Infant of a Diabetic
Mother (IDM)
Description
▪ May be SGA or LGA, with or without congenital anomalies
and with or without birth injury.
Aetiology
▪ IDM is caused by chronic hyperglycaemia in the mother
(e.g., gestational diabetes mellitus or long-term diabetes
mellitus with or without vascular changes).
Pathophysiology
1. Hyperglycaemia in the mother without vascular changes
causes large amounts of amino acids, free fatty acids, and
glucose to be transferred to the foetus, but maternal insulin
does not cross the placenta.
▪ The fetal response to these transferred substances
includes:
2.
▪ Islet cells of the pancreas enlarge (hypertrophy).
▪ Hypertrophic cells produce large volumes of insulin,
which acts as a growth hormone, and protein
synthesis accelerates.
▪ Fat and glycogen are deposited in fetal tissue, and the
foetus grows large (macrosomia), especially if
maternal blood glucose levels are not well controlled
in the third trimester.
, ▪ Various unknown factors also may contribute to
changes.
2. In maternal long-term diabetes with vascular changes, the
new born may be SGA because of compromised placental
blood flow, maternal hypertension, or pregnancy-induced
hypertension, which restricts uteroplacental blood flow.
3. Associated complications in IDM include:
▪ Fractures and nerve damage may occur from birth
trauma if the infant is LGA.
▪ Congenital anomalies (e.g., heart, kidney, vertebral, and
CNS) are three to five times more common, with
incidence decreasing if maternal blood glucose levels
remain controlled and normal during the first trimester.
▪ Risk for respiratory distress syndrome increases (high
insulin levels interfere with production of pulmonary
surfactant).
▪ Hypoglycaemia may result after birth from lack of
glucose from the mother, but continued production of
insulin by the new born.
▪ Hypocalcaemia may result from decreased parathyroid
hormone production.
▪ Polycythaemia (i.e., haematocrit exceeding 65%) may
result from placental insufficiency causing chronic fetal
hypoxia and increased fetal erythropoietin production.
▪ Organ damage may result from decreased blood flow
and renal vein thrombosis.
▪ Hyperbilirubinemia may result from breakdown of
excess RBCs after birth.
Assessment Findings
1. Clinical manifestations
▪ Congenital anomalies are more likely in IDMs who are SGA
than in other SGA new-borns.
▪ Size differences and variations are more common in IDMs
who are LGA than in other LGA new-borns.
Mother (IDM)
Description
▪ May be SGA or LGA, with or without congenital anomalies
and with or without birth injury.
Aetiology
▪ IDM is caused by chronic hyperglycaemia in the mother
(e.g., gestational diabetes mellitus or long-term diabetes
mellitus with or without vascular changes).
Pathophysiology
1. Hyperglycaemia in the mother without vascular changes
causes large amounts of amino acids, free fatty acids, and
glucose to be transferred to the foetus, but maternal insulin
does not cross the placenta.
▪ The fetal response to these transferred substances
includes:
2.
▪ Islet cells of the pancreas enlarge (hypertrophy).
▪ Hypertrophic cells produce large volumes of insulin,
which acts as a growth hormone, and protein
synthesis accelerates.
▪ Fat and glycogen are deposited in fetal tissue, and the
foetus grows large (macrosomia), especially if
maternal blood glucose levels are not well controlled
in the third trimester.
, ▪ Various unknown factors also may contribute to
changes.
2. In maternal long-term diabetes with vascular changes, the
new born may be SGA because of compromised placental
blood flow, maternal hypertension, or pregnancy-induced
hypertension, which restricts uteroplacental blood flow.
3. Associated complications in IDM include:
▪ Fractures and nerve damage may occur from birth
trauma if the infant is LGA.
▪ Congenital anomalies (e.g., heart, kidney, vertebral, and
CNS) are three to five times more common, with
incidence decreasing if maternal blood glucose levels
remain controlled and normal during the first trimester.
▪ Risk for respiratory distress syndrome increases (high
insulin levels interfere with production of pulmonary
surfactant).
▪ Hypoglycaemia may result after birth from lack of
glucose from the mother, but continued production of
insulin by the new born.
▪ Hypocalcaemia may result from decreased parathyroid
hormone production.
▪ Polycythaemia (i.e., haematocrit exceeding 65%) may
result from placental insufficiency causing chronic fetal
hypoxia and increased fetal erythropoietin production.
▪ Organ damage may result from decreased blood flow
and renal vein thrombosis.
▪ Hyperbilirubinemia may result from breakdown of
excess RBCs after birth.
Assessment Findings
1. Clinical manifestations
▪ Congenital anomalies are more likely in IDMs who are SGA
than in other SGA new-borns.
▪ Size differences and variations are more common in IDMs
who are LGA than in other LGA new-borns.
