Pregnancy and Diabetes Prof. M.C.Bansal MBBS,MS,MICOG,FICOG Professor OBGY Ex-Principal & Controller Jhalawar Medical College & Hospital Mahatma Gandhi Medical College, Jaipur.
‘My sugars are high and I must worry Since, within my womb a child I carryMust reduce the sugars before its too lateOr baby will end up being high birth weight’
Epidemiology Prevalence is 3.8 to 21.1% in different parts of country Incidence of diabetes among Asian women is rising & it is more frequently being diagnosed at younger ages Several women & their yet unborn offsprings are at potential risk of an adverse outcome More in urban areas than rural areas
What are the metabolic changes in normal pregnancy?Pregnancy is associated with 2 important changes1. Insulin resistance (permit foetus to draw on available fuel stores preferentially )2. Hormonal changes –Progesterone, HCG,HPL,cortisol, estradiol,prolactin- disturb glucose metabolism & result in Pregnancy: Insulin • Decreased FPG & Increased PPG resistant state Increased insulin levels •If β cells fail to β-cell hypertrophy & hyperplasia overcome this- results in GDM Decreased insulin sensitivity (IR) Enhanced lipolysis
WHO & NDDG Classification Pregestational Gestational diabetes diabetes impaired glucose Type 1 tolerance of Type 2 pregnancy Undiagnosed pre- existing diabetes Undiagnosed pre- existing IGT
When can Diabetes & Pregnancy coexist? DM & pregnancy coexist under 2 circumstances1. Known diabetic (type 1 or type 2) may become pregnant –Pregestational diabetes Known Diabetic2. Diabetes-first makes its appearance in a woman when she is pregnant-Gestational diabetes (GDM) Develops Non diabetes for Diabetic 1st time
What is GDM? GDM= Gestational Diabetes Mellitus The Third International Gestational Diabetes Workshop defined GDM as -Carbohydrate intolerance of variable severity with onset or first recognition during pregnancy If diabetic state regresses after delivery: diagnosis is confirmed If diabetic state does not regress : reclassified as type 1 or type 2
Risk Factors for GDM Strong family history Women who have given birth to large baby >4 Kg History of recurrent pregnancy loss Persistent glycosuria Age > 25 Yrs Past history of GDM Obese or overweight or show excessive weight gain during pregnancy
Risk Factors for GDM History of pre-eclampsia History of polyhydramnios Chronic hypertension History of still birth, congenital malformations Recurrent or severe moniliasis or UTI
Why all Indian womenshould be screened for glucose intolerance during pregnancy ?
Screening is essential in all pregnant womenas the Indian women have 11 fold increasedrisk of developing glucose intolerance during pregnancy compared to Caucasian women Dornhost A, Paterson CM, Nicholls JS, Wadsworth J, Chiu DC, Elkeles RS, Johnston DG, Beard RW: High prevalence of GDM in women from ethnic minority groups. Diabetic Med 1992: 9 (9): 820-2.
When to screen Optimally performed at 24- 28 wks of gestation In high risk patients it is wiser to screen in first antenatal visit Early detection causes better fetal outcome In pregnant woman with normal GCT in first trimester but if there is rapid maternal wt gain or fetal macrosomia suspected, then repeat test at 24-28 wks
Screening procedures American Diabetes Association (ADA ) World Health Organization (WHO ) AmericanCollege of Obstetrician and Gynecology ( ACOG )
• ADA recommends two step procedures for screening and diagnosis of diabetes in selective population.• An initial screening by measuring plasma glucose one hour after 50g oral glucose load (glucose challenge test [GCT]).• A glucose threshold value equal to or > 140mg/dl identifies GDM• Those found positive at the screening test are given 100g OGTT
ADA CRITERIA FOR DIAGNOSIS OF GDM 100 g OGTT Fasting 95 mg/dl (5.3mmol/L) 1 – hr 180mg/dl (10mmol/L) 2 – hr 155mg/dl (8.6mmol/L) 3 – hr 140mg/dl (7.8mmol/L)Two or more of the venous plasma concentrations must be met or exceeded for a positive diagnosis. Ref :O’Sullivan & Mahan → Carpenter & Couston; ADA Position Statement on GDM 2006)
Drawback Of ADA criteria Cut off values do not correlate with fetal outcome No of samples are drawn many ( Four ) Venous samples are needed Two visits are necessary so patient may not report back
WHO CRITERIA FOR DIAGNOSIS OF GDM2 hr pp after 75 Outside In pregnancy gm glucose pregnancy >200 mg/dl DM DM>140- 199 mg /dl GDM IGT>120-139mg/dl GGI - <120mg/dl Normal Normal
WHO CRITERIA FOR DIAGNOSIS OF GDM Drawback – Criteria not based on maternal and fetal outcome but easy adoptability Advantages – Need not to be fasting Both screening and diagnostic procedure Least disturbance in woman’s routine
