L3- Diabetes and Pregnancy-KHALID.ppt. .

Medical research

1. Diabetes and Pregnancy
Dr Khalid Akkour MD. FRCSC
Asst. Professor & Consultant
Gynecologic Oncologist

2. Two Types:
•Preexisting DM and pregnancy
•Gestational diabetes

3. Diabetes in pregnancy
Pre-existing diabetes Gestational diabetes
Pre-existing diabetes
IDDM
(Type1)
NIDDM
(Type2)
True GDM

4. Preexisting diabetes in
pregnancy
•Type 1 DM ( IDDM)
•Type 2 DM (NIDDM)

5. Preexisting DM in pregnancy
Effect of pregnancy on pre-existing DM
•Increase requirement for insulin doses
•Nephropathy , autonomic neuropathy may deteriorate
•Progress in diabetic retinopathy (2X)
•Hypoglycemia
•Diabetic ketoacidosis

6. Preexisting DM In Pregnancy
Effect of preexisting DM on pregnancy
(1)Maternal
1. increase risk of miscarriage
2. increase risk of preclampsia
3. increase risk of infection eg vaginal candidiasis, UTI,
endometrial or wound infection
4. increase LSCS rate

7. Preexisting DM in Pregnancy
(2) Fetal
1. increase risk of congenital abnormalities
sacral agenesis, congenital heart disease,
neural tube defects
Hba1c level Risk
normal not increased
<8% 5%
>10% 25 %

8. Preexisting DM in Pregnancy
2. Perinatal mortality (excluding congenital abnormality ) 2 fold
increased
3. Increase risk of sudden unexplained intrauterine fetal death.

9. Complications of pregnancy in pre-existing
DM
Maternal:
Increase insulin requirment’
Hypoglycemia
Infection
Ketoacidosis
Deterioration in retinopathy’
Increased proteinuria+edema
Miscarriage
Polyhydramnios
Shoulder dystocia
Preeclampsia
Increased caesarean rate
Fetal:
Congenital abnormalities
Increased neonatal and perinatal
mortality
Macrosomia
Late stillbirth
Neonatal hypoglycemia
Polycythemia
jaundice

10. Maternal hyperglycemia
|
Fetal hyperglycemia
|
Fetal pancreatic beta-cell hyperplasia
|
Fetal hyperinsulinaemia
|
Macrosomia,organomegaly, polycythaemia, hypoglycemia, RDS

11. Management
Aim
Achieve maternal near normoglycemic level to prevent adverse
perinatal outcomes

12. Diet
•Low-carbohydrate diet , high fibre with caloric restriction
•Frequent small snacks may be needed between meals
•Avoid starvation

13. Insulin
•3 pre-meal short acting insulin (actrapid) +/- intermediate-
acting insulin (protophane) as it allows maximum flexibility
•Target blood glucose:
fasting < 5mmol/L
2 hr <7 mmol/L

14. Oral Hypoglycemic agents
•Implicated as teratogeneic in animal studies esp first
generation sulfonyureas
•In humans, scattered case reports of congenital abnormality
•Risk of congenital abnormality related to maternal glycemic
control rather than mode of the anti-DM agents

15. Oral hypoglycemic agents
•For Type 2 DM patients,
to stop oral hypoglycemic agents and change to insulin
Reassure that the risk of congenital abnormality due to oral
hypoglycemic agents is very small

16. Oral hypoglycemic agents
•Biguanides ( metformin)
•Cat B drug
•Commonly used in Polycystic Ovarian Disease (PCOD)
to treat insulin resistance and normalize
reproductive function
•Not teratogeneic
•Reduce first trimester miscarriage
•10X reduce gestational diabetes
Glueck, Fertil Steril 2002
Reece, Curr Opin Endocrinol Diabetes, 2006
Hague, BMJ, 2003
Glueck, Human Reprod, 2004

17. Oral hypoglycemic agents
Sulfonylureas
•1
st
generation drug increase risk of neonatal
hypoglycemia
•2
nd
generation drug (Glyburide) no such effect and other
morbidities .
•Cat C drug
•4%-20% patients failed to achieve glucose control with
maximum dose of drug
•Increase risk of preeclampsia and need for phototherapy
Langer, N Eng Med J , 2000
Kremer, Am J Obst Gynaecol, 2004
Chmait, J Perinatol ,2004
Langer, Am J Obst Gynaecol, 2005

18. Insulin Analogues
•1. rapid-acting insulin analogs
(lispro) Cat B
concerns about teratogenesis, antibodies formation,
growth-promoting properties
majority of evidence showed that it does not cross placenta,
and has no adverse maternal or fetal effects

19. Insulin Analogues
2. Long acting analogs
glargine
Cat C drug
Not well studied systemically

20. Monitoring
•Regular home glucose monitoring
•Insulin may be need to be adjusted as gestation advances
•Hba1c monitoring
•Fetal monitoring with USG
•Refer to an ophthamologist

21. Delivery
•Timing and mode of delivery individualised
•Intrapartum insulin infusion with glucose monitoring
• no contraindication for Breast feeding either with insulin or
oral hypoglycemic agents

