Diabetes in Pregnancy
Diabetes in Pregnancy
Diabetes in Pregnancy
Suniti Rawal
Dept of OBGYN
DIABETES
is a state of carbohydrate intolerance resulting
from
1. Inadequacy of Insulin secretion or
3
Incidence
Gestational diabetes mellitus (GDM) accounts for
90% of the cases.
Type 2 diabetes mellitus accounts for 8% of the
cases and
Preexisting diabetes mellitus Type 1 affects 1% of
all pregnancies.
Baptiste-Roberts K et al. Risk factors for type 2 diabetes among women with
gestational diabetes: a systematic review. Am J Med. Mar 2009;122(3):207-
214.e4
4
Many placental hormones are secreted during
pregnancy which are thought to be responsible.
These are
Human Placental lactogen
Estrogen
Progesterone
Cortisol
5
Congenital Malformation
In normoglycemic pregnancy the risk of congenital
malformation is 1 – 2 % whereas it is increased to 6 –
10% in pregestational diabetes
No significant increase in malformation with GDM
Hyperglycemia at the time of organogenesis is thought
to be the culprit.
Risk of structural anomalies are increased rather than
chromosomal
Progressive rise with rates of congenital malformation
exceeding 8% where the HbA1c level is > 10%.
6
Specific malformations
1.Skeletal malformation: Caudal regression syndrome
2. CNS (4.2 fold): Spina bifida, Anencephaly,
encephalocele, microcephaly, meningomyelocele,,
3.Cardiovascular (3.4 fold): Transposition of great
vessels, VSD, ASD, hypoplastic left ventricle,
anomalies of aorta
4.Genitourinary: Absent kidneys (Potter syndrome),
Polycystic kidneys, Double ureter
5. Gastrointestinal: TOF, Bowel atresia, Imperforate
anus
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SPONTANEOUS MISCARRIAGE
Reported incidence: 8 – 43 %
Pederson hypothesis: Maternal hyperglycemia
leading to fetal hyperglycemia causes increase
insulin secretion.
Surfactant deficiency
RDS
TTN is also more common among the newborn
More insulin might be necessary to achieve metabolic
control
Increased risk of death for patients with diabetic
cardiomyopathy
Placenta Previa
Infection – chorioamnionitis, postpartum endometritis
Postpartum bleeding – caused by exaggerated uterine
distension and high incidence of infection
No need to screen
low risk women.
17
When a selective screening is used following
risk factors are considered:
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19
Screening in OBG/GYN dept is carried in 2 steps.
20
50 g glucose is dissolved in 200 ml water was
taken irrespective of fasting or fed status.
21
Blood glucose level Result
22
Screen positive women are subjected to 100 g
OGTT
23
The test should be performed in the morning
after an overnight fast of at least 8 h but not
more than 14 h and after at least 3 days of
unrestricted diet (150 g carbohydrate/day) and
physical activity.
The first glucose measurement is done in fasting
state. Thereafter subjected to 100 g glucose
dissolved in 200-400 ml water is given over 10
min and blood sample is drawn
24
To confirm the diagnosis of GDM by OGTT:
25
WHO recommendation of carrying out the one
step test for screening as well as diagnosis with
75 g OGTT is being considered in TUTH as well
and a new study is in progress……
28
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Proper nutrition is the most important component of
the care of Diabetes.
34
Insulin Therapy
35
Once the women is diagnosed with GDM , she is
admitted and a sugar profile is done 6-7 times
throughout the day.
1. Fasting
2. Post breakfast
3. Pre lunch
4. Post lunch
5. Pre dinner
6. Post dinner
7. Midnight
36
Types and Action of various Insulin
37
Starting Daily Insulin dose during Pregnancy
GDM: ≥ 4 times/day
1 fasting + 3 postprandial
39
Goals for glycemic control in GDM is
40
41
Metformin used as a treatment for PCOD has
been reported to reduce the incidence of GDM,
and can now is advised to be continued in
pregnancy too.
42
Principle of Obstetric care in a GDM
Strict control of blood sugar levels
Timing the delivery to improve maternal and
fetal outcome
Choosing the correct mode of delivery and
Adequate intrapartum and postpartum
management
43
REFERRAL TO A COMBINED MULTIDISCIPLINARY
DIABETIC & OBSTETRIC ANTENATAL CLINIC
44
Ideally a dating scan should be performed within
the first 10 weeks following conception as this
allows to know the viability of fetus, confirm the
gestational age and detect early congenital
anomalies if any ,esp. anencephaly.
46
Surveillance for medical obstetric complications:
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Assessment of Fetal growth
48
Optimization of Glycemic status:
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Assessment of fetal Growth
50
When glucose control is good and no other
complications supervene, pregnancy can be
prolong up to 40 weeks of gestation.
51
Expectant management beyond the estimated
due date is generally not recommended.
52
Suspected fetal macrosomia is related to traumatic
delivery including shoulder dystocia and brachial plexus
injury which can be prevented by elective Caesarean
section.
But Caesarean delivery results in higher rates of
maternal morbidity and two- to four-fold greater risk of
maternal mortality compared with vaginal delivery.
54
Insulin Management During Labor and Delivery
55
Following delivery, insulin requirement fall
immediately.
56
At TUTH
Following vaginal delivery or Cesarean delivery,
G I K regimen is continued until patient eats
normal diet.
57
It should be remembered that
Jovanovic L, ed in chief. Medical Management of Pregnancy Complicated by Diabetes. 3rd ed. Alexandria, Va: American Diabetes
58
Association; 2000:151
Contraception
Lactational Amenorrhoea
Barrier method
Low dose OCP
IUCD in cases of GDM
Sterilization
60
References
Williams Obstetrics.23rd edition ; Diabetes, 1169-1184
High Risk Pregnancy. DK James 4 th edition; Diabetes in Pregnancy, 665-
681
Avery’s Disease of the Newborn 8 th ed. Endocrine disorders in
pregnancy, pg:71-82
Dewhurst’s Textbook of obstetrics & Gynecology 6 th edition; Diabetes &
endocrine disorders in pregnancy, 197-209
Practical Guide to High risk pregnancy & Delivery. Fernando Arias 3r d
edition,; Diabetes & Pregnancy, 280-297
Medical Disorders in Obstetrics Practice. Michael de Sweit, 4 th edition;
Diabetes, 386-409
Progress in Obstetrics & Gynaecology. John Studd vol 16. GDM re-
appraised, 57-70
Harrison’s Principles of Internal Medicine 17 th edition; Diabetes Mellitus,
2152-2180
Pharmacology. Goodman & Gillman . Hypoglycaemic agents & the
pharmacology of the endocrine pancreas, 1679-1711
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