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© The Children’s Mercy Hospital, 2017
Lindsey Churchman, MSN, RN, NNP-BC
IDM: It’s not just about Sugar
Types of Diabetes
• Pregestational Diabetes:
• Type 1 or Type II Diabetes
– 1.8 percent prevalence
– Usually diagnosed if fasting
glucose ≥92 or random
glucose ≥200.
– Hgb A1C ≥6.5%
Gestational Diabetes:
• Diabetes first diagnosed during
pregnancy.
– 2-25% prevalence
Gestational Diabetes Classifications
• The White Classification system is used to differentiate between
gestational diabetes and diabetes that existed prior to pregnancy.
Gestational diabetes is class A with the following
subclassifications:
– A1GDM: diet controlled
– A2GDM: medication controlled- most common medications used to treat
mom’s are glyburide, metformin, and insulin
Who is at Risk:Gestational diabetes is more likely to occur in women who:
• Are >25 years of age
• Are overweight
• Have had a very large baby
• Have a close relative with diabetes
• Have had a stillbirth in a previous pregnancy
• Are African American, American Indian, Asian American, Hispanic,
Latina, or Pacific Islander
Screening For Gestational Diabetes
– All pregnant women should be screened for gestational diabetes using
history, clinical risk factors, and glucose screening tests
– Screening usually occurs some time between 24 and 28 weeks of
gestation
• 1 hour GTT
• 3 hour GTT
• Early screening is recommended in women with risk factors
Maternal and neonatal
Adverse Outcomes
Maternal
• Preeclampsia
• Macrosomia
• Birth trauma
• Increased need for C/S
• Stillbirth
• 10% chance of developing overt diabetes
immediately after pregnancy
• As high as 40% chance within 20 years
Neonatal
• Macrosomia
• Birth Trauma
• Fetal organomegaly(hepatomegaly, cardiomegaly)
• Increased perinatal mortality
• Respiratory distress syndrome
• Hypoglycemia
• Hyperbilirubinemia
• Hypocalcemia
• Polycythemia
• Congenital anomalies
• Increased risk of developing diabetes later in life
• Renal Vein Thrombosis
Neonatal Complications cont• Congenital Anomalies: Cardiac
• Heart defects are present in 3-9% of all
IDM’s
– Most common heart defects seen
are:
» Transposition of the Great
Vessels
» Double Outlet Right Ventricle
» VSD
» Truncus Arteriosus
» Tricuspid Atresia
» PDA
• Congenital Anomalies: CNS
– Anencephaly
– Spina Bifida
Other Congenital Anomalies
(less common)
– Flexion contracture of the limbs
– Vertebral anomalies
– Small left colon syndrome
– Caudal regression Syndrome
Case Study• 38 week infant born via C/S to a G1, P1 27 year old. Mother is obese, early
screening was positive for gestational diabetes. Initially given glyburide,
however insulin was added at 22 weeks gestation. All other serologies were
negative, including GBS.
• scheduled C/S for macrosomia, estimated fetal weight was 4.4kg.
• No complications with C/S, apgars 8,9. Birthweight was 4.6kg.
• Infant developed increased WOB shortly after delivery, oxygen saturations in
room air were in the mid 80’s. Infant brought to the NICU and placed in
head hood with 80% Fio2. Saturations improved to >95%.
macrosomia
• Definition: Infant with a
birthweight of >4kg, or
BW greater than the 90th
percentile on a
population appropriate
growth chart
macrosomia
• Can occur in all diabetic
pregnancies, but has a greater
incidence in pregestational diabetic
mothers
– One particular study using the
Swedish Medical Birth Registry
found that of the 3705 infants
born to mothers with type 1
diabetes between 1998-2007,
47% of the infant’s were LGA
macrosomia
• Associated with disproportionate
growth which results in increased fat
accumulation in the abdominal and
scapular regions of the body
• Increased risk for birth injury,
including brachial plexus injury,
clavicular or humeral fractures
• Increased risk for perinatal asphyxia
• Shoulder dystocia
What could be the cause of the Respiratory
distress and oxygen need?
• A. Respiratory Distress Syndrome
• B. C/S without labor
• C. Pulmonary Hypertension
• D. All of the above
Respiratory Distress in IDM’s
• Respiratory Distress Syndrome occurs more frequently in
IDM’s because:
– More likely to be delivered prematurely than infant’s born to nondiabetic mother
– Maternal hyperglycemia delays surfactant synthesis- proposed mechanism is
neonatal hyperinsulinemia is though to interfere with the induction of lung
maturation by glucocorticoids
– Other causes of respiratory distress in addition to RDS, include TTNB and
Cardiomypathy
Case Study Cont.
• Upon admission to NICU, CBC, ABG, and
glucose levels are drawn on the infant
• CBC: WBC 12, H&H are 23/70, platelet
count of 207k, normal diff
Which Value in the CBC is concerning?
• A. WBC of 12
• B. Platelet count of 207k
• C. H&H of 23/70
• D. Everything is fine….send the baby home!
