(Micali et al. J Psychosom.
Research, 2007)
  • N12,252
  • 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

21
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
22
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.

23
Eating Habits and Attitudes in the Post Partum
Period (Stein et al. Psychosomatic Med., 1996)
  • N97, 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.

24
Eating Habits and Attitudes in the Post Partum
Period (Stein et al. Psychosomatic Med., 1996)
p lt0.05, plt 0.01, plt0.001
25
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, n34
  • Control group, balanced for SES, age, and childs
    gender, n24
  • At one year
  • EDE
  • Childs growth
  • Structured observation of child and mother at
    task and mealtime

26
Mealtime Behaviors ( Stein et al., J Child
Psychol Psychiat, 1994)
27
Play Behaviors ( Stein et al., J Child Psychol
Psychiat, 1994)
28
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

29
www.anred.com
  • You could become depressed and frantic because of
    weight gain during pregnancy. You might feel so
    out of control of your life and body that you
    would try to hurt yourself or the unborn baby.
    You might worry and feel guilty about the damage
    you could be causing the baby.

30
  • Some women with eating disorders welcome
    pregnancy as a vacation from weight worries. They
    believe they are doing something important by
    having a baby and are able to set aside their
    fear of fat in service to the health of the
    child. Others fall into black depression and
    intolerable anxiety when their bellies begin to
    swell. Most fall somewhere between these two
    extremes.

31
  • You might underfeed your child to make her thin,
    or, you might overfeed her to show the world that
    you are a nurturing parent. Power struggles over
    food and eating often plague families where
    someone has an eating disorder. You could
    continue that pattern with your child.

32
  • Motherhood is stressful. If you are not strong in
    your recovery, you will be tempted to fall back
    on the starving and stuffing coping behaviors
    that are so familiar to you. Ideally, as you
    begin raising a family, you will already have
    learned, and will have had practice using, other
    more healthy and effective behaviors when you
    feel overwhelmed.

33
  • 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.

34
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
    counselors experiences

35
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

36
Clinical Interventions Nutrition
  • Frequent weigh-ins, lectures about weight gain,
    and even well-meaning comments my clinical staff
    can be triggers for increasing the frequency of
    eating disordered behaviors. (Mitchell et al. J
    midwifery womens 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

37
Clinical Interventions Exercise
  • Assess exercise level
  • Suggest joining exercise groups and new mothers
    groups to normalize experience of weight concerns

38
Clinical Intervention Infant Feeding
  • Offer assistance with parenting concerns
  • Offer information about infant feeding
  • infants ability to self regulate
  • attention to infant cues signals
  • use of food as reward or control mechanism

39
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.

40
Maternal Obesity
  • Rates of obesity are increasing world-wide
  • Obesity before pregnancy is associated with risk
    of several adverse outcomes

41
Pregnancy Concerns Associated with Maternal
Obesity
  • Nutrition and Pregnancy Outcome. Henriksen,
    Nutrition Reviews, 2006
  • Management of Obesity in Pregnancy. Catalono.
    Obstetrics and Gynacology, 2007

42
Diagnosis of Pregnancy Problems
  • 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

43
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 lt
    32.3, risk was 3.5 times that of controls)
  • Increased risk of GDM, IDD and NIDD
  • Increased twining
  • Increased UTI

44
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

45
Labor and Birth Outcomes
  • Increased incidence of cesarean births in
    nulliparous women
  • BMI lt 30 21
  • BMI 30-35 34
  • BMI 35-40 48
  • VBAC success rates
  • Normal weight women 71
  • Overweight women 66
  • Obese women 55

46
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

47
Postpartum Outcomes
  • Increased risk for endometrial infection
  • Increased prevalence of urinary incontinence

48
Infant Outcomes
  • Large infants - effect is independent of maternal
    diabetes- rates of macrosomia (gt4000 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
    lt 20

49
Long Term Risks to Infant
  • Children born to obese mothers twice as likely to
    be above 95th 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

50
Swedish population-based study (Cedergren, 2004)
  • n805,275
  • Morbid obesity (BMIgt40) compared to normal
    weight
  • 5 fold risk of preeclampsia
  • 3 fold risk of still birth after 28 weeks
  • 4 fold risk of LGA
  • BMI gt35, lt40, associations remain, but not as
    strong

51
Cost
  • Costs were 3.2 times higher for women with BMI gt
    35
  • Longer hospitalizations

52
Emerging Issues Bariatric Surgery
  • Outcomes
  • Challenges of studies
  • Appropriate control groups?
  • Outcomes to measure?
  • Selection bias
  • Changes in procedures over time
  • Clinical recommendations

53
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, B12)
  • Fetal abnormalities
  • SGA preterm birth
  • Cesarean delivery

54
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.

