Transcript Preconception and early post conception counseling

Preconception and early
post conception
counseling in D.M
Fakhrolmolouk Yassaee. MD. Assistant professor
OBS & GYN.
Obstetric & gynecologic department, perinatology
center Taleghani Hospital
Shaheed Beheshti medical science university Evin,
Tehran, IRAN
The question raised most frequently by diabetic
women are:
1) What is know about the heritability of diabetes?
2) What health measure can be implemented before
conception?
3) What type of obstetric care is recommended?
4) Will retinal and renal complications worsen during
pregnancy and shorten life expectancy?
5) What sort of malformations do infants of diabetic
mothers have and what causes them?
The obstetrician, internist, genetic counselor all
have important roles in providing advice to
diabetic women both before and throughout
pregnancy. Genetic transmission of diabetes
is complex and depends upon the type of
carbohydrate intolerance.
It is a chronic autoimmune disorder that occurs
in genetically susceptible individuals. Major
histocompatibility haplotype (HLA) strongly
influence susceptibility. No genetic marker has
been identified for IDDM but a major
component of genetic susceptibility has been
identified as a gene or genes located near
within the HLA complex on the short arm of
chromosome 6.
Genetic couseling and a careful medical
assessment before conception are
recommended for all diabetic women and
those with a history of gestational diabetes
during a previous pregnancy. In infants of
diabetic mother (IDM), congenital
malformation occur about 2-3 times as often
as in those of nondiabetic women. (Mill 1982)
Ylinen and associates (1984) have also
reported a higher risk of minor and major
malformation is infants of diabetic mothers
with elevated HbA1c concentrations.
The majority of lesions involve the central
nervous system and the cardiovascular
system, genitourinary and limb defects
(cousins 1991).
There is no increase in birth defects among
offspring of diabetic fathers, prediabetic
women, and women who develop gestational
diabetes after the first trimester, suggesting
that glycemic control during embryogenesis is
the main factor in the genesis of diabetesassociated birth defects.
Miller and coauthors( 1981) compared the
frequency of congenital anomalies in patients
with normal or high first- trimester maternal
glycohemoglobin and found only 3.4% rate of
anomalies with HbA1c less than 8.5%
whereas the rate of malformations in patient
with poorer glycemic control in the
periconceptional period (HbA1c > 8.5) was
22.4%
Because the critical time for teratogenesis is
during the period 3-6 weeks after conception,
nutritional and metabolic intervention must be
institutes preconseptionally to be effective.
Fetal overgrowth is a major problem in pregnancies
complicated by diabetes. Defined typically as birth
weight above the 90th percentile for gestational age
or greater than 4000 g, macrosomia occurs in 1545% of diabetic pregnancies.
Neonatal morbidity: hypoglycemia, macrosomia,
neonatal jaundice, one fifth of IDMS had
disproportionate macrosomia (Hunter ,1993)
(abdominal circumference greater than head
circumference) compared with 1% control infants
(Ballard, 1993)
Birth injury, including shoulder dystocia and brachial
plexus trauma is more common among IDM, and
macrosomic fetuses are at the highest risk.( Keller
1991)
Acceleration of growth, stimulated by excessive
glucose delivery during diabetic pregnancy, may
extend into childhood and adult life. Silverman
(1995) reported on the follow up of macrosomic
IDMS through 8 years of age in which half of the
IDMS weighed more than the heaviest 10% of
the nondiabetic children. These investigator also
found that the diabetic offspring have permanent
derangement in glucose- insulin kinetics,
resulting in increased incidence of impaired
glucose tolerance in later childhood.
The macrosomic IDM dose not follow the
growth pattern observed in euglycemic
pregnancies. During the first and second
trimesters, differentiation of diabetic from
nondiabetic fetuses is extremely difficult
using ultrasound measurements, suggesting
that the period of fetal fat deposition (28
weeks and onward) is when abnormal fetal
growth primarily occurs.
Morphologic studies of the IDM neonate
indicate that the increased growth of the
abdominal circumference (AC) is due to
deposition of fat in the abdominal and
interscapular area. This central deposition of
fat is a key characteristic of diabetic
macrosomic and underlies the dangers
associated with vaginal delivery in these
pregnancies. Acker (1980) reported that
although the incidence of shoulder dystocia is
3% among infants weighing greater than
4000g, 16% of infant from diabetic
pregnancies weighing greater than 4000g,
sustained shoulder dysticia.
Key features of a preconceptional diabetes management
program should include the following:
 A through assessment of cardiovascular, renal,
ophthalmologic, status. Blood pressures, 24- hour protein
and creatinine, and retinal examination should be
performed. Thyroid function ( TSH and FT4) should be
evaluated. Antihypertensive agents should be initiated and
regulated
 A regimen of frequent and regular monitoring of both preprandial and postprandial glucose capillary glucose levels.
Target levels are fasting glucose 80- 95 mg/dl and 1- hour
postprandial glucose less than 130mg/dl or 2 hour
postprandial glucose less than 120 mg/dl
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The insulin regimen should result in a smooth
glucose profile throughout the day with no
hypoglycemic reaction between meals or at night.