Glycosylated Haemoglobin (A1c) Normal A1c level in pregnancy is 5.3 – 6 Not reliable as they reflect too long a time period. May serve as a prognostic value
Glycosylated Haemoglobin (A1c)May be useful to find out whether the woman is a pre GDM or GDMUseful in monitoring the control during pregnancy but not for day to day management
Measuring other parameters BP monitoring – if >130/80 alpha methyldopa should be started Retinal examination Microalbuminuria to be looked for Thyroid functions
Clinical parameters to be monitored Pre-pregnancy weight Weight gain during ANC Edema Pallor Thyroid enlargement Uterine height more than period of gestation
MATERNAL COMPLICATIONS Effects of diabetes on mother Risk of recurrent abortions –in first trimester Infections Postpartum bleeding High Caesarean section rate Risk of pre-eclampsia
GDM ~ 35% DEVELOP DIABETES By 10 YEARSGDM AFTER PARTURITION
Effects of pregnancy on diabetes Moreinsulin is necessary to achieve metabolic control Progression of diabetic neuropathy Worsening of diabetic nephropathy Increase cardiomyopathy and myocardial infarctions
Effect of Maternal Fuels on Fetal & Offspring’s Development Mother Fetus Neonate Child Hypoglycemia & other complications P Insulin l macrosomia Obesity a c IGT e n Plasma t Insulin Glucose a Amino acids “Mixed Diabetes lipids Nutrients”
Fetal Complications Congenital malformations – Mainlyin type I –due to metabolic derangements present at the time of conception, during blastogenesis and organogenesis Hyperglycemia – macrosomia Hypocalcemia Intermittent hypoglycemia- risk of IUGR Hyperviscosity syndrome
Fetal Complications Hyaline membrane disease Apnea and bradycardia Unexplainedfetal demise – during last 4- 8 weeks of gestation
Common congenital malformations Cardiovascular System – TGV, VSD,Coarctation of aorta, PDA, ASD, Single ventricle Central Nervous System – spina bifida, anencephaly, holoprosencephaly, neural tube defects Skeletal – cleft lip and palate, caudal regression syndrome
Neonatal complications Respiratory distress Hypoglycemia Hypocalcemia Hyperbilirubinemia Hyperviscosity Syndrome Cardiac hypertrophy Perinatal Deaths Long term effects on cognitive developments
Management of pregnancy in a woman with diabetes Women with DM (pregestational DM) planned in advance good control-established before conception- avoid risks of hyperglycaemia / glucotoxicityand ketoacidosis during embryogenesis / organogenesis If it occurs accidentally or unaware of DM risks are explained Pregestational •planned pregnancy •tight control at conception
Management of GDM Patienteducation Medical nutrition therapy (MNT) Physical activity Self monitoring blood glucose Self administration of Insulin
Medical Nutrition Therapy Adequate calories/nutrition to meet the need of pregnancy Wt gain expected in pregnancy – 300-400 gm/wk total 10-12 kg Avoid excess wt gain and post prandial hypoglycemia
Calorie allotment and wt gainCurrent wt Recommended daily Recommended( %of ideal calorie intake Kcal/kg total wt gain in kgbody wt ) < 80-90 36-40 12.5-18 100-120 30 11.5-16 120-150 24 7-11.5 >150 12-18 At least 6
Calorie counting Breakfast – split in two equal halves and eat at 2 hr interval – to avoid undue peak in plasma glucose level Dawn phenomenon – peaking of plasma glucose is high with breakfast than with lunch or dinner, in GDM mother first phase of insulin is deficient so it is divided in two halves
FETAL MONITORING Risk based on glycemic Procedure control, vascular disease Low risk high risk Dating ultrasound 8 - 12 weeks 8 - 12 weeks Prenatal genetic diagnosis As needed As neededTargeted perinatal ultrasound: 18 - 22 weeks 18 - 22 weeks fetal echocardiography Fetal kick counts 28 weeks 28 weeks 28 and 37 Ultrasound for fetal growth Monthly weeks1 Antepartum FHR monitoring, 36 weeks, 27 weeks, 1 - 3/week modified BPP weeklyAmniocentesis for lung maturity - 35 - 38 weeks Induction of labor 40 weeks2 35 - 38 weeks
Fetal Ultrasound Indirectly indicates glycemic control Ultrasound scan for fetal growth and liquor volume every two weeks from 26th week Fetal abdominal circumference provides a baseline for further serial measurements which can indicate growth acceleration or restriction.
Insulin Therapy MNT for 2 weeks, if even then fasting Plasma glucose >90 mg/dl and post meal glucose >120 mg/dl – Begin Insulin Premix Insulin 30/70 of any brand 4 units BBF- increase every 4 th day by 2 units till 10 units If FPG >90 mg/dl give 6 units BBF and 4 units BD
Insulin Therapy If post breakfast glucose is high begin with premix 50/50 If 2 hr Plasma glucose >200 mg/dl at diagnosis start 8 units of premixed insulin BBF and titrate it on follow up.