55
Pregnancy following gastric-bypass (Dao, 2006)
lt 1 year (21) gt 1 year (13)
Mean BMI At surgery At pregnancy 49 35 46 28
Mean weight gain 4 34
Mean birthweight 2868 g (2 sets twins) 2727 g (3 sets twins)
Major pregnancy complications 5 1
Minor pregnancy complications 5 3
56
Birth Outcomes in Obese Women After Laparoscopic
Adjustable Gastric Banding
  • Dixon et al. Obstet Gynecology. 2005
  • N79 (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.

57
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.

58
Pregnancy Outcome of Patients with Gestational
Diabetes Mellitus Following Bariatric Surgery
  • Sheiner et al. Am J Obstet Gynecol. 2006
  • N 28 (16 gastric banding)
  • Compared to 7988 GDM pregnancies without surgery
  • Israel between 1988 and 2002
  • No differences in obstetric characteristics,
    perinatal outcomes, congenital malformations,
    Apgar, Hgb A1c, fasting glucose.

59
Sheiner et al. conclusions
  • Previous bariatric surgery in patients with GDM
    is not associated with adverse perinatal
    outcome.
  • Note not associated with better outcomes
    either.

60
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, B12

61
Hypertensive Disorders During Pregnancy
  • Incidence
  • Definitions
  • Etiology/pathophysiology
  • Nutritional Implications

62
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
WORKING GROUP REPORT ON HIGH BLOOD PRESSURE IN
PREGNANCY
July 2000
63
Incidence
  • Second leading cause of maternal mortality in US
  • 15 of maternal deaths (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

64
High risk
  • First pregnancy and under age 17 or over 35
  • Family history of hypertension
  • Poor nutritional status
  • Smoking
  • Overweight
  • Other health problems such as renal disease,
    diabetes
  • Multiple gestation
  • Some Fetal anomalies

65
Chronic Hypertension
  • Known hypertension before pregnancy or rise in
    blood pressure to gt 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.

66
Gestational Hypertension
  • Hypertension in pregnancy is present when
    diastolic BP is 90 or greater, systolic BP is 140
    or greater
  • the use of BP increases of 30 mm Hg systolic and
    15 mm Hg diastolic has not been recommended -
    women in this group not likely to have increased
    adverse outcomes
  • ¼ of women with gestational htn advance to
    preeclampsia

67
Preeclampsia
  • Preeclampsia is defined as the presence of
    hypertension accompanied by proteinuria
  • In the absence of proteinuria the disease is
    highly suspect when increased blood pressure with
    headache, blurred vision, and abdominal pain, or
    with abnormal laboratory tests, specifically, low
    platelet counts and abnormal liver enzymes.

68
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

69
Findings that increase the possibility of
Eclampsia and indicate need for FU Severe
Preeclampsia
70
(No Transcript)
71
Edema
72
Dx of Preeclampsia Superimposed on Chronic Htn.
73
Eclampsia
  • Occurrence in a woman with preeclampsia, of
    seizures that can not be attributed to other
    causes
  • Rare 4 of women with preeclampsia advance to
    eclampsia

74
Etiology
  • Not fully understood
  • Primary pathophysiology is placental function
  • Secondary pathophysiology involves endothelial
    cell dysfunction due to factors released because
    of insufficient placental blood supply

75
Characterized by
  • Vasospasm
  • Activation of the coagulation system
  • Perturbations in systems related to volume and
    blood pressure control

76
Pathogenic Mechanisms
  • Delivery is only known cure - research has
    focused on placenta
  • failure of the spiral arteries (terminal branches
    of uterine artery) to remodel
  • alterations in immune response at the maternal
    interface
  • increase in inflammatory cytokines in placenta
    and maternal circulation, natural killer cells,
    and neutrophil activation

