2. Increasing Prevalence of GDM
Abnormal maternal glucose regulation
occurs in 3-10% of pregnancies
GDM accounts for 90% of cases of DM in
pregnancy
Overt - 35% type 1 DM, and 65% type 2 DM
3.
Not limited to western countries
Increase is noted in India and China
3.8-20% in different part of India, more in
urban – DIPSI
Compared with white women the RR of GDM
in Indian women is 11.3
4. Increase is attributable to:
Sedentary lifestyles
Changes in diet
Immigration from high-risk populations
Childhood and adolescent obesity
5. CLASSIFICATION
GESTATIONAL DIABETES: 1 abnormal value on
GTT or hgbA1c - 5.7 to 6.4%.
A1 - Euglycemia achieved with diet and
exercise.
A2 - Require medication
PREEXISTING DIABETES
Type I. No endogenous insulin, ketosis
prone
Type II. Late onset,insulin resistant
6. Gestational Diabetes Mellitus
Glucose intolerance with onset or first recognition
during pregnancy.
Many are denovo pregnancy induced
Some are type 2 ( 35-40%)
Whether insulin or only diet modification is needed
Persists or not after Delivery.
9. Metabolism in Pregnancy
Goal is uninterrupted nutrient supply to
fetus
Metabolic goals of pregnancy are
In early pregnancy to develop anabolic
stores to meet metabolic demands in late
pregnancy
In late pregnancy to provide substrate for
fetal growth and energy needs.
11. Meal sets in motion a complex series of
hormonal actions,
Increase in blood glucose
Sec. secretion of pancreatic insulin,
glucagon, somatomedins, & adrenal
catecholamines.
These adjustments ensure that an ample,
but not excessive, supply of glucose is
available to mother & fetus.
12. Placental steroid & peptide hormones (eg,
E, P, chorionic somatomammotropin) ↑se
linearly throughout 2nd & 3rd trimesters.
↑se insulin resistance
↑sed insulin secretion.
24 hr mean insulin levels are 50% higher
in 3rd trimester compared with
nonpregnant state
14. GDM
Precise mechanisms unknown
Hallmark is ↑sed insulin resistance
Inability to secrete sufficient insulin to
compensate for the increased nutritional
needs of gestation due to:
↑sed adiposity of pregnancy,
↑sed anti-insulin hormones, such as HPL,
HPGH, prolactin, cortisol (potent), P & E
(weak)
enzymes with insulinase activity
Oxytocinase, histaminase, alkaline phosphatase
18. PEDERSEN THEORY
Maternal Diabetes
Glucose crosses placenta
Carbohydrate surplus of fetus
Increased secretion of
insulin
Free amino acid
Stimulation of protein, lipid &
glycogen synthesis
Stimulatory effect on
development of B cells
Release Insulin like
growth factor
MACROSOMIA
30. Criteria of Diagnosis
ADA recommendations
WHO criteria
Urine Glucose
Spot Test
HbA1C, Serum fructosamine
31. Whom and When to Screen? Indian
Scenario - The DIPSI Guidelines
75 gm GCT with single PG at 2 hrs
≥ 140 mg/dL is GDM
≥ 120 mg/dL is DGGT
Universal screening
First trimester, if negative at 24 – 28 wks
and then at 32 – 34 weeks
32. First visit
Hb A1C
Collect 24 hr urine (protein, creatinine clearance,
creatinine)
CVS status - ECG and echocardiogram
Eye exam
Bl urea nitrogen, serum creatinine,
TSH, and free thyroxine levels
33. 2nd Trimester Laboratory Testing
Spot urine protein-to-creatinine study in
women with elevated value in first
trimester
MSAFP
HbA1C
Capillary blood sugar 4-7 times daily
34. Ultrasound
Dating scan at 8 – 12 wks
Nuchal translucency 11-14 wks
Targeted scan including fetal echo at 18-20
wks
Growth scan at 26 wks and every 4 wks
thereafter
NST + AFI twice wkly starting at 32 wks; 28
-wks if poorly controlled or class D- T.
39. Artificial Sweeteners and
Caffeine:
Avoid saccharin as it crosses the placenta.
Aspartame , acesulfame-K and sucralose allowed
in limited amounts. Artificial sweeteners containing
CHO counted as part of total CHO
Caffeine is allowed in moderation. <300 mg/day is
allowed to limit potential harm to the fetus
40. Exercise
ACOG recommends – 30 min/day of moderate
exercise .
Begin with 5 – 10 min of warm up period involving
stretching exercises.
In sedentary women, exercise HR should not
exceed 140 bpm.
Exercising lowers maternal glucose conc in GDM .
43. When to Start Insulin Therapy in
GDM
Fastinga
Postprandial
Reference
105b
None
Metzger
>95
2 h> 120
Langer et al.
>100
1 h > 130
Ramus and Kitzmiller
>90
1 h> 120
Jovanovic–Peterson
a – Glucose concentrations (mg/dl) measured in finger–stick
wholeblood samples unless designated otherwise.
b – Venous plasma sample.
