Download Hypertension

10/25/2002
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Disordered Eating
Hypertensive Disorders
Gestational Diabetes
Adolescence
Disordered Eating &
Pregnancy
• Few data on prevalence of disordered eating
in pregnancy
• Difficult to adequately capture this information
from women
• No good, prospective studies
• Results of published studies are confusing some find improvement with pregnancy others find increased symptoms
Disordered Eating &
Pregnancy
 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.
 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.
Disordered Eating &
Pregnancy
• Many women experience concerning
food and body image behaviors in
pregnancy
Attitudes to body weight, weight gain and
eating behavior in pregnancy, (Abraham et al J
Psychosom Obstet Gynecol, 1994)
• N=100, exclusions were no hx of drug
use or major psychiatric illness, baby
not in ICU
• Questionnaires completed at 3 days pp.
Attitudes to body weight, weight gain and
eating behavior in pregnancy,
(Abraham et al J
Psychosom Obstet Gynecol, 1994)
Did you:
% Before preg. % During
preg.
% Worse in
preg.
Watch your weight
65
71
34
Preoccupation with
food/weight
42
52
23
Binge eating
37
44
22
Feel out of control
of eating/weight
30
30
20
Use weight control
methods
81
76
-
Methods of Weight Control Used
(Abraham et
al J Psychosom Obstet Gynecol, 1994)
% Before Preg
% During Preg.
"Dieting"
82
37
Avoiding certain foods
56
42
Compulsive/excessive
exercise
Diet drugs
15
4
15
1
Fasting or fluid only diet
13
3
Smoking cigarettes
14
4
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
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)
Reported complications of pregnancy and
eating disorders: Anorexia Nervosa
Maternal Complications
Infant/Birth Complications
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Inadequate Weight Gain
Miscarriage
Vaginal bleeding
Decreased uterine size
Hyperemesis
Low Birth Weight
Delayed Development
Premature Birth
Prenatal death
Reported complications of pregnancy and
eating disorders: Bulemia Nervosa
Maternal Complications
Infant/Birth
Complications
 Increased symptoms
 Excessive exercise
 Low and high weight gain
 Miscarriage
 Hypertension
 Stillbirth
 Low birth weight
 Low apgar scores
 Breech delivery
 Cleft palate
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.
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.
Eating Habits and Attitudes in the Post
Partum Period
Preconception
(Stein et al. Psychosomatic Med., 1996)
Late pregnancy 3 mos pp
6 mos pp
Concern about 0.91
shape***
1.14
1.34
1.08
Concern about 0.96
weight****
0.80
1.34
1.63
Concern about 0.13
eating**
0.04
0.15
0.09
Dietary
restraint*
0.94
0.90
1.08
0.90
Global
EDE***
0.60
0.58
0.79
0.77
** = p <0.05, ***= p< 0.01, ****=p<0.001
Number Meeting DSM-IV Diagnostic Criteria for Clinical
Eating Disorder NOS (Stein et al. Psychosomatic Med., 1996)
Preconception
Early
Late
pregnancy pregnancy
3 mos pp
6 mos pp
3
3
4
4
4
Eating Habits and Attitudes in the Post
Partum Period
(Stein et al. Psychosomatic Med., 1996)
• No cases of bulimia nervosa or anorexia
nervosa
• No women who met criteria before pregnancy
were cases during pregnancy
• All cases during pregnancy were do novo but two had history of bulimia nervosa
• At postpartum, three cases were de novo
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
Play Behaviors ( Stein et al., J Child Psychol Psychiat, 1994)
Index
Control
Negative Expressed 0.47
emotion toward child
1.34
Intrusiveness
16.23
5.83**
% of maternal
controlling
statements
51.23
44.5*
* p< 0.05, ** 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:
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maternal height,
infant birthweight
conflict during meals
mothers concern about own body shape
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.
• 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.
• 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.
• 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.
• 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: Psychosocial
• Making the fetus as real as possible to
the patient very early.
• 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 Interventions: Nutrition
• 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 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
Hypertensive Disorders
During Pregnancy
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Incidence
Definitions
Etiology/pathophysiology
Nutritional Implications
NATI O NAL I N STITUTE S O F
HEALTH
NATI O NALH EART, LU N G ,AN D
BLOOD
INSTITUTE
WORKING GROUP
REPORT ON HIGH
BLOOD PRESSURE
IN PREGNANCY
July 2000
Incidence
• Second leading cause of maternal
mortality in US
• 15% of maternal deaths (abruptio placentae,
disseminated intravascular coagulation, cerebral hemorrhgae,
hepatic failure, acute renal failure)
• Hypertensive disorders occur in 6 to 8%
of pregnancies
• Contribute to neonatal morbitidy and
mortality
High risk
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First pregnancy and under age 17 or over 35
Family history of hypertension
Multiple gestation
Poor nutritional status
Smoking
Overweight
Other health problems such as renal disease,
diabetes
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.
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)
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.
