Title: Hx
Author: Celestino Monzon Menchavez
Last saved by: mirkil
Company: Unknown Organization

Holy Cross Hospital Newborn Nursery Rotation
Topic #6
Infant of Diabetic Mother
 
Case
Baby boy E. is the 40-week product of a 33 y.o. G5P4A1 mother with gestational diabetes requiring insulin.  Maternal prenatal labs were negative.  The infant was delivered via NSVD, complicated by late decelerations, Apgars were 4/9. The infant weighed 8 lbs. 14 oz. (4040g).

At delivery, the infant appeared dusky with a fetal heart rate below 50 and a poor respiratory effort.  The infant was given 100% O2 x 1½  minutes with improvement. 

Physical Exam:
T:  99.3
RR: 56
HR: 148
Weight: 4040g (>90 %ile)		
Length: 53.4 cm (>90%ile)		
HC: 36.2 cm (>90%ile)
Physical exam was significant for facial and chest petechiae and bruising, molding and caput of the head, crepitus of the right clavicle and a right subconjunctival hemorrhage.  The remainder of the exam was within normal limits. 

Assessment:
•	Term male infant
•	Large for gestational age
•	Infant of a diabetic mother
•	Fracture right clavicle

Discussion:
The frequently occurring problems of IDMs result from the exaggerated provision of maternal metabolic fuels to the fetus resulting in pancreatic B-cell hypertrophy and fetal hyperinsulinemia. Macrosomia is a well-known characteristic of IDM in which the infant tends to have an excess of fatty tissue with weights above 4000g.  Since insulin does not influence head size, they develop asymmetric macrosomia and are at an increased risk for shoulder dystocia resulting in birth trauma.  Cesarean deliveries are also more frequent because the infants are large for gestational age.  Even with excellent glycemic control maintained throughout pregnancy, approximately 20% to 30% of IDMs are born with excessive weight and size.  

About 75% of IDMS and 25% of infants of mothers with gestational diabetes develop hypoglycemia.  Hypoglycemia results from fetal hyperinsulinemia and usually manifests within the first 2-6 hours of life.  Infants can appear jittery, tachypneic, and diaphoretic with unstable vital signs.   Infants should be evaluated with rapid blood glucose checks confirmed by the laboratory. Blood glucose levels less than 35mg/dL are an indication for early feeding of the infant with a blood glucose level of at least 45mg/dL as a therapeutic goal. When necessary, IV or NG therapy can be instituted to maintain normal serum glucose levels but treatment may take anywhere from several hours to several days.

Other metabolic abnormalities can also develop; hypocalcemia and hypomagnesemia are seen in up to 40% to 50% of IDMs.  The cause of hypomagnesemia and hypocalcemia is not fully understood and may be a result of maternal losses related to the diabetes during pregnancy. Magnesium deficiency may cause a functional hypoparathyroidism that could result in neonatal hypocalcemia when the newborn is without maternal calcium.  In the pregnant mother with diabetes, hyperinsulinemia and hyperglycemia lead to reduced fetal arterial oxygen content, which stimulates erythropoiesis.  Neonatal polycythemia (venous hematocrit >65%) can develop and may be associated with cardiopulmonary failure, decreased renal function, renal vein thrombosis, and CNS damage.  Hyperbilirubinemia can also develop when RBC breakdown occurs. 

Maternal diabetes is also a predisposing factor for respiratory distress syndrome of the newborn.  Hyperglycemia and hyperinsulinemia are associated with a delay in pulmonary maturation by inhibiting enzymes needed for the phospholipid component of surfactant.  With improved glycemic control in the mother, the incidence of respiratory distress syndrome can approach levels similar to the general population.

The incidence of congenital anomalies is increased significantly in IDMs and has emerged as the single most common cause of perinatal mortality among these infants.  It is felt that poor glycemic control during the first trimester increases the likelihood for a defect in organogenesis to occur.  The most common defects are cardiac malformations (Hypertrophic cardiomyopathy, VSD, ASD, transposition of the great arteries, and coarctation of the aorta) and lumbosacral agenesis.  Additional anomalies include neural tube defects, hydronephrosis, renal agenesis, duodenal or anorectal atresia, and holoprosencephaly.  Abdominal distension may also develop with a transient delay in the development of the left colon leading to small left colon syndrome.

Key Points:
•	IDMs are at risk for hypoglycemia and macrosomia.
•	IDMs have an increased incidence of congenital anomalies including hypertrophic cardiomyopathy and microcolon.
•	Polycythemia/Hyperviscosity, hyperbilirubinemia and other metabolic abnormalities are seen in IDMs.
•	Early feeding is usually sufficient to treat hypoglycemia.  Occasionally, IV dextrose is needed for persistent or recurrent hypoglycemia.