1. Outline Case presentation Discussion
Screening and Management of neonatal glucose hemostasis
Neonatal effect of infant of a diabetic mother (IDM)

2. Patient profile Name:許O敏之子 Chart number: 1775xxxx Age: 1 d/o
Gender: male
Admission date: 105/8/25

3. Chief complaint
Short of breath soon after delivery

4. Present illness 1-day-old boy infant
Born to a 38 year-old mother, G2P2, GA 38+4 weeks, NSD
Mother had DM type II (baseline sugar 130 mg/dL), HTN before pregnancy, with medication controlled
Prenatal was uneventful
Level II ultrasound showed no congenital anomaly
Did not have amniocentesis test
Perinatal
Apgar 7-9
SpO2 82%
Suction: medium amount

5. Physical examination T/P/R: 36.2/162/40 BP: 79/41 (54) O2: room air
Abundant lanugo (forehead)
T/P/R: 36.2/162/40
BP: 79/41 (54)
O2: room air
SpO2: %
BH: 51.2cm(75-90%)
BW: 3760gm (>90 %)
Ponderal index 2.8
(50-90%)
Chest:
Symmetrical expansion
Bilateral diffused crackles breathing sounds
Suprasternal/ subcostal retraction
Negative findings:
No tremor/ jitteriness/seizure/apnea/cyanosis
No irritable/ high peach crying
No shoulder dystocia/ neurological defect
No specific heart murmur
No hepatosplenomegaly
Large for gestational age

6. Apgar 7-9 T/P/R: 32.6/162/40 BP: 79/41 (54) O2: room air SpO2:88-100 %
BH: 51.2cm(75-90%)
BW: 3760gm (>90 %)
Ponderal index 2.8
Chest:
Symmetrical expansion
Bilateral diffused crackles breathi
Suprasternal/ subcostal retraction
Abundant lanugo (forhead)

7. Lab (8/25 10:30) Peripheral artery Micro gas Micro dextrose 33mg/dl
CK (4-8 HR)
CK isoenzymes (MB)
WBC
Hct 腳跟 70 周邊65 實驗室 55 (coulter counter)
Hct 60.4%(8/26)→58.7%(8/27) micro K 5.34, micro Ca 0.991

8.  CXR: patch in right lower lung
-->TTNB

9. Impression and plan LGA Infant with diabetic mother
 Hypoglycemia & Polycythemia
Closely monitor sugar and hematocrit level
Sufficient IV hydration and nutrition support
Monitor breathing pattern
Further check electrolyte, esp. Ca, Mg
Dyspnea, r/o Pneumonitis, r/o TTNB
On NPO with fluid support
Blood work including CBC/DC, CRP, B/C
Empirical antibiotics with
ampicillin and gentamycin
Closely monitor vital signs

10. GIR 5.54 mg/kg/min check dex Q4H-Q6H check dex Q8H-QD
After delivery 10:30
D10W
12.5 ml/hr
(80 ml/kg/day)
10:30 (report at 14:05)
Sugar(random) 9 mg/dl
11:15
Micro dextrose 33mg/dl
11:15
D10W 7.4ml IVP in 3min
GIR 5.54 mg/kg/min
11:45
Micro dextrose 57 mg/dl
This calculation is a simple conversion of units (into mg/kg/min):
GIR = [IV Rate (mL/hr) * Dextrose Conc (g/dL) * 1000 (mg/g)] / [Weight (kg) * 60 (min/hr) * 100 (mL/dL) ]
where the dextrose concentration is expressed as a whole number, e.g. 5 or 10.
A GIR of 5-8 mg/kg/min is typical.
Infants who are not feeding should not be allowed a rate less than 5 mg/kg/min for any significant period of time. The GIR needed to optimize nutrition in neonates is 14 mg/kg/min.
check dex Q4H-Q6H
19: mg/dl
23: mg/dl
check dex Q8H-QD

11. 14:00 micro Hct: 69% 16:00 micro Hct: 67% 20:00 65% 23:25 58% D10W
12.5 ml/hr
(80 ml/kg/day)
After delivery
Artery Hct : 58%
(10:30 sample)
(13:40 report)
14:00
micro Hct: 69%
D10W
15.7 ml/hr
(100 ml/kg/day)
16:00
micro Hct: 67%
Q4H check Hct
20:00 65%
23:25 58%

13. Calcium level since day 2
8/26
Micro K
5.18 mg/dl ( )
Micro Ca
1.00 mg/dl ( )
8/27
Micro K
5.34 mg/dl
Micro Ca
1.00mg/dl
8/28
Micro Ca
1.057 mg/dl

