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Infant of diabetic mother (IDM) 

 

• Women with diabetes mellitus during pregnancy (Type 1, Type 2, and gestational) are all at 

increased risk for adverse pregnancy outcomes.  

• Adequate glycemic control before and during pregnancy is crucial for improving outcome. 
• Most infants born to diabetic mothers are large for gestational age. 
•  If the diabetes is complicated by vascular disease, infants may have growth restriction, 

especially those born after 37 wk gestation.  

• The neonatal mortality rate is over 5 times that of infants of non diabetic mothers  
 
Problems of Infants of Diabetic Mothers 

Birth trauma 
Birth asphyxia 
Hypoglycemia 
Hypocalcemia 
Hypomagnesemia 
Hyperbilirubinemia 
Surfactant deficiency, related respiratory distress syndrome (hyaline membrane disease) 
Polycythemia 
Renal vein thrombosis 
Cardiac septal hypertrophy and cardiomyopathy 
Congenital malformations  

 
Diabetic mothers have a high incidence of; 

polyhydramnios  
preeclampsia 
pyelonephritis  
preterm labor   
chronic hypertension  
High fetal mortality rate at all gestational ages, especially after 32 wk  

 
Pathophysiology 
• Maternal hyperglycemia causes fetal hyperglycemia, and increased the fetal pancreatic 

response leads to fetal hyperinsulinemia;  

• Fetal hyperinsulinemia and hyperglycemia cause increased hepatic glucose uptake and 

glycogen synthesis, accelerated lipogenesis, and protein synthesis . 

• Related pathologic findings are hyperplasia of the pancreatic β islet cells, increased weight of 

the placenta and infant organs, myocardial hypertrophy, except for the brain.  

• Hyperinsulinism and hyperglycemia produce fetal acidosis, which may result in an increased 

rate of stillbirth.  

• Separation of the placenta at birth suddenly interrupts glucose infusion into the neonate 

without a proportional effect on the hyperinsulinism, and hypoglycemia and poor lipolysis 
develop during the 1

st

 hr after birth. 

 
CLINICAL MANIFESTATIONS 
• Infants tend to be large and plump as a result of increased body fat and big viscera.  
• They have puffy, plethoric facies.   
• These infants if delivered before term or the mother had associated vascular disease, then may 

have normal or low birth-weight. 

 


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Hypoglycemia 
• Develops in 25–50% of infants of diabetic mothers  
• Occurs in 15–25% of infants of gestational diabetes mothers, and only small percentage of 

these infants become symptomatic.  

• The nadir in an infant's blood glucose concentration is usually reached between 1 - 3 hr after 

birth; and spontaneous recovery may begin by 4–6 hr after birth.  

• The infants tend to be jumpy, tremulous, and hyper-excitable during the 1

st

 3 days of life, 

although hypotonia, lethargy, and poor sucking may also occur.  


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Tachypnea
 
• Develops in many infants of diabetic mothers during the 1

st

 2 days of life.  

• Infants of diabetic mothers have a higher incidence of respiratory distress syndrome may be 

related to the antagonistic effect of insulin on stimulation of surfactant synthesis by cortisol. 

 
Cardiomegaly
 
• Cardiomegaly is common in 30% of IDM 
• Heart failure occurs in 5–10% of infants of diabetic mothers.  
• Congenital heart disease is more common in infants of diabetic mothers. 
• Asymmetric septal hypertrophy may occur, and inotropic agents worsen the obstruction and so 

are contraindicated.  

 

 

 
Birth trauma is also a common sequel of fetal macrosomia. 
Neurologic development and ossification centers tend to be immature and correlate with 
brain size (which is not increased) and gestational age rather than total body weight.   
Hyperbilirubinemiapolycythemia, and renal vein thrombosis; are increased, and the 
incidence of the latter should be suspected in infants with a flank mass, hematuria, and 
thrombocytopenia. 
 
Congenital anomalies
 
• The incidence  is 3X in infants of diabetic mothers;  
• cardiac malformations (VSD, ASD, TGA, coarctation of the aorta, others)  
• lumbosacral agenesis are most common.  
• neural tube defects 
• hydronephrosis, other renal  anomalies.  