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 and24-hour urine protein in
preeclampsia it is recommended that the diagnosis
be based on a 24-hour urine if at all possible
Findings that increase the possibility of
Eclampsia and indicate need for FU
Edema
Dx of Superimposed Preeclampsia
Eclampsia
• Occurrence in a woman with
preeclampsia, of seizures that can not
be attributed to other causes
Etiology
• Not fully understood
• Characterized by:
– Vasospasm
– Activation of the coagulation system
– Perturbations in systems related to volume
and blood pressure control
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
Pathophysiology
 Decreased blood flow
 Decreased renal blood flow, decreased GFR, Na
retention
 Tissue hypoxia
 Damage to organs
Pathophysiology
 Decreased blood volume
 Decreased placental blood flow may
occur 3-4 weeks before increased BP
 Hypoxia
 Decreased nutrient delivery
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.
Focus of Possible
Interventions
 Smooth muscle contraction
 Prostaglandin synthesis
Calcium
 Epi studies suggest inverse relation between dietary
calcium and PIH
 Intraerythrocyte calcium levels and intracellular
calcium ion conc. increased in women with preeclampsia
 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.
Calcium, cont.
 Recent meta-analysis found Ca intake of 1.52 g associated with sig. reductions in systolic
and diastolic BP without adverse effects.
 Question remains: does lowering BP have
effect on pathophysiology of PIH?
Cochrane: Calcium supplementation during
pregnancy for preventing hypertensive
disorders and related problems
• Nine studies met criteria
• Modest reduction in hbp and risk of
preeclampsia with Ca supps.
• Effect greatest in those with high risk of
htn and those with low baseline Ca
intake.
Cochrane: Calcium supplementation during
pregnancy for preventing hypertensive
disorders and related problems
Reviewer’s conclusions:
“Calcium supplementation appears to be
beneficial for women at high risk of
gestational hypertension and in
communities with low dietary calcium
intake.”
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
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.
Other Nutrition Related Factors
 Na: Pregnant women with proteinuric
hypertension have lower plasma volume Na.
restriction is associated with accelerated
volume depletion – not recommended
 Mg: Not found beneficial in prevention,
unclear about benefits in treatment
 Energy and Protein intake: increases not
found to be useful
 Weight reduction or limited gain in
pregnancy: not found to be useful
Report of the Canadian Hypertension Society
Consensus Conference: Non pharmacologic
management and prevention of hypertensive disorders
in pregnancy (Can Med Assoc J., 1997)
• A normal diet without salt restriction is
advised.
• Promising preventive interventions may
include:
• Calcium supplementation (2g/d)
• Fish oil supplementation and low-dose
acetylsalicylic acid therapy, particularly in
women at high risk for early-onset gest. htn.
Canadian Consensus Report: Calcium
• Calcium supplementation of 2 g/d is
associated with a reduction of blood
pressure in gestational hypertension
with or without proteinuria in both low
and high risk women
• There is no apparent effect on the
prevention of more severe gestational
hypertension in women with established
gestational hypertension.
Canadian Consensus Report: Fish Oil
• “Trials with larger samples of Canadian
women are required to assess reliably
the potential benefits or adverse effects
of fish oil supplementation during
pregnancy.”
• “Fish oil supplementation potentially
prevents proteinuric gestational
hypertension.”
2002 Working Group Report Current Knowledge of Nutrients and
Hypertensive Disorders of Pregnancy
• Calcium supplements only beneficial for
prevention in high risk women
• Magnesium not effective for prevention
• Fish oil not effective for prevention
• Studies of vitamins C and E encouraging, but
needs further work
Position Statement
Gestational Diabetes Mellitus
American Diabetes Association
2002
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.
Diagnosis
• Assess risk at first visit
• If high risk (marked obesity, personal
history of GDM, glycosuria, or a strong
family history of diabetes) GTT ASAP
• Women of average risk should have
testing undertaken at 24–28 weeks of
gestation
• Low-risk status requires no glucose
testing
Low Risk Criteria
• Age <25 years
• Weight normal before pregnancy
• Member of an ethnic group with a low
prevalence of GDM
• No known diabetes in first-degree relatives
• No history of abnormal glucose tolerance
• No history of poor obstetric outcome
Non GTT dx
• A fasting plasma glucose level >126
mg/dl (7.0 mmol/l) or a casual plasma
glucose >200 mg/dl (11.1 mmol/l) meets
the threshold for the diagnosis of
diabetes, if confirmed on a subsequent
day, and precludes the need for any
glucose challenge
One-step Approach
• Perform a diagnostic oral glucose
tolerance test (OGTT) without prior
plasma or serum glucose screening
• May be cost-effective in high-risk
patients or populations (e.g., some
Native-American groups).
Two-step approach
• Initial screening by measuring the
plasma or serum glucose concentration
1 h after a 50-g oral glucose load
• Diagnostic OGTT on that subset of
women exceeding the glucose threshold
value on the GCT
Table 1— Diagnosis of GDM with a 100-g oral glucose load
mg/dl
mmol/l
Fasting
95
5.3
1-h
2-h
3-h
180
155
140
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.
Infant Concerns in GDM
• Higher risk of:
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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
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
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 glucose-lowering agents have generally not
been recommended during pregnancy
Exercise
• Programs of moderate physical exercise
have been shown to lower maternal
glucose concentrations in women with
GDM
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.
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