Insulin Therapy If GDM only has post prandial hyperglycemia with normal FBG then start with rapid and regular insulin 2- 3 times a day with each meal. Human insulin does not cross placenta. Usually women with GDM do not require >20 units of insulin/day in comparison to type I or II who may require higher doses
Oral Hypoglycemic Agents Trialand work reveals beneficial role of glibenclamide and metformin No consensus evolved ACOG do not recommend use of OHA in pregnancy
Significance of control of maternal glucose levels Increase maternal carbohydrate intolerance – increase adverse fetal and maternal outcome If maternal Blood Glucose level is 120- 139 mg/dl - Risk of Type II DM is 19% in offspring 140-199 mg/dl – risk increases to 30%
Management guidelines Obstetricmanagement Glycemic control : Pre Induction Monitoring Insulin : Low dose sliding scale High dose sliding scale Insulin infusion Management of Hypoglycemia Elective caesarean section Postpartum Neonatal Management
Preterm labour Choice – Nifedipine Rule out infection ( seen in 40% of cases) Beta Adrenergics : X Increase glycogenolysis and lipolysis tendency to metabolic acidosis
Insulin Type / Regimen Aim: To mimic Natural pattern of insulin secretion To Avoid: •Post prandial Hyperglycemia •Pre meal Hypoglycemia •Nocturnal Hypoglycemia
Obstetric management The standard management of labour for a high risk pregnancy Continuous electronic fetal monitoring Ensure adequate analgesia with a lower threshold for epidural in labour. Labour should not be prolonged Prepare for the possibility of shoulder dystocia. Active management of third stage.
Monitoring labor in Type 1 & Type 2 Diabetes Mellitus Stable Unstable Deliver at 38 wks Delivered as soon CBG during induction as lung maturity is normal range : 0.9% saline attained >120mg/dl : continous insulin infusion <70 mg/dl : DNS Active phase : DNS
GDM : When to deliver ? High risk Low risk Induce at 38 wks Delivery planned at 40 wks gestation Spontaneous onset of labour is awaited Avoid prolonged pregnancy At 40 wks <4500 gms : induce >4500 gms : elective CS ACOG
Elective caesarean section Usual insulin the night before Caesarean section Morning of Caesarean section - withhold usual insulin Measure blood glucose level in theatre prior to anesthesia Avoid IV Dextrose unless hypoglycemic. If indicated, insulin and glucose infusions are given to keep the blood glucose under 140 mg/dl. Postoperatively use low-dose sliding scale then, fasting and before each meal.
Insulin during labour in GDM ? Most do not require it Capillaryblood glucose measured 2-4 hrly : upward deviation corrected with small doses of regular insulin / low dose IV insulin infusion Very low blood glucose : 50-100 ml bolus of 5-10%DS
Intravenous insulin infusionFor patients requiring intensive therapy and/or poorcontrol on a sliding scale,e.g. severe preeclampsia.Via syringe pump50 units regular insulin in 50 mLs of Normal salineAim : blood glucose level 72 – 126 mg/dl(4-7mmol/L)
Plasma Glucose and Insulin flow at the time of onset of labor<70 mg/dl 5% GNS – 100 ml/hr90-120 mg/dl NS – 100 ml /hr120 -140 mg/dl NS 100 ml/ hr + 4 units of regular insulin (in 500ccNS)140 -180 mg/dl NS 100 ml/hr +6 units of regular insulin>180 mg/dl NS 100 ml/ hr +8 units of regular insulin
Blood glucose monitoring Type 1 and Type 2 and GDM on insulin 2-hourly GDM not on insulin 4-hourly Intravenous therapy Not routinely required for diabetes management Normal Saline should be used if requires IV therapy, no need for routine IV Dextrose Caution with fluid overload in severe pre-eclampsia
Management of GDM – Post partum Blood glucose monitoring B.D. for 48 hours Insulin is ceased post delivery : >95% cases do not require it any more If blood glucose levels > 126mg/dl , continue to monitor until discharge - fasting and 2 hours after meals If blood glucose levels are persistently elevated after 72 hours, contact Diabetes Consultant
Management of Type 1 & 2 – Post partum Type 2 will usually not require insulin in the postnatal period unless blood glucose levels are consistently elevated. Start at ½ or 2/3 of pre delivery dose Oralhypoglycemic agents (sulfonylureas, glitazones) are usually not recommended while breastfeeding
Neonatal Management Commence feeding within one hour of birth and feed 3 - 4 hourly. Measure Blood Sugar Level (BSL) : at four hours of age or before the second feed (whichever comes first) immediately - if clinical signs of hypoglycemia present before each subsequent feed until 3 consecutive readings ≥ 2.6 mmol/L Recommence glucose monitoring if change in feeding or clinical condition.
Follow Up of GDM OGTT with 75 gm Glucose using WHO criteria at 6-8 wks postpartum. If normal repeat at 6 months and every yr Toavoid neural tube defects in unplanned pregnancy daily folic acid is recommended
Counseling Ifwoman plans pregnancy she should have very good control of DM – FPG <90 mg/dl at the time of conception to avoid fetal malformations contraceptives – low dose hormones may be given
Preventive measures start fromintrauterine life and continuesthrough out life from earlychildhood.
A short termintensive care givesa long term pay off in the primary prevention of obesity, IGT and diabetes, as‘Preventive medicine starts before birth’