Infant of diabetic mother
PATHOPHYSIOLOGY
maternal hyperglycemia → fetal hyperglycemia→
fetal hyperinsulinemia.
→↑
hepatic glucose uptake &glycogen synthesis,
accelerated lipogenesis
augmented protein synthesis.
-hypertrophy and hyperplasia of the pancreatic islet β cells.
-increased weight of the placenta and infant organs except brain.
-myocardial hypertrophy.
-extramedullary hematopoiesis.
-fetal acidosis, increased rate of stillbirth.
Interruption of glucose infusion + diminished epinephrine and glucagon
responses→ hypoglycemia.
Congenital anomalies correlate with poor metabolic
control& hyperglycemia during the periconception &
organogenesis periods.
Chronic fetal hypoxia(elevated amniotic fluid erythropoietin
levels)is associated with increased fetal and neonatal
morbidity
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CLINICAL MANIFESTATIONS
-large , plump ( increased body fat and enlarged viscera).
-puffy, plethoric facies (corticosteroids )
-normal or low birthweight.
-Hypoglycemia. between 1 and 3 hr; spontaneous recovery
may begin by 4–6 hr.
jumpy, tremulous, and hyperexcitable during the 1st 3 days
of life, hypotonia, lethargy, and poor sucking, tachypnea
hypothermia, transient tachypnea, cerebral edema RDS
Hypocalcaemia, Hypomagnesaemia, Perinatal asphyxia.
hyperbilirubinemia , polycythemia.
Cardiomegaly , heart failure.
Asymmetric septal hypertrophy .
Congenital heart disease .
Birth trauma
renal vein thrombosis;( flank mass, hematuria, and thrombocytopenia The
incidence of congenital anomalies is increased threefold in IDM
cardiac malformations and lumbosacral agenesis are most common.
neural tube defects, hydronephrosis, renal agenesis and dysplasia, duodenal
atresia, and holoprosencephaly.
the small left colon syndrome.
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prognosis
-incidence of diabetes mellitus in infants of diabetic mothers is increased.
-oversized infants may be predisposed to childhood obesity
-impaired intellectual development
TREATMENT
.
-prenatal evaluation of all pregnant with overt or gestational diabetes.
-planning the delivery of these infants in hospitals.
-Periconception glucose control & during labor.
Asymptomatic infants
-blood glucose determination within 1 hr of birth and then every hour for
the next 6–8 hr.
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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Hypoglycemia
prematurity, hypothermia, hypoxia, maternal diabetes, maternal glucose
infusion in labor, and intrauterine growth restriction (IUGR).
Serum glucose levels decline after birth until 1–3 hr of age, when levels
spontaneously increase in normal infants. In healthy term infants, serum
glucose values are rarely <35 mg/dL between 1 and 3 hr of life, <40 mg/dL
from 3 to 24 hr, and <45 mg/dL (2.5 mmol/L) after 24 hr.
CLINICAL MANIFESTATIONS
jitteriness or tremors, apathy. limpness or lethargy
episodes of cyanosis, convulsions,
intermittent apneic spells, difficulty feeding.
tachypnea, weak or high-pitched cry.
eye rolling. Episodes of sweating,
sudden pallor, hypothermia.
cardiac arrest and failure.
TREATMENT
.
-symptoms other than seizures :
intravenous bolus of (2 mL/kg) of 10% glucose.
-convulsions, 4 mL/kg,10% glucose bolus injection.
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Followed by glucose infusion at 8 mg/kg/min.
If hypoglycemia recurs, the infusion rate and concentration increased until
15–20% glucose.
-diazoxide 15mg/kg.
-octreotide .
-subtotal pancreatectomy.
S.glucose level measured every 2 hr after initiating therapy until several
determinations are above 40 mg/dL, then every 4–6 hr and the treatment
gradually reduced and finally discontinued( 24–48 hr). few days to a week.
risk for hypoglycemia :
•
serum glucose measured within 1 hr of birth, every 1–2 hr for the
1st 6–8 hr, and then every 4–6 hr until 24 hr of life.
•
Normoglycemic should receive oral or gavage feeding with human
milk or formula started at 1–3 hr of age and continued at 2–3 hr
intervals for 24–48 hr.
•
IV infusion of glucose at 4 mg/kg/min if oral feedings are poorly
tolerated.
PROGNOSIS
good in asymptomatic patients with hypoglycemia of short duration.
prolonged, recurrent, and severe symptomatic hypoglycemia is associated
with neurologic sequelae.
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Hypocalcemia
.
S ca <7 mg/dl
Early onset hypocalcemia<3days.
Preterm, IDM, perinatal asphexia, IUGR, maternal anticonvulsive.
Late onset >3days.
Mg, ↑ ph, hypoparathyroid, vit D def. malabsorption, renal failure
Treatment
Symptomatic:
2ml/kg ca gluconate diluted 1:1 N/S or GW
10-15 min, cardiac monitor .
Maintenance 4-6ml/kg/24 hr every 6hr.
For 72 hr
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