Gestational dm
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Transcript of Gestational dm
DM in Pregnancy DM in Pregnancy
Dr.Sushma Sharma
Prof.,Dept. of ObGyn,
MIMER Medical college,
Talegaon
Dr.Sushma Sharma
Prof.,Dept. of ObGyn,
MIMER Medical college,
Talegaon
Increasing Prevalence of GDM 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
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
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
Increase is attributable to: Sedentary lifestyles
Changes in diet
Immigration from high-risk populations
Childhood and adolescent obesity
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
Gestational Diabetes Mellitus 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.
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.
D M D M
conceptionconception
Preexisting type 2Preexisting type 2
Incipient type 2Incipient type 2
type 1type 1
10 20 30 40
True GDMTrue GDMdeliverydelivery
Follow upFollow up
Maternal-fetal Metabolism in Normal Pregnancy
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.
Metabolic Changes
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.
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
Glucose Metabolism in Pregnancy
Fetus
Fat
Glucose Aminoacids
Insulin resistance
Hyperinsulinemia
FASTINGaccelerated starvation
(maternal hypoglycemia,
hypoinsulinemia,
hyperlipidemia,
hyperketonemia)
FEDhyperglycemia, hyperinsulinemia,
hyperlipidemia,
reduced sensitivity to insulin
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
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
Compartment Metabolic Effect
MotherMother
PlacentalHormones
HPLHPGH
CortisolOestrogen
Progesterone
PlacentaPlacenta
FoetusFoetus
Insulin resistance
Impaired insulin action
Aberrant Fuel Mixture
Mode oftransport
Glucose Amino acids Cholesterol TG Ketones
FacilitatedFacilitatedDiffusionDiffusion
By GLUT3 carriers
ActiveActive Diffusion
Lipase
DiffusionDiffusionFFAFFA GlycerolGlycerol
DiffusionDiffusion
Aberrant fuel mixture
HyperinsulinemiaHyperinsulinemia
Fuel Mediated TeratogenesisFuel Mediated TeratogenesisFuel Mediated TeratogenesisFuel Mediated Teratogenesis
Perinatal Mortality, Morbidity & Birth Injury
Maternal Hyperglycemia
Fetal Hyperglycemia
Fetal Hyperinsulinemia
↑Fetal substrate uptake ↑Oxygen uptake Lung Surfactant↓
Respiratory Distress Syndorme
Lipids / Amino acid ↑ Hypoxemia
Polycythemia Marosomia
↑Erythropoietin
? SB
↑BMR
Hypotrophy Pancreaticislet & B cells
PATHOGENIC EVENTS
PEDERSEN THEORY
Maternal Diabetes
Glucose crosses placenta
Carbohydrate surplus of fetus
Increased secretion of insulin
Stimulation of protein, lipid & glycogen synthesis Free amino acid
Stimulatory effect on development of B cells
Release Insulin like growth factor
MACROSOMIA
MACROSOMIA
SHOULDER DYSTOCIA
Perinatal Mortality to Maternal Blood Glucose During Last Weeks of Pregnancy
Mean glucose level Perinatal mortality
>150 mg%100–150 mg% <100 mg%
24%15%4%
Fetal Consequences
First Trimester Second Trimester Third Trimester
-Malformations-Growth Restriction-Fetal Wastage
-Hypertrophic cardiomyopathy-Polyhydramnios-Erythraemia-Placental Insufficiency-Preeclampsia-Fetal loss-Low IQ
-Hypoglycemia-Hypocalcemia-Hyperbilirubinemia-Respiratory distress syndrome-Macrosomia-Hypomangnesmia-Intrauterine Death
Malformations in infants of Diabetic Mothers, No Risk in GDMMalformations in infants of Diabetic Mothers, No Risk in GDM
Anomaly Onset
Caudal regressionSpina bifida
3 wks6 wks
AnencephalyMyeloceleHydrocephalus
4 wks4 wks5 wks
DextrocardiaConus arteriosus defectsVSD
4 wks5 wks6 wks
Renal agenesis/hypoplasia
6 wks
Neonate
ChildAdult
RDSHypoglycemiaHypocalcemia
HypomagnesemiaThrombocytopenia
RDSHypoglycemiaHypocalcemia
HypomagnesemiaThrombocytopenia
Polycythemiaheel-stick blood
Renal vein thrombosis
HyperbilirubinemiaHyperbilirubinemia
Behavior - Intellect deficitObesity
Diabetes mellitusDiabetes mellitusDiabetes mellitusDiabetes mellitus
Maternal Complications
Worsening retinopathy – 10% new DR, 20% mild NPDR and 55% mod-severe NPDR progresses
Worsening proteinuria.
