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PHYSIOLOGICAL CHANGES OF GLUCOSE METABOLISM IN PREGNANCY. Pregnancy is a state of insulin resistance
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1. DIABETES IN PREGNANCY DR. SALWA NEYAZI
CONSULTANT OBSTETRICIAN GYNECOLOGIST
PEDIATRIC & ADOLESCENT GYNECOLOGIST
2. PHYSIOLOGICAL CHANGES OF GLUCOSE METABOLISM IN PREGNANCY Pregnancy is a state of insulin resistance & relative glucose intolerance
This is due to placental production of anti-insulin hormones : hPL, cotisol, and glucagon
FBS ??
Postprandial glucose ? ?
Insulin production ? ? 2 folds in N women
Insulin requirements ? ? in diabetic women
?? renal threshold for glucose ? glycosuria
3. DIAGNOSIS OF GESTATIONAL DIABETES MELLITUS Women in whom the criteria of DM are met in pregnancy ? include a gp of diabetics who were undiagnosed before pregnancy
FBS ? > 7 mmol/L on 2 occasions
Or
RBS ? > 11.1 mmol/L on 2 occasions
Borderline cases ? GTT ? DM is Dx if FBS ? > 7 mmol/L or 2 hrs > 11.1 mmol/L
Impaired glucose tolerance ? 2hrs G 8-11 mmol/L with a N FBS
4. EFFECT OF PREGNANCY ON DM
Insulin requirement ? ? in pregnancy reaching a max at term & being at least 2 X the pre-pregnancy requirement
Pt with diabetic nephropathy ? deterioration in renal function with ? in creatinine clearance & proteinuria
? this deterioration in renal function is usually reversed after delivery
5. EFFECT OF PREGNANCY ON DM 2 X ?? in retinopathy
? rapid improvement in glycemic control ? worsening retinopathy due to ?? retinal blood flow
?? icidence of hypoglycemia
Ketoacidosis is rare unless associated with hyperemesis, infections, tocolytic & corticosteroid Rx
6. EFFECTS OF DM ON PREGNANCY ?? incidence of congenital abnormalities
The risk is related to the degree of glycemic control ? 5% with Hb A1c > 8%
? 25% with Hb A1c > 10% with ?? risk
of abortions
Sacral agenesis, congenital heart defects, skeletal abnormalities & neural tube defects
Perinatal & neonatal mortality ?? 2-4 X
Unexplained IUFD at term / more in macrosomic babies
7. EFFECTS OF DM ON PREGNANCY Macrosomia ? the incidence is ?? with poor diabetic control
? not eliminated by tight control
? associated with ?? risk of operative delivery, birth trauma, & shoulder dystocia
Hyperglycemia ? fetal polyuria ? polyhydramnios ? PROM, preterm delivery
Prematurity pose an added problem as pulmonary surfactant production is slightly delayed in babies of diabetic mothers
8. EFFECTS OF DM ON PREGNANCY Postnatally, babies are at risk of hypoglycemia & jaundice
?? risk of PET especially in pt with pre-existing hypertension & nephropathy where it reaches almost 30%
9. MANAGEMENT Multidisciplinary team including obstetricians, endocrinologists, dieticians, & midwives ? optimize outcome
Preconception councelling
To achieve normoglycemia as far as possible
?FBS < 5 mmol/L
?PP < 7.5 mmol/L
Dietary advice on a low sugar, low fat, high fiber diet
Regular capillary glucose series (7 point profile)
Combined short acting & intermediate acting insulin
10. MANAGEMENT Regular assessment of Hb A1c
Ophthalmologic examination & Rx of retinopathy
Regular monitoring of renal function in Pt with diabetic nephropathy
Detailed U/S screening for congenital malformations in the 2nd trimester (20wk) ? to exclude NTD, sacral agenesis, & cardiac defects
Frequency of antenatal visits needs to be individualized
11. ANTENATAL FETAL SURVELANCE ?? incidence of IUFD justify close monitoring in the 3rd trimester
Serial U/S biometry ? to detect macrosomia, hydramnios, IUGR
Umbilical artery doppler in Pt with IUGR
CTG
BPP
12. LABOR & DELIVERY With well controlled DM with appropriately grown fetus ? pregnancy is allowed to proceed till term
When there is concern about fetal well being or macrosomia ? the risk of IUFD must be weighed against the risk of RDS
½ of the babies are >90th centile ? CS rate of 50-60%
Intrapartum care should focus on meticulous diabetic control & continuous electronic fetal monitoring . Blood glucose should be 4-7 mmol/L achieved by 5% Dextrose infusion & insulin infusion
13. LABOR & DELIVERY After delivery mternal insulin requirement rapidly returns to the pre-pregnancy level
If abnormal glucose tolerance was 1st Dx in pregnancy ? GTT should be done 6 wk post-partum
14. Gestational diabetes Carbohydrate intolerance of variable severity 1st Dx in pregnancy ? will include women with undiagnosed DM
There is no consensus on the optimal screening for GDM
?Universal screening
?Screening pt > 25 Y
?Clinical risk factors: previous GDM, family Hx , previous macrosomic baby, previous unexplained IUFD, obesity, glycosuria, polyhdramnios, LGA in current pregnancy
? The timing of screening also contraversal
15. Implications of GDM ? perinatal mortality & morbidity but to a lesser extent than DM
No ? risk of congenital malformations
Macrosomia is the main risk factor for adverse outcome
? risk of operative deliveries
? incidence of PET
Women with GDM have a significantly ? risk of DM later in life (50% over 10-15 Y)
16. Management Combined diabetic obstetric approach
Initial approach by dietery modification including caloric reduction in obese Pt
The need for insulin is manifested by persistent PP hyperglycemia (7.5-8 mmol/l) or persistant fasting hyperglycemia (>5.5-6 mmol/L)
Regular U/S scans to assess fetal growth & well being
Early delivery is not advised unless there is a complicating factor
17. Management Intrapartum management
?Depends on whether the pt is on diet control alone or on insulin
? Pt on insulin need to be on sliding scale
?Following delivery insulin must be discontinued
GTT should be done 6 wks postpartum
18. MACROSOMIA Fetal Wt >4000-4500 gm regardless of gestational age
Risks of macrosomia include ? shoulder dystocia, erb’s palsy, ? 5 min APGAR score, admission to NICU & obesity later in life
Risk factors for the development of macrosomia:
? prior HX of macrosomia
?? maternal pre-pregnancy Wt
?excessive Wt gain in pregnancy
?multiparity
19. MACROSOMIA (risk factors) ?male fetus
?gestational age >40wks
?race
?maternal birth Wt
?maternal Ht
?maternal age
?+ve GCT with-ve GTT
?GD, DM
20. MACROSOMIA How macrosomic infants of diabetic mothers differ from those without diabetes?
How is macrosomia predicted?
How does it affect the management of labor & delivery?
When is CS recommended for macrosomia?
What is the role of induction of labor?