15. Hospital course
Glucose level and Hematocrit level was within normal value after management
No further complication was noted
The patient was discharged on 8/30

16. Discussion
Screening and Management of
neonatal glucose hemostasis

23. Discussion
The neonatal effect of Infant of a diabetic mother

24. INTRODUCTION
Diabetes in pregnancy is associated with an increased risk of fetal, neonatal, and long-term complications in the offspring
The outcome is generally related to the onset and duration of glucose intolerance during pregnancy and severity of the mother's diabetes

25. NEONATAL EFFECTS
IDMs are at increased risk for mortality and morbidity compared with neonates born to a nondiabetic mother

26. NEONATAL EFFECTS Overview
Neonatal complications in offspring of diabetic mothers include:
Congenital anomalies
Prematurity
Perinatal asphyxia
Macrosomia
Metabolic complications
(hypoglycemia and hypocalcemia)
Low iron stores
Hyperbilirubinemia
Cardiomyopathy
Respiratory distress
Hematologic complications
(polycythemia and hyperviscosity)

27. NEONATAL EFFECTS Congenital anomalies
IDMs are at significant risk for major congenital anomalies due to maternal hyperglycemia at the time of conception and during early gestation
Congenital malformations account for half of the perinatal deaths in IDMs
In a study of 13,030 infants with congenital anomalies and 4895 without birth defects, when compared with a reference group of nondiabetic control mothers, the risk of isolated and multiple congenital anomalies was highest in infants of mothers with pregestational diabetes followed by infants born to mothers with gestational diabetes
Congenital malformations account for half of the perinatal deaths in IDMs
 The Risk can be reduced by strict glycemic control during the pre- and periconceptual (first eight weeks of pregnancy) periods.

28. NEONATAL EFFECTS Congenital anomalies
2/3 of the anomalies in IDMs involve the cardiovascular system or central nervous system (CNS)
Cardiovascular malformations occur in 9 % of diabetic pregnancies  TGA, VSD, PDA, truncus arteriosus, and tricuspid atresia
Central nervous system occur in 5.3 % of diabetic pregnancies  Anencephaly and spinal bifida are 20 times more frequent among IDMs

29. NEONATAL EFFECTS Perinatal asphyxia
Fetal heart rate abnormalities during labor, low Apgar scores & intrauterine death
IDMs are at increased risk for intrauterine or perinatal asphyxia due to macrosomia (failure to progress and shoulder dystocia) and cardiomyopathy (fetal heart rate abnormalities)
Perinatal asphyxia defined here as fetal heart rate abnormalities during labor, low Apgar scores, and intrauterine death  
IDMs are at increased risk for intrauterine or perinatal asphyxia due to macrosomia (failure to progress and shoulder dystocia) and cardiomyopathy (fetal heart rate abnormalities)
In a study of 162 IDMs, for example, 27 percent had perinatal asphyxia. Perinatal asphyxia correlated with hyperglycemia in labor, prematurity, and nephropathy. Maternal vascular disease, manifested by nephropathy, may contribute to the development of fetal hypoxia and subsequent perinatal asphyxia

30. NEONATAL EFFECTS Macrosomia
BBW > 90th percentile or BBW above 4000 gm
A common complication in IDMs
The incidence is greater in infants born to mothers with pregestational diabetes
IDMs with macrosomia are more likely than those who are not macrosomic to have hyperbilirubinemia, hypoglycemia, acidosis, respiratory distress, shoulder dystocia, and brachial plexus injury
In a population-based study using the Swedish Medical Birth Registry (MBR) of 3705 infants born to mothers with type 1 diabetes between 1998 and 2007, 47 percent of the infants were LGA, defined as BW greater than 90th percentile.
In another Swedish study based on all births from the Swedish MBR from 1998 to 2007, infants born to mothers with gestational diabetes were 2.5 times more likely to be LGA than infants born to nondiabetic mothers (26 versus 11 percent)

31. NEONATAL EFFECTS Respiratory distress syndrome
RDS due to surfactant deficiency occurs more frequently in IDMs:
IDMs are more likely to be delivered prematurely
Neonatal hyperinsulinemia interferes with the induction of lung maturation by glucocorticoids
RDS due to surfactant deficiency occurs more frequently in IDMs for the following two reasons:
IDMs are more likely to be delivered prematurely than infants born to nondiabetic mothers.
At a given gestational age, IDMs are more likely to develop RDS because maternal hyperglycemia appears to delay surfactant synthesis. The proposed underlying mechanism is neonatal hyperinsulinemia, which interferes with the induction of lung maturation by glucocorticoids. The risk of RDS in preterm infants of mothers whose diabetes is well-controlled approaches that of infants born to nondiabetic mothers at a similar gestational age.
The clinical manifestations, diagnosis, prevention, and management of RDS are discussed separately