Hypertension and Cardiovascular disease
Neuropathy – No worsening
Infection
Hypoglycemia Diabetic Ketoacidosis Preeclampsia: 18 % Preterm delivery: 42 % Cesarean delivery: 56 %
50% lifetime risk in developing Type II DM in GDM
Recurrence risk of GDM is 30-50%
MANAGEMENT
Patient education
Medical Nutrition therapy
Glycemic monitoring: SMBG and targets
Pharmacological therapy
Fetal monitoring: ultrasound
Planning on delivery
Interdisciplinary team effort
PRENATAL MANAGEMENT
Screening Tests for GDM
Best method still controversial
Criteria of Diagnosis
ADA recommendations
WHO criteria
Urine Glucose
Spot Test
HbA1C, Serum fructosamine
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
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
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
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.
Fetal Evaluation
Procedure Low risk High risk
Fetal kick counts 28 28
USG for fetal growth
28 & 37 weeks Monthly
NST In GDM 36weeks Semiweekly
28-34 weeks, Semiweekly
FHS/BPP/Doppler 36 weeks, weekly
27 weeks-1-3/week
AmniocentesisFor lung maturity
- 35 - 38 wks
Tx Targets - Controversial
ACOG F venous plasma ≤ 95 mg/dl 1 hr PP ≤ 140 mg/dl 2 hr PP ≤ 120 mg/dl Pre-meal ≤ 100 mg/dl A1C ≤ 6%
ADA Premeal 80-110 2 hr PP not >155
These are venous plasma targets, not glucometer targets
Medical Nutrition Therapy
Goals Achieve normoglycemia Prevent ketosis Provide adequate weight gain Contribute to fetal well-being
Nutritional plan Calorie allotment Calorie distribution CH2O intake
Dietary Therapy Avoid single large meals with large %
of simple CHOs
6 feedings/day, with 3 major & 3 snacks
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
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 .
Exercise
Absolute Contraindication Preterm Labor PROM Incompetent Cervix Persistent 2nd or 3rd trimester bleeding IUGR Placenta Previa beyond 26 week PIH
INSULIN
MEDICATION ORAL DRUGS
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.
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
Why Insulin?
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.
Regimen and timing of insulin injections different from non-pregnant state because as pregnancy progress:
↑sing fetal demand for glucose
Progressive lowering of maternal F & PPBG
↑ses the risk of symptomatic hypoglycemia
.
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
%)
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%
Cross placenta.
Fetal hperinsulinemia.
Prolonged fetal hypoglycemia
OHA in Pregnancy
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
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
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.
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
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
Insulin During Labor
Postpartum Care
Prevent infection
Insulin infusion is discontinued
GDM on diet-no monitoring
GDM on insulin /Pre-gestational DM-
-Monitor BS
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
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
Contraception
Low dose EP can be used
Progestin only pills shown to ↑se risk of T2DM in GDM
IUCD – ↑sed PID
Women and Diabetes
Diabetes no longer means› Abstinence› Amenorrhea › Inability to
conceive› Inability to
deliver healthy children
› Death during pregnancy
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.