diabetes in pregnancy[1]
TRANSCRIPT
Epidemiology
• Most common medical complication of Pregnancy
• affects 2-3% of pregnancies– Gestational DM 90%– Preexisting DM 10%
CHO Metabolism
• Effects of Pregnancy– mild fasting hypoglycemia; postprandial
hyperglycemia– due to inc plasma volume in early gestation and
inc fetal glucose utilization as pregnancy advances– progressive increase in tissue resistance to insulin– increase insulin secretion to maintain euglycemia– suppressed glucagon response– inc prolactin, cortisol– HPL has GH like effects
Glucose Metabolism
• Normal pregnancy : Diabetogenic state– increase in pc BG– insulin resistance
– Early Pregnancy• Anabolic state
– increase in maternal fat stores
– decreased FFA concentration
– decrease in insulin requirements
Type I Diabetes
• Abrupt onset• usually young age• occasionally occurs in 30’s or 40’s
• lifelong requiremnent for insulin replacement• may have genetic predisposition for islet cell
ab• concordance in MZ twins for dev of DM is
33%• suggests other factors also imp
(environmental)
Type 2 DM
• Abnormalities of insulin sensitive tissues– decreased skeletal muscle and hepatic
sensitivity to insulin
– abnormal B cell response• inadequate response for a given degree of glycemia• usually older• increased BMI• insidious onset• strong genetic component
– MZ twin data lifetime risk 58-100%
Diagnosis of DiabetesNon Pregnant
• Fasting plasma BG >7.0mmol/l• Casual plasma BG >11.1mmol/l
Impaired Fasting Glucose• FPG 6.1-7.0 mmol/l
Impaired Glucose Tolerance • normal FPG• 2 h 75gOGTT test with BG 7.8-11.1 mmol/l
Canadian Diabetes Association 1998
Classification and Risk Assessment
Class DM onset Duration Vascular Dis Insulin Need
Gestational Dm
A1 Any Any - -
A2 Any Any - +
Pregestational DM
B >20 <10 - +
C 10-19 10-19 - +
D <10 >20 + +
F Any Any + +
R Any Any + +
T Any Any + +
H Any Any + +
Gestational Diabetes
• Definition• CHO intolerance of variable severity first diagnosed in
Pregnancy
• Prevalence 2-4%• Risk Factors
• maternal age >25
• Family history
• glucosuria
• prior macrosomia
• previous unexplained stillbirth
• ethnic group: Hispanic, Black, First Nations
Gestational Diabetes
• Screening
– PC 50/Trutol
– 1 hr after 50g load of glucose – >7.8mmol/l abnormal*– 15% of patients screen positive
* value >10.3 diagnostic of GDM (no OGTT needed)
Gestational Diabetes
• Screening
– 24-28 weeks routine
– no need to fast– screen at 1st prenatal visit if hx of previous
GDM– screen earlier (12-24 weeks ) if risk factors
• Diagnosis OGTT
• 2 or more values greater than or equal to above cutoffs diagnostic of GDM
• single abnormal value indicates CHO intolerance
Gestational Diabetes
Fasting 5.31h 10.62h 9.23h 8.1
Fasting 5.31h 10.62h 8.9
3 H 2H
Maternal Risks
• birth trauma• operative delivery
• 50% lifetime risk in developing Type II DM
• recurrence risk of GDM is 30-50%
Gestational Diabetes
Fetal Risks
• no increase in congenital anomalies• increased risk of stillbirth if fasting+ pc
hyperglycemia• macrosomia• birth trauma-shoulder dystocia and
related complications
Gestational Diabetes
• Management
– goal is to optimize BG levels to minimize risk of adverse perinatal outcomes
– diet – exercise– insulin therapy
Gestational Diabetes
• Management : Diet