77
Pathophysiology
  • Decreased blood flow
  • Decreased renal blood flow, decreased GFR, Na
    retention
  • Tissue hypoxia
  • Damage to organs multi-organ disease affecting
    the liver, kidneys, and brain

78
Pathophysiology
  • Decreased blood volume
  • Decreased placental blood flow may occur 3-4
    weeks before increased BP
  • Hypoxia
  • Decreased nutrient delivery

79
Outcomes
  • Increased LBW and IUGR for infant
  • There is mounting evidence that children born to
    mothers whose blood pressure was elevated during
    pregnancy are at greater risk for elevated blood
    pressure during childhood and adolescence
  • Also long term maternal health may be affected by
    consequences of maternal damage to renal and CV
    systems.

80
Focus of Possible Interventions
  • Smooth muscle contraction
  • Prostaglandin synthesis

81
Calcium
  • Epi studies suggest inverse relation between
    dietary calcium and PIH
  • Intraerythrocyte calcium levels and intracellular
    calcium ion conc. increased in women with
    pre-eclampsia
  • HO Ca supplementation reduced serum parathyroid
    hormone reduced intracellular Ca conc. in
    vascular smooth muscle cells and reduces response
    to pressure stimuli
  • Several RCT have found reduced risk of PIH with
    Ca supplementation to prevent (not treat) PIH.

82
Calcium, cont.
  • Recent meta-analysis found Ca intake of 1.5-2 g
    associated with sig. reductions in systolic and
    diastolic BP without adverse effects.
  • Question remains does lowering BP have effect on
    pathophysiology of PIH?

83
Cochrane Calcium supplementation during
pregnancy for preventing hypertensive disorders
and related problems (2006)
  • 12 studies met criteria
  • Randomized trials comparing at least one gram
    daily of calcium during pregnancy with placebo.
  • RR of high blood pressure with Ca supplements
    0.70 (95 CI, 0.57-0.86)
  • RR of preeclampsia with Ca supplements 0.48
    (95 CI, 0.33-0.69)

84
Cochrane Calcium supplementation during
pregnancy for preventing hypertensive disorders
and related problems (2006)
  • 5 trials of Ca supplements in high risk women
  • RR 0.22 (95 CI, 0.12-0.42)
  • 7 trials in women with low baseline Ca
  • RR 0.22 (95 CI, 0.18-0.70)

85
Cochrane Calcium supplementation during
pregnancy for preventing hypertensive disorders
and related problems updated 2006
  • Reviewers conclusions
  • Calcium 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 no other clear
    benefits, or harms.

86
Cochrane Magnesium supplementation in
pregnancy updated 2001
  • There is not enough high quality evidence to show
    that dietary magnesium supplementation during
    pregnancy is beneficial.

87
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, n22 cases, 40 controls
  • adjusted for parity and pre-pregnancy BMI

88
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
    CI1.4-40.6) for developing preeclampsia.

89
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
  • 2 trials, lower risk of giving birth before 34
    weeks
  • RR 0.69 (95 CI 0.49-0.99)

90
Antioxidants and Preeclampsia Definitions
  • Antioxidants any substance that, when present in
    low concentrations compared to that of an
    oxidizable substrate, significantly delays or
    inhibits oxidation of that substrate
  • Free radical scavengers include vitamin C
    (ascorbate), vitamin E (tocopherols), carotenoids
  • Antioxidant enzymes include glutathione
    peroxidase, superoxide dismutase and catalase,
    which are dependent on the presence of co-factors
    such as selenium, zinc and iron

91
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, 2005
92
Cochrane Antioxidants for preventing
pre-eclampsia (2005)
  • 7 trials involving 6082 women
  • Only 3 of 7 were rate high quality
  • All randomized and quasi-randomized trials
    comparing one or more antioxidants with either
    placebo or no antioxidants during pregnancy for
    the prevention of pre-eclampsia, and trials
    comparing one or more antioxidants with another,
    or with other interventions.

