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Newborn Nursery Curriculum
Julee Waldrop, MS,PNP
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Diabetes in Pregnancy Diabetes in pregnancy 4%
Pre-gestational diabetes 12%
Gestational diabetes 88%
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Classification of Severity Whites Classification for diabetes
A Abnormal GTT treated with diet
A1 Medication controlled GDMA2 Insulin-treated GDM
B Onset at age >/=20 and duration of < 10 yr
C Onset at 10-19 years or duration > 10-19 years
D Onset before 10 yrs, duration > 20 yrs, somemacrovascular to microvascular disease
R-T Various complications have already occurred
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Pathophysiology Reduced insulin activity in the mom leads to a
hyperglycemic environment for the baby
In the first trimester this can cause embryopathy(birth defects and spontaneous abortions)
Highest risk are women with type 1 DM
In the 2nd & 3rdtrimesters can cause fetopathy
Macrosomia
Neonatal hypoglycemia
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Pathophysiology Intermittent maternal hyperglycemia leads to to
premature maturation of fetal pancreatic isletsand hypertrophy of the beta cells which producemore insulin causing hyperinsulinemia.
Hyperinsulinemia stimulates storage of glycogenin the liver, increased activity of hepatic enzymesin lipid synthesis and accumulation of fat inadipose tissue.
All this leads to increased fetal growth especiallyin insulin sensitive tissues, muscle and fat.
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Pathophysiology These increased metabolic needs require more O2
and leads to relative hypoxemia in the fetus
It also promotes catecholamine production which canlead to HTN and cardiac hypertrophy which may beinvolved in the 20-30% rate of stillbirth seen in poor
control
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Congenital Anomalies Type 1 DM RR was ~8 times greater
Account for about 50% of the perinatal deaths
Systems most frequently affected: CV and CNSAnencephaly and Spina bifida- 13-20 x more likely
DM during pregnancy accounts for most ofinfants born with caudal regression syndrome
(defects of the caudal region of the spinal cord) 200 x more likely
Spinal cord injury results in significant sequelae likeincontinence to paraplegia
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Prematurity Related consequences
Perinatal aspyxia can be related to many things Examples:
Maternal vascular compromise
Macrosomia
Prematurity
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Macrosomia Increased growth occurs after the 24th week of
pregnancy. There is a linear relationship between elevated blood
glucose and birth weight. Disproportionate growth
Excessive fat in the abdomen and scapular areas.
Increased risk for: Hyperbilirubinemia
Hypoglycemia
Acidosis
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Complications of Macrosomia Birth injury
Shoulder dystocia (1/3rd of infants > 4000gms)
1.7 times more likely to occur Brachial plexus injury
Clavicular or humoral fracture
Perinatal asphyxis
Facial palsy cephalohematomas
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IUGR If hypertension is significant enough with
vasculopathy then growth restriction may occur
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Respiratory Distress More common in IDMs when delivered prematurely
Delayed maturation of surfactant synthesis caused byhyperinsulinemia
TTNB 2-3 x more likely
Decreased fluid clearance in diabetic fetal lung
Cesarean delivery
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Metabolic Disorders Hypoglycemia
Definition: BGL < 40 mg/dL
Incidence: 14-21% Most common in macrosomic infants
Can also occur in IUGR
Persistent hyperinsulinemia in the newborn
Depressed counter response to hypoglycemia Glucagon
catecholamines
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Metabolic Disorders Hypocalcemia
Infrequent in term infants
Routine evaluation not recommended but maycontribute to persistent hypoglycemia
Hypomagnesemia
Infrequent in term infants
If hypocalcemia occurs is more likely
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Polycythemia Definition: HCT > 65%
Incidence: 13-33%
Fetal hypoxemia stimulates synthesis of erythropoietinwhich leads to polycythemia
Puts infants at risk for renal vein thrombosis (morecommon in IDMs)
Recommend measurement within 12 hours of birth
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Hyperbilirubinemia Incidence: 11-29%
Risk factors
Prematurity Polycythemia
Macrosomia
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Cardiomyopathy Hypertrophic cardiomyopathy
30-50% of IDMs
Increased thickening of the interventricular septum Hyperinsulinemia leads to increased deposition of
fat in myocardial cells
Symptomatic in only 15-20%
Resolves on its own as insulin levels decrease
Echo normalizes in 6-12 months