32. NEONATAL EFFECTS Other causes of respiratory distress
Transient tachypnea of the newborn (TTNB) & Cardiomyopathy
TTNB occurs 3 times in IDMs than in normal infants
Reduced fluid clearance in the diabetic fetal lung
In infants born to mothers with GDM, the risk for respiratory distress increases for those with BBW >4000 g
Transient tachypnea of the newborn (TTNB) and cardiomyopathy.
TTN occurs two to three times more commonly in IDMs than in normal infants. The mechanism may be related to reduced fluid clearance in the diabetic fetal lung. Cesarean delivery, which is more frequently performed in diabetic versus nondiabetic pregnancies, may be a contributing factor
In infants born to mothers with gestational diabetes mellitus (GDM), the risk for respiratory distress increases for those with BW >4000 g

33. NEONATAL EFFECTS Hypoglycemia
Blood glucose levels below 40 mg/dL in the first 24 hours
Occurs frequently in IDMs (27 %)
likely caused by persistent hyperinsulinemia in the newborn after interruption of the intrauterine glucose supply from the mother
The onset typically occurs within the first few hours after birth
The hyperinsulinemic state typically lasts days
Blood glucose levels below 40 mg/dL in the first 24 hours, occurs frequently in IDMs (27 %)
The onset of hypoglycemia typically occurs within the first few hours after birth. Thus, IDMs require close blood glucose monitoring after delivery and frequently need glucose supplementation, including parental glucose infusion. In our experience, the hyperinsulinemic state typically lasts two to four days. In neonates requiring glucose supplementation, the maintenance of normal plasma glucose levels while supplemental glucose is being weaned is evidence of resolving hyperinsulinism. Further testing should be undertaken to define the cause of persistent hypoglycemia in infants who continue to require glucose infusions at rates exceeding 8 to 10 mg/kg per minute to maintain normal plasma glucose levels beyond the first week of life.

34. NEONATAL EFFECTS Hypoglycemia
Macrosomic IDMs are more likely to develop hyperinsulinemia and hypoglycemia
Further testing should be undertaken to define the cause of persistent hypoglycemia in infants who continue to require GIR > 8 mg/kg/min to maintain normal glucose levels in the first week
Strict glycemic control during pregnancy decreases, but does not abolish, the risk of neonatal hypoglycemia

35. NEONATAL EFFECTS Hypocalcemia
Total serum Ca < 7 mg/dL (1.8 mmol/L) or
An ionized Ca < 4 mg/dL (1 mmol/L) or
An ionized Ca < 3.2 mg/dL (0.8 mmol/L) in ELBW infant
At least 5 percent of IDMs

36. NEONATAL EFFECTS Hypocalcemia
The lowest serum Ca concentration occurs between 24 & 72 hours after birth
Hypocalcemia in term IDMs usually is asymptomatic and resolves without treatment  Routine screening is not recommended
Should be measured in infants with jitteriness, lethargy, apnea, tachypnea, or seizures, and in those with prematurity, asphyxia, respiratory distress, or suspected infection

37. NEONATAL EFFECTS Polycythemia
Central venous Hct > 65 percent
Pathogenesis :
Chronic fetal hypoxemia Increased erythropoietin concentrations
More likely in IDMs
Higher Hb and Hct values are associated with fetal exposure to oxidative stress

38. NEONATAL EFFECTS Polycythemia and hyperviscosity syndrome
Polycythemia may lead to hyperviscosity syndrome, including vascular sludging, ischemia, and infarction of vital organs
To detect polycythemia, the Hct should be measured within 12 hours of birth

39. NEONATAL EFFECTS Cardiomyopathy
IDMs are at increased risk for transient hypertrophic cardiomyopathy
The most prominent change is thickening of the interventricular septum with reduction in the size of the ventricular chambers, resulting in obstructed left ventricular outflow

40. NEONATAL EFFECTS Cardiomyopathy
Infants often are asymptomatic
10 % have respiratory distress or signs of poor cardiac output or heart failure
Cardiomyopathy is transient and resolves as plasma insulin concentrations normalize
Symptomatic infants typically recover after 3 weeks of supportive care, and echocardiographic findings resolve within 6 to 12 months
Supportive care includes increased IV fluid administration and propranolol
Inotropic agents are contraindicated because they may decrease ventricular size and further obstruct cardiac outflow.