diabetes & pregnancy by: carolyn connors. diabetics and pregnancy euglycemia is very important!...
TRANSCRIPT
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Diabetes & PregnancyBy: Carolyn Connors
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Diabetics and Pregnancy
Euglycemia is very important!Decreases likelihood of:
Miscarriage
Congenital anomalies
Macrosomia
Fetal death
Neonatal morbidity
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Diabetic Embryopathy
Occurs in 6-7th weeks GA
Maternal Hyperglycemia leads to vascular disruption and yolk sac failure
Increased spontaneous abortions
Major malformations
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Fetal Effects
Pathophysiology – Maternal hyperglycemia
Fetal hyperglycemia
Premature maturation of pancreatic islets
Hypertrophy of beta cells
Hyperinsulinemia
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Hypertrophy of Beta Cells
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Fetal Hypoxemia
Chronic fetal hyperinsulinemiaIncreased activity hepatic enzymes
Increased glycogen and lipid storage
Increased metabolic rates
Oxygen consumption increased
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Fetal Hypoxemia
Stimulates erythropoietin polycythemia
Promotes catecholamine productionHTN
Cardiac hypertrophy
Contributes 20-30% stillbirth rate in poorly controlled diabetics
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Neonatal Effects
Congenital anomalies –
Accounts for 50% of perinatal deaths of infants of diabetic mothers (IDM)
Relative risk increased 7% with IDM over general population
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Congenital Anomalies
Two-thirds involve CVS or CNSAnencephaly and Spina bifida 20x more common in IDM
GU, GI, MSK defects increased
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Congenital Anomalies
Left Colon Syndrome - Transient inability to pass meconium
Resolves spontaneously
Condition unique to IDM’s
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Congential Anomalies
Caudal Regression Syndrome –
200x more common in IDM
Incomplete development of sacrum/lumbar region
Distal spinal cord disruptedNeurologic impairment varied
Leg deformities
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Premature Delivery
Increased Iatrogenic premature delivery
Maternal preeclampsia
Increased spontaneous premature labour
Associated with poor glycemic control
High rates of UTI’s
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Perinatal Asphyxia
Defined to include:Fetal heart rate abnormalities during labor
Low Apgar scores
Intrauterine death
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Perinatal Asphyxia
Correlated with:
Maternal vascular diseaseEg: nephropathy
Hyperglycemia during labor
Prematurity
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Increased Fetal Growth
Mostly during 3rd trimester
Disproportionate growthInsulin sensitive tissue eg. Liver, muscle, cardiac muscle, subcutaneous fat
Head circumference normal
Increased risk of hyperbilirubemia, hypoglycemia, acidosis
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Macrosomia
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Macrosomia
Birth weight > 90th percentile or > 4000g
Predisposes to birth injury Eg: Shoulder Dystocia
Brachial plexus injury
Clavicular/Humeral Fractures
Perinatal asphyxia
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Shoulder Dystocia
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Shoulder Dystocia
Occurs in 1/3 IDM > 4000g
Disproportionate growth contributes
C-Section often recommended if fetal weight > 4300g
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Intrauterine Growth Restriction
Maternal Vasculopathy
Preclampsia
Congenital Anomalies
Very strict BG control
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Respiratory Distress Syndrome
Causes amoung IDM:
Delayed maturation of surfactant synthesis
Hypertrophic cardiomyopathy
Retained lung fluid (TTN)
Increased rates of c-section
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Hypertrophic Cardiomyopathy
Fetal hyperinsulinemia increases fat/glycogen deposit in cardiac muscle
Thickening interventricular septum30-50% IDM with hypertrophy on Echo
Obstructed left ventricular outflow5-10% symptomatic
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Hypertrophic Cardiomyopathy
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Hypertrophic Cardiomyopathy
Transient condition
Echo normalizes 6-12 months
Symptomatic infants recover after 2-3 weeks supportive care
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Hypoglycemia
BG levels < 2.2
Occurs within hours of birth
Increased risk with both LGA and SGA infants
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Polycythemia
13-33% IDM’s
Hct should be measured 12hrs after birth
Can lead to Hyperviscosity SyndromeRenal vein thrombosis
Vascular sludging, ischemia, infarction of vital organs
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Polycythemia
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Hyperbilirubinemia
Associated with:Poor maternal glycemic control
Polycythemia
Macrosomic infants
prematurity
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Neurodevelopmental Outcome
Few studies available which adequately control confounders
Maternal ketones Poorer psychomotor development
Elevated HbA1c levels during pregnancy
Poorer intellectual performance
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Neurodevelopmental Outcomes
Developmental Delay IUGR
Congenital malformations
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Risk of Developing Diabetes
Type 1 DM:
Some genetic component:Offspring – 6%
Siblings – 5%
Identical twins – 30%