93
Cochrane Antioxidants for preventing
pre-eclampsia (2005)
  • Supplementing with any antioxidants during
    pregnancy compared to control
  • RR of preeclampsia 0.61 (95 CI, 0.50,0.70)
  • RR SGA 0.64 (95 CI, 0.47,0.87)
  • Increased risk of preterm birth RR 1.38 (95 CI,
    1.04,1.82)

94
Cochrane Antioxidants for preventing
pre-eclampsia (2005)
  • These results should be interpreted with
    caution, as most of the data come from poor
    quality studies. Nevertheless, antioxidant
    supplementation seems to reduce the risk of
    pre-eclampsia. There also appears to be a
    reduction in the risk of having a
    small-for-gestational-age baby associated with
    antioxidants, although there is an increase in
    the risk of preterm birth. Several large trials
    are ongoing, and the results of these are needed
    before antioxidants can be recommended for
    clinical practice.

95
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

96
Position StatementGestational Diabetes Mellitus
American Diabetes Association2004
97
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.

98
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.

99
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 2428 weeks of gestation
  • Low-risk status requires no glucose testing

100
Low Risk Criteria
  • Age lt25 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

101
Non GTT dx
  • A fasting plasma glucose level gt126 mg/dl (7.0
    mmol/l) or a casual plasma glucose gt200 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

102
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).

103
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

104
Table 1 Diagnosis of GDM with a 100-g oral
glucose load
mg/dl mmol/l

Fasting 95 5.3
1-h 180 10.0
2-h 155 8.6
3-h 140 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.
105
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

106
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

107
Maternal Concerns
  • Higher risk of
  • hypertension
  • preeclampsia
  • urinary tract infections
  • cesarean section
  • future diabetes

108
Nutritional Therapy in GDM
  • 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

109
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.

110
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

111
Nutrition Management
  • All women with GDM should receive nutritional
    counseling, by a registered dietitian when
    possible
  • For obese women (BMI gt30 kg/m2), a 3033 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 3540 of
    calories has been shown to decrease maternal
    glucose levels and improve maternal and fetal
    outcomes

112
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 glucose-lowering agents have generally not
    been recommended during pregnancy

113
Exercise
  • Programs of moderate physical exercise have been
    shown to lower maternal glucose concentrations in
    women with GDM

114
Long Term
  • 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
  • education regarding lifestyle modifications that
    lessen insulin resistance, including maintenance
    of normal body weight through MNT and physical
    activity.

115
Long Term
  • Avoid medications that worsen insulin resistance
    (e.g., glucocorticoids, nicotinic acid)
  • Seek medical attention if develop symptoms
    suggestive of hyperglycemia.
  • Use family planning to assure optimal glycemic
    regulation from the start of any subsequent
    pregnancy

116
Emerging Understandings 5th International
Workshop-Conference on Gestational Diabetes
Mellitus
  • Diabetes Care. Supplement July 2007
  • Pathophysiology
  • Therapy
  • Impact on infants
  • Maternal follow-up

117
Emerging Issues Pathophysiology
  • Basic In GDM insulin levels are insufficient to
    meet insulin demand
  • Categories of dysfunction chronic exposed by
    the general insulin resistance of pregnancy
    rather than acute due to
  • Autoimmune b-cell dysfunction (fast
    deterioration)
  • Genetic abnormalities that lead to impaired
    insulin secretion (5, monogenic forms of
    diabetes such as maturity-onset diabetes of the
    young (MODY) and mitochondrial diabetes
  • b-cell dysfunction associated with chronic
    insulin resistance

118
Therapeutic Interventions During Pregnancy
  • Recent RCT found treatment started before 30
    weeks reduced likelihood of serious neonatal
    morbidity
  • Individualize MNT
  • Daily self monitoring of blood glucose (SMBG)
  • Insulin when needed (20 needed)

119
Treatment, cont.
  • Metabolic management based on fetal growth
    measures is promising technique
  • Oral antihyperglycemic agents
  • Glyburide (glibenclamide) studies indicate may
    be useful adjunct to MNT/PA may be less
    successful with obese patients
  • Metformin crosses placental, insufficient
    evidence that prevents GDM
  • Acarbose safety not fully evaluated

120
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

121
Maternal Follow-up
  • Majority will eventually develop diabetes-
  • 35-60 percent within 10 years
  • risk continues at least 1-2 decades after GDM
    pregnancy
  • Increased risk of congenital anomalies in
    subsequent pregnancies
  • 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.
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