44. Why Insulin?
Gold standard because of its safety and efficacy
it can not cross placenta because large
mol wt (6000Da)
NPH
insulin is the only basal insulin that
has been adequately studied in
pregnancy
45.
Insulin regimen should:
Result in a smooth glucose profile throughout
the day, with no hypoglycemic reactions bet
meals or at night.
HbA1C is (< 6.5%) at least 3 months before
conception
1.0 mg/day of folic acid for at least 3
months before conception to minimize
the risk of neural tube defects in the fetus.
46.
Regimen and timing of insulin injections
different from non-pregnant state
because as pregnancy progress:
Progressive lowering of maternal F & PPBG
.
↑sing fetal demand for glucose
↑ses the risk of symptomatic hypoglycemia
47. Monitoring BG
At least 4 times (SMBG)
Fasting and 3 one hr postprandial
Pre vs. postprandial monitoring
Better glycemic control (HbA1c value 6.5 vs.
8.1 %)
↓ incidence of LGA infants (12 vs. 42 %)
↓rate of CS delivery for CPD (12 vs. 36 %)
48. Monitoring BG
Home monitoring
Maintain log book
Use a memory meter
Calibrate the glucometer frequently
HbA1C
Ancillary test for feedback to the pt
Lower values when compared to non-pregnant
state – lower BG – measured every 2-4 weeks
Target < 5.1%
51. WHEN TO DELIVER
Class A1
Labor spontaneously or induce 40-42 weeks,
Cochrane review-”little evidence to support
elective induction at 38wks
Class A2 -C ( good control with nl antepartum
testing)
Induce at 39 – 40 weeks
Class D - T or class A2 - C with poor control
Deliver at 37-38 weeks
52. Mode of Delivery
Vaginal route – preferred
Indications of C.S.
-EFW->4.5 Kg [ACOG ]
-H/O shoulder Dystocia, previous stillbirth
-other obstetric indications
EFW - 4 - 4.5Kg - Role of CS controversial
53. Scheduled C-Section
Usual medication (insulin or glyburide) at
bedtime
Eat nothing after midnight
Do not take morning medication
Check blood glucose
Perform CS within 2 hrs
If unable to perform surgery immediately
or pt in poor control, start insulin drip,
Perform CS after 4-6 hrs euglycemia.
54. Vaginal delivery : Management
•
•
•
•
•
•
Strict asepsis
Restrict number of PV examinations
Electronic fetal heart rate monitoring
Partogram
Obstetrician to be well versed with the
Mx of SHOULDER DYSTOCIA
Call Paediatrician
55. Insulin During Labor
Tight control of maternal glycaemia is
essential throughout labor.
In labor no extra insulin is required
because labor is a form of exercise
Monitor BS- 1 hourly
Target BS-70-100 mg/dl
Monitor urine sugar & ketone 2-4 hourly
57. Postpartum Care Continued
Type 1 DM-restart insulin [0.5-0.6U/Kg] on day 2-5
post delivery.
Breast feeding: helps in weight loss.
Insulin, tolbutamide compatible.
Chlropropamide secreted small amounts
Glyburide and glipizide not secreted
Metformin secreted - no adverse effects
58.
Check BG before discharge
Lifestyle modification: exercise, weight reduction &
healthy diet
75 OGTT at 6-12 wks postpartum: classify patients
into normal/impaired glucose tolerance and
diabetes
59. Contraception
Low dose EP can be used
Progestin only pills shown to ↑se risk of
T2DM in GDM
IUCD – ↑sed PID
60. Women and Diabetes
Diabetes no longer
means
›
›
›
›
›
Abstinence
Amenorrhea
Inability to
conceive
Inability to deliver
healthy children
Death during
pregnancy
61. Teachable Moments
Women with a history of GDM present an ideal
group for diabetes prevention, not only in
preventing diabetes in themselves, but for their
family, for whom they are often the gatekeepers
for nutrition and exercise.
Pregnancy is a teachable moment when women
are usually very focused on their own health and
the health of their baby.
Notas do Editor
Memory-based self-monitoring of blood glucose (SMBG).
See comment
Carbohydrate CHO
plasma value is approximately 12% higher than a whole blood value. A finger stick yields arterialized blood, which does not influence the fasting glucose concentration because in the fasting state there is little glucose uptake by muscle tissue. After eating, however, muscle glucose utilization becomes a factor. Measurement of glucose concentrations in blood samples obtained by a finger stick yields higher values than if a venous sample had been obtained. This is because the arterialized blood has not yet traversed muscles and hence glucose removal by this tissue has not occurred.
Levels of HbA1c are related to the rate of congenital anomalies and spontaneous early abortions in pre-existing diabetes, but the use of this measure, which retrospectively reflects glycemic profile in the last 10 weeks, for treatment evaluation in GDM is questionable. In addition, the association between glycosylated hemoglobin and pregnancy outcome in GDM or prediction of macrosomia is poor