Diabetes in Pregnancy

Ryan Agema MS III

Diabetes in Pregnancy
Epidemiology
Classification
Pathophysiology
Morbidity

Fetal
Maternal

Diagnosis
Treatment and Management
References

Epidemiology

4-6% of pregnancies in the U.S are

complicated by DM, accounting for 50150 thousand babies per year.

88% GDM, 8% Type II DM, 4% Type 1 DM

Prevalence also varies by race

1.5-2% in Caucasians, 5-8% in Hispanic,

Asian and African Americans, and up to
15% in some SW Native American groups.

Classification

Pathophysiology

Normal pregnancy is
characterized by:

Mild fasting hypoglycemia

Postprandial hyperglycemia
Hyperinsulinemia

Due to peripheral insulin

resistance which ensures
an adequate supply of
glucose for the baby.

Pathophysiology

Human Placental Lactogen (HPL)

Produced by syncytiotrophoblasts of
placenta.
Acts to promote lipolysis increased FFA
and to decrease maternal glucose uptake
and gluconeogenesis. Anti-insulin

Estrogen and Progesterone

Interfere with insulin-glucose relationship.

Insulinase

Placental product that may play a minor

role.

A Vicious Cycle???

Fetal Morbidity

Miscarriages
Frequency directly related to degree of
maternal glycemic control.
Up to 44% with poorly controlled DM
(HbA1C >12).

Preterm Delivery

Increase in both spontaneous and

indicated preterm labor (<35 wks).

Fetal Morbidity

Birth Defects
1-2% risk among the general population.
4-8 fold increased risk among preexisting
diabetics.
Most common defects are CNS and CV,
but also an increase in renal and GI
abnormalities.
Up to a 600 fold increase in caudal
regression syndrome.

Fetal Morbidity

Macrosomia
Defined as birthweight above 90th % or
>4000 grams.
Occurs in 15-45% of diabetic
pregnancies, a 4-fold increase over
normal.
Carries many morbidities including birth
trauma, RDS, neonatal jaundice and
severe hypoglycemia.

Fetal Morbidity

Growth Restriction
Although we typically associate maternal
DM with macrosomia, growth restriction
is fairly common among Type 1 diabetic
mothers.
Best predictor is presence of maternal
vascular disease.

Fetal Morbidity

Fetal Morbidity

Polycythemia

Hyperglycemia stimulates fetal erythropoeitin

production.
Can lead to tissue ischemia and infarction.

Hypoglycemia

Think of as an overshoot mechanism.

Baby is used to having lots of maternal glucose so
it makes lots of insulin. When born, maternal
glucose is no longer available but insulin remains
high hypoglycemia.
Can lead to seizures, coma and brain damage.

Fetal Morbidity

Postnatal hyperbilirubinemia
Occurs in appox. 25%, double that of
normal.
Thought to be due in large part to
polycythemia.

Respiratory distress syndrome

5-6 fold increased frequency.
May be due to a delay in lung maturation
or simply due to the increased frequency
of preterm deliveries.

Fetal Morbidity

Polyhydramnios
Amniotic fluid volume >2000 mL.
Occurs in 10% of diabetics.
Increased risk of placental abruption and
preterm labor.

Maternal Morbidity
Increased risk of DKA due to
increasingly resistant DM.
Increased incidence of UTI due to
glucose-rich urine and urinary stasis.

Glucosuria is a normal finding of

pregnancy but may be much higher in
diabetics.

Diabetic retinopathy
Diabetic nephropathy

Maternal Morbidity
Diabetic neuropathy
Preeclampsia

2-fold increase

Diagnosis

Glucose Challenge Test (24-28 wks)

50 gram glucose load with blood level 1
hour later.
Does NOT require fasting state.
Normal finding is <140 mg/dl.
If >140, need to do a 3 hour glucose
tolerance test.

Diagnosis

Glucose Tolerance Test

Draw a fasting glucose level (normal<95).
Give 100 gram glucose load with glucose
levels drawn after 1, 2 and 3 hours.
Normal levels vary widely depending on
who you ask but should be in the
following ranges:

hr:<180 2 hr:<155 3 hr:<140

2 or more abnormal values = GDM.

Treatment and Management

Obviously the main goal is to

maintain good glycemic control.

Typically controlled with insulin but oral

hypoglycemic agents like glyburide are
also showing promise.

Treatment and Management

Obstetrical management

Serial US to trend fetal growth, AFI and fetal

anatomy
Fetal well-being monitored with kick counts,
NSTs, BPPs

Postpartum, 95% of GDM mothers return

to normal glucose tolerance, and require
no further insulin.

Glucose tolerance screen 2-4 mo. postpartum

to detect those that remain diabetic.

References
www.acog.org
Current Obstetric & Gynecologic
Diagnosis & Treatment (2003)
Williams Obstetrics (2005)