 
 


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TREATMENT:
 

 Prenatal evaluation of all pregnant women with overt or gestational diabetes, and planning the 

delivery in hospitals where expert obstetric and pediatric care is available.  

 Preconception glucose control reduces the risk of anomalies and other adverse outcomes, and 

glucose control during labor reduces the incidence of neonatal hypoglycemia.  

 Regardless of size, all infants of diabetic mothers should initially receive intensive care.  

 Hypoglycemia is defined; plasma glucose of 30 to 45 mg/dl (25 to 40 mg/dl in whole blood) in 

term infants. 

  The best treatment of mild, transient neonatal hypoglycemia is early feeding, whether the 

neonate is an IDM or not. 

 A plasma or blood  glucose level of less than 20 or 25 mg/dl, respectively, requires 

intravenous glucose administration unless the infant readily takes a good feeding and remains 
normoglycemic.  

 Asymptomatic infants should have a blood glucose determination within 1 hr of birth and then 

every hour for the next 6–8 hr;  

 If clinically well and normoglycemic, oral or gavage feeding with breast milk or formula 

should be started as soon as possible and continued at 3 hr intervals. If any question arises 
about an infant's ability to tolerate oral feeding, the feeding should be discontinued and 
glucose is given by peripheral intravenous infusion at a rate of 4–8 mg/kg/min.  

 Hypoglycemia should be treated, even in asymptomatic infants, by frequent feeding and/or 

intravenous infusion of glucose. 

 Bolus injections of hypertonic glucose should be avoided because they may cause further 

hyperinsulinemia and potentially produce rebound hypoglycemia  

 
 
 
 
 
 
 
 
 
 
 


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HYPOCALCEMIA 
• Calcium concentration in the immediate newborn period decreases in all newborn infants. 
• Hypocalcemia is usually defined as a total serum concentration less than 7 mg/dl.    
 
Clinical Findings 
• Hypocalcemic tetany; includes a high-pitched cry, jitteriness, tremulousness, and seizures.  
• Apnea, muscle twitching, laryngospasm.  

The next 2 signs are rare in the immediate newborn period. 

• Chvostek sign :facial muscle spasm when the side of the face (over the 7

th

 nerve) is tapped. 

• Trousseau sign :carpopedal spasm induced by partial inflation of a blood pressure cuff  
 
Hypocalcemia tends to occur at two different times in the neonatal period:  
Early-onset hypocalcaemia; occurs in the first 2 days of life and is associated with 

prematurity, maternal diabetes, asphyxia, and, rarely maternal hypoparathyroidism.  

Late-onset hypocalcemia; occurs at approximately 7–10 days and is observed in;  

•  Infants receiving modified cow's milk rather than infant formula (high phosphorus intake).  
•  In infants with hypoparathyroidism 
•  In infants with hypomagnesemia. 
•  Mothers with vitamin D deficiency  .  

 
Treatment 
A. oral calcium therapy:  
• The oral administration of calcium salts is a preferred method of treatment for chronic forms 

of hypocalcemia resulting from hypoparathyroidism but is rarely used in early-onset 
hypocalcemia.  

• Calcium in the form of calcium gluconate can be given as a diluted solution or added to 

formula feedings several times a day.  

•  If a 10% solution of calcium gluconate is used, the dose is 5–10 ml/kg/day given orally in 

divided doses, every 4 - 6 hours.  

 B. intravenous calcium therapy: 
• Intravenous calcium therapy given in symptomatic hypocalcemia  
• The infusion must be given slowly so that there is no sudden increase in calcium concentration 

of blood entering the right atrium, which could cause severe bradycardia and even cardiac 
arrest.  
 
Hypomagnesaemia
  
•  Hypomagnesemia occurs when serum magnesium levels fall below 1.5 mg/dl 

(0.62 mmol/l).  

•  It occurs during exchange transfusion with citrated blood, which is low in magnesium 

because of binding by citrate, approximately 10 days are required for return to normal.  

•  Hypomagnesemia should also be suspected in any patient with tetany not responding 

to calcium therapy. 

•  Immediate treatment consists of intramuscular injection of magnesium sulfate. For newborn 

infants, 25-50 mg/kg/dose every 8 hr for 3-4 doses usually suffices.  

 
 
 
 
 
 
 


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