The regimen should be initiated early enough
before pregnancy so that the glycohemoglobin
level is lowered into the normal range for at least
3 months prior to conception.
Taking a daily prenatal vitamin ( including 400 μg
of folic acid ) at least 3 months prior to
conception to minimize risk of neural tube defects
in fetus.
Particular attention should be paid to support
systems that permit extended bed rest in the third
trimester if necessary.
The goals of management of diabetic
pregnancy are to prevent stillbirth and
asphyxia while minimizing maternal morbidity
associated with delivery. This involves
monitoring fetal growth in order to select the
proper timing and route of delivery. The first
is testing fetal well- being at frequent intervals
and fetal size.
Fetal surveillance in type I and type II diabetic pregnancies
Time
Test
Preconception Maternal glycemic control
8-10 w
sonographic crown –rump measurement
16 w
Maternal serum alpha- fetoprotein level
20-22 w
high – resolution sonography, fetal cardiac
echography in women in in suboptimal diabetic control (HbA1c ) at
first prenatal visit
24w
Baseline sonographic growth assessment of the fetus
28 w
Daily fetal movement counting by the mother
32 w
Repeat sonography for fetal growth
34 w
Biophysical seting:
2X weekly NST or
weekly CST
or
weekly biophysical profile
36w
Estimation of fetal weight by sonography
37-38.5 w
Amniocentesis and delivery for patients in poor control
(persistent daily hyperglycemia)
38.5 – 40 w
Delivery without amniocentesis for patients in good control who
have excellent dating criteria
TESTS OF FETAL WELL - BEING
test
frequency
Reassuring result
comment
Fetal movement
counting
Every night Ten movement in <60 min Performed in all
from 28 w
patients
Non- stress test
Twice
weekly
Two heart – rate
Being at 28-34 w with
acceleration in 20 minutes insulin dependent
diabetes
Contraction stress
test
weekly
No heart rate decelerations Same as for non stress
in response to ≥ 3
test
contrations in 10 minutes
Ultrasound
weekly
biophysical profile
Score of 8 in 30 minutes
3 movement =2
1 flexion = 2
30 sec breathing = 2
2 cm amniotic fluid = 2
CHOOSING TIMING AND ROUTE OF
DELIVERY
Timing of delivery should be selected to minimize
maternal and neonatal morbidity and mortality and
mortality. Delivery delaying as near as possible to
the EDC helps maximize cervical ripeness and
improves the chances of spontaneous labor and
vaginal delivery. Yet at the risks of fetal macrosomia,
birth injury, and fetal death increase.
( Rasmussen, 1992). Although earlier delivery at 37
wks. gestation might reduce the risk of shoulder
dystocia, an increase in failed labor induction and
poor neonatal pulmonary status must be
considered. Thus, an optimal time for delivery of
most diabetic pregnancies is between 38.5 and 40
wks.
Indication for delivery diabetic pregnancy
Fetal
Non reactive NST
Positive CST
Reactive NST, positive CST, mature fetus
Sonographic evidence of fetal growth arrest
Decline in fetal growth rate with decreased amnionic
fluid 40 – 41 w gestation
Maternal
Severe preeclampsia
Mild preeclampsia, mature fetus
Markedly falling renal function
Obstetric
preterm labor with failure of tocolysis
Mature fetus , inducible cervix
CONFIRMATION OF FETAL MATURTY BEFORE
INDUCTION OF LABOR OR PLANNING CESAREAN
DELIVERY W DIABETIC PREGNANCY
1.
2.
3.
4.
5.
6.
Phosphatidyl glycerol > 3% in amniotic fluid collected
from vaginal pool or by amniocentesis
Completion of 38.5 weeks gestation
Normal LMP
First pelvic examination before 12 weeks confirm
dates.
Sonogram before 24 weeks confirm dates
Documentation of more than 18 weeks by fetoscope of
FHT
After 38.5 weeks gestation, the obstetrician can
await spontaneous labor if the fetus is not
macrosomic and biophysical testing is
reassuring. In patients with GDM and super
glycemic control, continued fetal testing and
expectant management can be considered
until 41 weeks ( Lurie 1992)
In the fetus with on AC measurably greater than
head circumference, induction should be
considered. After 40 + weeks, the benefits of
continued conservative management are
likely to be less than the danger of fetal
compromise. Induction of labor 42 weeks in
diabetic pregnancy- regardless of the
readiness of the cervix- is prudent.
Given these data, the decision to attempt
vaginal delivery or perform a cesarean is
inevitably based on very limited data. The
patient’s past obstetric history, the best EFW,
a fetal adipose profile (abdomen larger than
head), and clinical pelvimetry should all be
considered. Most large series of diabetic
pregnancies report a cesarean section rate of
30- 50%. The best means by which this rate
can be lowered is by early and strict glycemic
control in pregnancy. Conducting long labor
inductions in patients with a large fetus and
marginal pelvis may increase morbidity and
costs.