• patients without fasting hyperglycemia• average 8000-9000 kj/day.• BMI>27 -- 25 kcal/kg/ideal body weight/d• BMI 20-26 -- 30 “• BMI<20 -- 38 “
Gestational Diabetes
• Diet : general principles
• 55% CHO 25% Protein 20% fat
• Normal weight gain 10-12 kg• avoid ketosis
• liberal exercise program to optimize BG control
Gestational Diabetes
• If persistent hyperglycemia after one week of diet control proceed to insulin
• 6-14 weeks 0.5u/kg/day• 14-26 weeks 0.7u/kg/day• 26-36 weeks 0.9u/kg/day• 36-40weeks 1 u /kg/day
Gestational Diabetes
• If fasting hyperglycemia start with NPH hs • initial dose 6-8 U • if only pc hyperglycemia use humalog 2-4u ac
the specific meal
• adjust 2u/time 1 formula /time
• BG target ac <5.3 2 h pc <6.7
Gestational Diabetes
• Postpartum• often will not require insulin• if fasting hyperglycemia - more likely to
develop persistent Diabetes• 6 weeks post partum 75g OGTT• yearly fasting BG
• emphasize importance of maintaining N weight, exercise
Gestational Diabetes
Neonatal Risks
• hypoglycemia 50% in macrosomic 5-15% if N BG control in Pgy
• Hyperbilirubinemia• polycythemia• hypocalcemia• hypomagnesiumia
Gestational Diabetes
Preexisting Diabetes
• Preconception Counselling
• risk of NTD ~1-2%
• Folic Acid 1-4 mg /day• BG 3.5-5.3 prior to meals• switch to MDI regimen (insulin ac meals and
HS)
• keep track of cycles
• Normoglycemia prior to conception • ideally HBA1C 6% or less• Team approach• glucose monitoring qid• ACE contraindicated : should be D/C at
conception or use Diltiazem instead• baseline HBA1C, 24h urine for protein Cr Cl ,
opthalmology review• switch from OHA to insulin
Preexisting Diabetes
• Assess for end organ disease– assess for nephropathy - inc risk of PIH– Assess and treat retinopathy - may
progress– assess for neuropathy
• generally remains stable during pregnancy
– assess and treat vasculopathy• CAD is a relative C/I for pregnancy
Preexisting Diabetes
• Maternal Risks– PIH /PET– polyhydramnios– preterm labour
– operative delivery ~50%
– birth trauma– infection– increase in insulin requirements– DKA
Preexisting Diabetes
• Fetal Risks
• congenital anomalies 3X inc risk
• unexplained stillbirth • shoulder dystocia
• macrosomia
• IUGR
Preexisting Diabetes
• Neonatal Risks • hypoglycemia• hypocalcemia• hyperbilirubinemia/polycythemia• idiopathic RDS• delayed lung maturity• prematurity• predisposition to diabetes
Preexisting Diabetes
• Congenital anomalies
• 3x the general population risk • approaches the gen pop risk (2-3%) if
optimal control in periconception period
• related to glycemic control during embryogenesis
Preexisting Diabetes
• CVS– ASD/VSD,coarctation,transp
osition,– cardiomegaly
• CNS– anencephaly, NTD,
microcephaly
Preexisting Diabetes
• GI– duodenal atresia,
anorectal atresia, situs inversus
• GU• renal agenesis • Polycystic kidneys
• MSK• caudal regression• siren
Congenital anomalies
• Maternal Surveillance
• Blood pressure • renal function *• urine culture **• thyroid function
• BG control HB A1C*
• * q trimester
• ** monthly
Preexisting Diabetes
• Fetal Surveillance
• U/S for dating/viability ~ 8 weeks• Fetal anomaly detection
– nuchal translucency 11-14w– maternal serum screen– anatomy survey 18-20 w
– Fetal echo 22 w
Preexisting Diabetes
Preexisting Diabetes
Multidose Insulin
• breakfast 25% H
• lunch 15% H• supper 25% H• hs 35%