Polycythemia
Neonatal polycythemia in a term infant is defined by a peripheral venous hemoglobin and hematocrit more than 2 standard deviations above the mean; this translates to a hemoglobin greater than 22 g/dl and a hematocrit greater than 65%.
*More likely to occur in IDMs than in infants born to nondiabetic mothers*
*Underlying pathogenesis is due to increased erythropoietin concentrations*
* Can lead to hyperviscosity syndrome, which may then contribute to the increase incidence of renal vein thrombosis seen in IDMs*
Treatment of polycythemia1. Treatment should be based on presence of clinical signs and symptoms, not
just on laboratory values alone
2. Peripheral hematocrits >65% should be confirmed with a central sample
3. Asymptomatic infants with Hct of 60-70% may be monitored closely with
adequate hydration and glucose levels
4. Some institutions choose to treat (partial exchange transfusion) infants
regardless of symptoms if repeated Hct levels are above 70% or in patients who
are symptomatic (ie cardiopulmonary or neurologic symptoms) with a Hct >65%.
Maternal Hyperglycemia
Fetal
Hyperglycemia
Fetal
Hyperinsulinemia
Fetal substrate
uptake increased
Decreased
lung surfactant
Resp Distress
Synrome
Macrosomia
Oxygen uptake
increases
Hypoxemia
?stillbirth
Erythropoietin
increased
Polycythemia
From Schwartz R, et al: Infant of
the diabetic mother, J. Pediatric
Endocrin. 5:197, 1992
Case Study Cont.
The infant is closely monitored over the next 24 hours and develops
delayed cap refill of 4-5seconds, decreased pulses in all extremities,
and becomes tachypneic.
Vital signs are otherwise normal, and repeat CBC continues to have
no shift.
What is the most likely cause of this
baby’s poor perfusion?• A. Septal Hypertrophy
• B. VSD
• C. Respiratory Distress Syndrome
• D. Hypoglycemia
Cardiomyopathy– Increased risk of transient cardiomyopathy thought to be caused by fetal hyperinsulinemia
increasing the synthesis and deposition of fat and glycogen in myocardial cells, ie septal hypertrophy
– Septal hypertrophy decreases size of ventricles, possibly obstructing outflow of the left ventricle
– Cardiac output is significantly reduced
– The severity of IDM cardiomyopathy can vary from an incidental finding on echocardiograph, to an infant with severe symptoms of congestive heart failure
– Diagnosis is made by echocardiography, chest radiograph may show cardiomegaly.
Treatment of Cardiomyopathy• Treatment for Cardiomyopathy from septal hypertrophy is supportive care
• Supportive care includes, IV fluid administration, oxygen support as needed,
diuretics as needed, and/or beta blockers.
• Digoxin and inotropes which are often used in heart failure associated with
structural heart defects, are contraindicated if hypertrophic cardiomyopathy
is present as they increase LVOT obstruction.
• Resolution of symptoms usually occurs within 2-4 weeks, and resolution of
septal hypertrophy occurs during the first 2-12 months of life.
Case Study Cont.• The baby is currently receiving D15W @ 70ml/kg/day. The baby has a BMP
drawn at 36 hours of age with the following results:
• Na 139
• K 3.5
• Cl 102
• CO2 20
• BUN 12
• Cr 0.8
• Ca 6.7
Which lab value is
worrisome?
Alterations in Calcium and magnesium homeostasis
• IDM’s demonstrate an exaggerated drop in circulating calcium
levels compared to infants of non-diabetic mothers
• Occurs in about 50% of infant’s born to insulin dependent
diabetic mothers
• Usually is most apparent at 24-72 hours of age, and is related to
the severity and duration of maternal diabetes
• Mechanism of hypocalcemia is most likely the failure of the IDM
to mount an appropriate parathyroid hormone response,
persistently high calcitonin, and possibly alterations in vitamin D
metabolism
• In most infant’s hypocalcemia and hypomagnesemia are
transient events that improve spontaneously, but serum levels
should be monitored in infant’s with jitteriness, lethargy, apnea,
tachypnea, or seizures.
Treatment of hypocalcemia
• Treatment for hypocalcemia is
administration of calcium salts
• Treatment may be given orally
after the initial correction has
been given and the infant can
tolerate oral solution
• Complications of IV calcium
therapy include extravasation
into soft tissues and bradycardia.
Long Term effects/Summary
• Morbidity and mortality lessen with adequate glucose control
during pregnancy, especially during the early part of gestation
when organogenesis is occurring
• May also negatively effect neurodevelopmental outcomes as well
• Long term outcome data suggest that exposure to hyperglycemia
increases the risk of postnatal metabolic complications, including
diabetes, increased BMI, and impaired glucose metabolism
Any
Questions??
References:• Fanaroff, A., Martin, R., & Walsh, M. (2011). Neonatal-Perinatal
Medicine: Diseases of the Fetus and Infant. St. Louis, MO:
Elsevier.
• Riskin, A., Garcia-Prats, J., Infant of a Diabetic Mother [PDF
document]. Retrieved from Online Web site:
http://www.uptodate.com
• Gardner, S., Carter, B., Hines, M., & Hernandez, J. (2016).
Neonatal Intensive Care. St. Louis, MO: Elsevier.