ACOG Practice Bulletin - #60 March 2005

Pregestational DM

Observed in 1% of all pregnancies

o 90% of diabetes cases during pregnancy = GDM, but >50% of these cases eventually develop type 2
PGDM.
Type II PGDM is the most common
o characterized by onset later in life; peripheral insulin resistance; relative insulin deficiency; obesity
Type I PGDM
o characterized by early onset in life; autoimmune process that destroys pancreatic cells
Pregnancy characterized as insulin resistant state with reduced insulin sensitivity which is greatest in the 3rd
tri (resistance 2/2 placental hormones: human placental lactogen, progesterone, prolactin, placental growth
hormone, cortisol, leptin)
o Late in 1st tri risk of maternal hypoglycemia due to estrogen effects of increasing insulin sensitivity
Management of diabetes in pregnancy focuses on glu control via combo of diet, exercise, and insulin therapy
o Patient checks can be as frequent as 1-2 weeks in 1st tri & 2nd tri and weekly after 28-30 weeks
gestation
o Caloric requirements are ~300 kcal > basal; carb counting beneficial in avoidance of weight gain, and
for correlation with insulin dosages and exercise
o Insulin requirements increase throughout pregnancy (marked gestational weeks 28-38); on average
needs range from
.7-.8 U/kg/d in 1st tri
.8-1 U/kg/d in 2nd tri
.9-1.2 U/kg/d in 3rd tri
Generally, insulin doses are cy 20% in response to hyper or hypoglycemia
o Management goal = maintain capillary glu levels as close to normal as possible (100 mg/dL w/ [Hb
A1C] no higher than 6%)
fasting glu level of 95 mg/dL or less
premeal values of 100 mg/dL or less
1-hour postprandial levels of 140 mg/dL or less
2-hour postprandial values of 120 mg/dL or less
Night glu levels should not decrease to less than 60 mg/dL
Check HbA1c each trimester
8% reflects mean of 108 mg/dL w/ each 1% higher or lower than 8 = to a change of
30 mg/dL.
o Short or rapid acting insulin administered prior to
meals to avoid glu spikes
o Longer acting insulin administered to restrain glu
production between meals and in the fasting state
o Intermediate-acting insulin given before breakfast
with rapid or short acting insulin and before the
evening meal or bedtime
o Note that lispro and regular insulin not temporally
interchangeable
o Experience w/ glargine in pregnancy limited
o Oral agents not well studied (glyburide no cross)
o Bedtime dosing preferred as injection given w/
evening meal may increase risk of nocturnal
hypoglycemia
o Achieving euglycemic state w/o significant
hypoglycemia during pregnancy requires frequent self-monitoring
Check and record glu levels in the fasting state, before and 1 or 2 hrs after each meal, &
before bed. Check urine ketones when glu >200 mg/dL.
Teach patients and families to recognize and respond to hypoglycemia (<60 mg/dL; more
frequent in preg); milk preferable to fruit juices; have glucagon on hand for severe/LOC
Maternal morbidity
o Pregnancy can exacerbate DM related complications and poorly controlled PG DM which has lead to
end-organ disease can affect obstetric outcomes
o rapid institution of strict glycemic control in women with diabetes during pregnancy has been
associated with acute progression of retinopathy (especially if HTN present)

Diabetic nephropathy ~ 510% of pregnancies; progression to ESRD reported when serum creatinine
levels exceeded 1.5 mg/dL or severe proteinuria (>3 g per 24 hrs)
o Preexisting diabetic nephropathy -> higher risk for obstetric complications 2/2 worsening renal fxn i.e.
hypertensive disorders, uteroplacental insufficiency, & iatrogenic preterm birth
o Establish baseline evaluation of renal function before conception and f/u regularly
o Chronic HTN ~5-10% pts w/ PG DM; ideally control before conception; discontinue ACE/ARB
o HTN especially + nephropathy -> increases risk of preeclampsia, uteroplacental insuff, and stillbirth
o Pre-existing symptomatic CAD may be potential contraindication to pregnancy 2/2 risk of MI and 2/2
pregnancy related hemodynamic changes
Perinatal Morbidity and Mortality
o Best when preconception glu control w/o maternal vascular dx
o Leading cause of mortality= congenital anomalies (6-12% of infants); other= spontaneous abortion;
HbA1c near 10% associated w/ fetal anomaly rate of 20-25% vs 2-3% nml
o Hyperglycemia during organogenesis has critical role in abnormalities vs hypoglycemia
o Complex cardiac defects, CNS anomalies (ie. anencephaly, spina bifida), skeletal malformations (ie.
sacral agenesis) are most common
o Fetal hyperglycemia can be seen w/ facilitated diffusion of glucose across the placenta-> stimulation
of the fetal pancreatic cells-> fetal hyperinsulinemia -> excessive fetal growth, particularly in
adipose tissue
Poor control: risk of intrauterine fetal death w/ weight > 4,000
g and
Disproportionate [fat] around shoulders & chest-> 2x dystocia
risk at vaginal delivery
o Neonatal consequences of poor control: profound hypoglycemia, a
higher rate of respiratory distress syndrome, polycythemia,
organomegaly, electrolyte disturbances, and hyperbilirubinemia
Obstetric Complications
o Spontaneous preterm labor more common (some 2/2 hydraminosis)
o Preeclampsia seen in 1520% of pregnancies complicated by T1 DM
w/o nephropathy & ~ 50% w/ nephropathy
o HTN + nephropathy doubles risk of fetal IU growth restriction
o Rate of primary c-section increased
L&D
o Early delivery can be indicated in pts w/ vasculopathy, nephropathy, poor glu control, or prior stillbirth;
consider cesarean if fetal weight >4,500g; induction not indicated for macrosomia
o W/ poor control, fetal lung maturity amnio before 39 weeks gestation; if admin steroids increase
insulin requirement over next 5 days
o Induction: control maternal glycemic w/ IV regular insulin->
titrate to hourly reading <110 mg/dL
o Avoid intrapartum maternal hyperglycemia as may prevent
fetal hyperglycemia and reduce subsequent neonatal
hypoglycemia
o Insulin requirements decrease post-delivery; half of
predelivery dose after regular diet started
DKA in 5-10%; fetal mortality 10-35%; RFs= new onset diabetes;
infections ie. influenza, UTI; poor pt compliance; insulin pump
failure; & treatment with -mimetic tocolytic meds and antenatal
corticosteroids
o Presentation: abdominal pain, nausea and vomiting, and
altered sensorium
o Labs: low arterial pH (<7.3), a low serum bicarbonate
level (<15 mEq/L), an elevated anion gap, and positive
serum ketones
o Strip: recurrent late decelerations (resolved w/ maternal
improvement)
o Treat: hydration, IV insulin, glucose and K replacement
o