Transcript WEEK 5

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 for 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)
Index
Control
Negative Expressed 3.27
emotion toward child
0.90**
Intrusiveness
8.91
1.20**
% of maternal
controlling
statements
27.3%
26.11%
** p<0.01
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 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
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, B12)
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, B12
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
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/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
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
&
5th 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
Fasting
1-h
2-h
3-h
mg/dl
mmol/l
95
180
155
140
5.3
10.0
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/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
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.”