22. Pre-conception Counselling
•Allows for optimisation of diabetic control prior to
conception, and assessment of the presence of
complications like hypertension, nephropathy, and
retinopathy
•Should counsel that good control and lower hba1c lower
the risk of congenital abnormalities and improve
outcome
•If necessary, proliferative retinopathy may be treated
with photocoagulation prior to conception
•Contraindications to pregnancy only :ischemic heart dx,
untreated proliferative retinopathy, severe renal
impairment(creatinine>250 mmol/L)

23. Gestational diabetes
Definition
Carbohydate intolerance of variable severity first recognised
during the present pregnancy.
This includes women with preexisting but previously
unrecognised diabetes

24. Pathophysiology
•Significant hormonal changes affects carbohydrate
metabolism during pregnancy .
•This happens because of the increase of human placental
lactogen HPL and cortisol, both of them are insulin
antagonist.
•These changes are most marked during the 3
rd
trimester .
•To balance these changes maternal pancreas secretes
increased amounts of insulin to maintain carbohydrate
metabolism.
•It affects 2-4% of pregnancies

25. Gestational diabetes
No consensus for 4 decades!

26. Gestational diabetes
•Should all pregnant women be screened or only
those with risk factors?
•Is it safe to screen all?
•Which screening test and which diagnostic test
are the most reliable?
•Which cut-off values should we use?
•What are the risk for mothers and babies and
can treatment improve outcome?
•What are the connection between gestational
diabetes and type 2 DM?
•Is it physiological or pathological ?

27. Gestational diabetes
•Screening of diabetes in pregnancy 24-28 weeks
•No single test proved to be perfect.
•Urinary glucose is completely unreliable.
•A full glucose tolerance test is would be ideal but is
expensive and time consuming .
•Random blood sugar of 5.8 mmol, has only 60% sensitivity .
•Glucose challenge test GCT is using 50 gm glucose without
fasting and measure the blood glucose after one hour and
should not be greater than 7.8 mmol , the sensitivity is
improved by 80%

28. •Definition of diabetes .
•WHO has defined diabetes as either fasting blood glucose of
7.8 mmol/l or more than 11mmol/l 1-2 hours following 75
grams of oral glucose load.
•A good glycemic control during pregnancy or even before is
needed because of the direct relationship between the
blood glucose level and the fetal and maternal
complications.
•Any diabetic woman who plan to get pregnant should insure
that their diabetes is optimally controlled to reduce the risk
of obstetrical complications.

29. Gestational diabetes
•Screening and diagnosis
In general, risk factor includes:
1. age>25y
2. BMI > 25
3. previous GDM
4. Family hx of DM in 1
st
degree relative
5. previous macrosomic baby (>4 kg)
6. polyhydramnios
7. large for date baby in current pregnancy
8. previous unexplained stillbirth

30. Gestational diabetes
Screening
Fasting / random glucose/ glucose challenge test(50gm)
Diagnosis
Glucose tolerance test

31. Gestational diabetes

32. Gestational diabetes
•Incidence
2-4%
more common in Asian and Indian women
In developed countries, increasing trend because of epidemic
of obesity

33. Gestational diabetes
Clinical significance of GDM
1.High incidence of macrosomia, and adverse pregnancy
outcomes,
2.A significant proportion(30%) identified as GDM in fact have
DM before pregnancy

34. Gestational diabetes
•Women with glucose intolerance just above normal range are
at low risk for pregnancy complications, those with more
severe glucose intolerance approaching the criteria of
diabetes are at risk of neonatal complications

35. Fetal complications
•Macrosomia (>4 kg)
risk is 16-29% as compared to 10% in control
•Increase in caesarean delivery, intrumental deliveries
( forceps/vacuum), birth trauma, such as brachial plexus
injuries , clavicular fractures
•Increase in neonatal hypoglycemia (24% ),
hyperbilirubinemia, hypocalcemia, polycythemia
•Children are at risk of type 2 DM and obesity in life

36. Maternal complications
•Increase risk of hypertensive disorders
•Increase risk of caesarean and intrumental deliveries
•Increased Risk (40-60%) of developing type 2 DM within10-15
yr.

37. Gestational diabetes
•Management is similar as preexisting DM
•Need for glucose monitoring
•Start with Diet control
•Commence insulin for poor control
•Delivery plan should be individualised

38. Gestational diabetes
•In view of risk of developing type 2 DM 30%,
the woman should be screened annually for DM on yearly
basis.

39. Diabetes and Pregnancy
Conclusion
(1)Preexisting DM in pregnancy
•Good glucose control is important for decreasing
morbidities
•Insulin is still the gold standard of tx in pregnancy
•Increasing evidence for clincial effectiveness for treatment
with oral hypoglycemic agents

40. Diabetes and pregnancy
conclusion
(2) Gestational diabetes
• no consensus
•The morbidities increases as glucose level
approaching the diagnosis as DM
•Possible that treatment improves outcomes
•Overlap with preexisting DM, esp type2
•Long term implication for health of the mother
and baby

41. Thank You