(general population – 0.4%)
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Risk of Developing Diabetes
Type 2 DM:
Much larger genetic component
Abnormal intrauterine metabolic environment
IDM – 45%
Prediabetic – 8.6%
Nondiabetic – 1.4%
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ObesityIncreased BMI noted in offspring of diabetic mothers (ages 5-19 yrs)
Birth weight not indicative
Impaired Glucose Tolerance
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Prepregnancy Counselling
Required to decrease complications in known diabetics:
Macrosomia: 63% (10%)
C-Section: 56% (20%)
Preterm delivery: 42% (12%)
Preeclampsia: 18% (6%)
Congenital Malformations: 5% (3%)
Perinatal Mortality: 3% (<1%)
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Complete History/Physical Exam
Duration/Type of DM
Acute complications
Chronic complications
Glucose management
Physical activity
Medication
Obs/Gyne History
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Laboratory Investigations
UrinalysisTreat asymptomatic bacteriuria
Baseline renal functionTotal protein, serum Cr, CrCl
Thyroid FunctionTSH, Free T4
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Comprehensive eye examWithin 12 months prior to pregnancy
Within 1st trimester
Followed closely up to 1 year postpartum
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Assessing Glycemic Control
HgbA1C: mean blood glucose concentration over preceding 6 - 8 weeks
HgbA1A – In Pregnancy: Mean BG concentration over 4 – 6 weeksLife span of RBC shortened due to increased production
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Hemoglobin A1C
Measured every 4-6 weeks
Goal < 6.1 prior to d/c contraceptionAssociated with lowest rate of adverse pregnancy outcome
Spontaneous abortion
Congenital malformation
Perinatal death
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Assessing Glycemic Control
Glucose monitoring:Pregnancy associated with exaggerated rebound from hypoglycemia
Urine Ketones:Type 1 DM with illness or BG > 11.1
DKA associated with high fetal mortality rate
Ketonemia may have adverse developmental effects.
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Target Blood Glucose Values
Fasting glucose < 5.2
1 hr postprandial glucose < 7.7
2 hr postprandial glucose < 6.6
Qhs < 5.9
Strict glycemic control decreases adverse fetal outcomes
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Hazards of Strict Glycemic Control
1. Hypoglycemia – does not appear to be teratogenic in humans
Extremely strict control (BG < 4.8) can cause small-for-gestational age infants
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Hazards of Strict Glycemic Control
2. Diabetic Retinopathy – Related to degree of baseline retinopathy
Magnitude of reduction of chronic hyperglycemia
Mediated by closure of small retinal blood vessels that were narrowed but patent
Frequent retinal evaluation recommended in high risk women
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Retinopathy
Comprehensive eye examWithin 12 months prior to pregnancy
Within 1st trimester
Followed closely up to 1 year postpartum
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Nutritional Therapy
Achieve euglycemia
Prevent ketosis
Provide adequate weight gain
Contribute to fetal well-being
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Caloric Requirements
Increase 300 kcal/day in pregnancy
Based on BMI:30-40 kcal/kg/day – BMI < 22
30-35 kcal/kg/day – BMI 22-27
24 kcal/kg/day – BMI 27-29
12-15 kcal/kg/day – BMI > 30
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Maternal obesity can cause:Excessive fetal growth
Increase glucose tolerance
Caloric restriction may be useful treatment
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Oral Anti-hyperglycemic Agents
Sulfonylureas –
can cross the placenta causing fetal hyperinsulinemia:
Macrosomia
Neonatal hypoglycemia
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Oral Anti-hyperglycemic Agents
Glyburide –
High protein binding so placental passage low
Several studies have not shown harmful effects
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Oral Anti-Hyperglycemic Agents
Metformin and Thiazolindiones –Minimal information available
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Recommendations
Oral anti-hyperglycemics not recommended in pregnancy
Some question as to usage in non-compliant patients on individualized basis
Insulin - patients unable to obtain euglycemia through diet alone
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Insulin Therapy
Type 2 DM:Insulin during preconception period
Obtain adequate HgbA1C
Avoid excessive weight gain
Moderate low-impact exercise
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Insulin Therapy
Rapid Acting Insulin (Lispro/Aspart)
Acceptable safety profiles
Minimal transfer across the placenta
No evidence teratogenesis
Note: Compared to Regular Insulin
Improves postprandial BG
Decreases risk hypoglycemia
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Insulin Therapy
Longer Acting Insulin:
NPH recommended
Glargine:high affinity for IGF-1 receptor
Risk of macrosmia
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Intrapartum Management
Latent phase – insulin to maintain BG 3.9-5.0
Active Phase – insulin resistance rapidly decreases
BG check hourly
Avoid boluses of glucoseIncreases risk of neonatal hypoglycemia
Fetal hypoxia
Fetal/neonatal acidosis
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Postpartum Management
Postpartum - insulin requirements drop sharply
Short ½ lives of placental growth hormone and placental lactogen
Insulin doses readjusted 24-72 hrs
Note: Breast-feeding patients should remain on insulin
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The End!