NPH
• indicates insulin as a % of total daily dose
Gabbe Obstet Gynecol 2003
Insulin Therapy
onset (h) peak duration
• insulin analogs .25 0.5-1.5 6-8
• rapid acting 0.5 2-4 8-12
• intermediate 1-1.5 4-8 12-18
• Insulin Pump– Allows insulin release close to physiologic – Use short acting insulin– 50-60% of total dose is basal rate– 40-50% given as boluses– Potential complications
• Pump failure• Infection• Increased risk of DKA if above happens
Insulin Therapy
Peripartum Management
• Withhold subcutaneous insulin from onset of labour or induction
• IV D10 @50cc/h• IV short acting insulin in NS usually
starting at 0.5-1u/h* *10cc insulin in 100 cc NS(1U=10cc)
• insulin rate usually based on BG and pre-delivery insulin requirement
• eg. For each 75-100 total units /24h of pre-delivery insulin, 1 unit per hour needed
• measure capillary BG hourly VPG q2-3h• target: 4-6mmol/L
Peripartum Management
• Following delivery– stop insulin infusion – begin sub Q insulin
– resume previous MDI schedule at 1/2 -2/3 the pre pregnancy dose
– maintain IV D5W @50cc/h until oral feeds tolerated
Peripartum Management
Oral Hypoglycemic agents
• Traditionally not recommended in pregnancy
• Recent RCT of oral glyburide vs insulin for GDM
• 440 patients• BG measured 7x daily• Treatment started after 11 weeks gestation
Langer NEJM 2000
Glyburide Insulin
Achieved N BG 82% 88%LGA infants 12% 13%Macrosomia 7 4C Section 23 24Hypoglycemia 9 6Preeclampsia 6 6Anomalies 2 2
Oral Hypoglycemic agents
Langer NEJM 2000
• Goals– Minimize/eliminate the risk of fetal death– Early detection of fetal compromise – Prevent unnecessary premature delivery
• Main benefit is the NPV of these tests– Provides reassurance that fetus with a N test
unlikely to die in utero– Allow prolongation of pregnancy – fetal maturation
Fetal Surveillance
Fetal Surveillance
• Gestational Diabetic Diet controlled
– Can start fetal surveillance at term (40 weeks)
• GDM on insulin/Type II DM/ Type I DM
– Start weekly BPP from 32 weeks– Consider earlier testing if
• suboptimal control• Hypertension• vasculopathy
Timing of Delivery
GDM Diet controlled– Same as non diabetic
– Offer induction at 41 weeks if undelivered
GDM on Insulin/Type II/Type I– If suboptimal control deliver following confirmation
of lung maturity if <39 weeks– Otherwise deliver by 40 weeks– Generally do not allow to go postterm
Mode of Delivery
• Macrosomic infants of diabetic mothers have higher rates of shoulder dystocia than non diabetic mothers
• Ultrasound estimates of fetal weight become significantly inaccurate after 4000g
• Reasonable to recommend C/S delivery if EFW is >4500g
Diabetic Ketoacidosis
• 5-10% of pregnant Type 1 pts
• Risk factors– New onset DM– Infection– Insulin pump failue
– Steroids– B mimetics
• Fetal mortality 10%
• Management– ABC’s and ABG
• Assess BG, ketones electrolytes
– Insulin • .2-.4U/Kg loading and 2-10U/h maintenance
– Begin 5% dextrose when BG is 14 mmol/l– When potassium is N range begin 20mEq/h– Rehydration isotonic NaCl
• 1L in 1st hour • .5-1l/h over 2-4h• 250cc/h until 80% replaced• Replace Bicarb and phosphate as needed
Diabetic Ketoacidosis
– Rehydration isotonic NaCl• 1L in 1st hour • .5-1l/h over 2-4h• 250cc/h until 80% replaced
– Replace Bicarb and phosphate as needed
Diabetic Ketoacidosis