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Infants of diabetic mothers ( IDM)
1. INFANTS OF DIAETIC
MOTHERS
( I.D.M .).
By;
Mr. Manulal .V.S
Senior Lecturer
SP Fort College of Nursing
Thiruvananthapuram.
2. INFANTS OF DIAETIC MOTHERS
( I.D.M .).
• Diabetes is one of the common endocrine disorders
affecting pregnancy. Sometimes, the foetus may suddenly
die during the last trimester of pregnancy or macrosomia
and its attending risks during delivery such as birth trauma ,
asphyxia , and increased possibility of L.S.C.S.
• The newborn may have neonatal respiratory distress,
hypoglycemia, hypocalcemia, hyperbilirubinemia,
cardiopulmonary and persistent pulmonary hypertension,
polycythemia and increased viscocity of blood etc.
3. THE PEDERSON HYPOTHESIS.
• States that maternal hyperglycemia leads to foetal
hyperglycemia.
– Before 20 weeks of gestation , foetal islets cells are not capable
of response to insulin secretion. After 20 weeks of gestation the
foetus has a functioning pancrease responsible for for its own
glucose homeostasis , as maternal insulin does not cross the
placenta in appreciable amount.
– Unregulated hyperglycemia results in hypertrophy of foetal
pancreatic isletsand hyperinsulinemia.
– Foetal hyperglycemia, hyperinsulinemia or the combined effect
of the two.
4. PATHOPHYSIOLOGY OF I.D.M
Maternal hyperglycemia
Foetal hyperglycemia
Stimulation of foetal pancreatic beta cellsand
increased production of insullin by the foetus.
Insulin concentration of the foetus is elevated.
( insulin is an anabolic hormone and promotes
growth .) .
5. PATHOPHYSIOLOGY OF I.D.M
Mother’s insulin turn over is high during pregnancy
due to hormonal effects , leading to excess
maternal glucose and amino acids.
Increased synthesis of protein, lipids, and glucogen
in the foetus. ( most part of the foetal size is due
to the accumulation of fat .) .
The mechanism of hypoglycemia in these cases is
diminished production of glucose and increased
removal by insulin.
6. CLINICAL MANIFESTATIONS IN
THE BABY.
• Large baby
• Hypoglycemia = The foetus is exposed to high
glucose concentrations in utero and hence has
correspondingly high insulin levels in blood ; after
delivery , glucose from the Mother is suddenly
cut off but the baby’s blood has high insulin levels
; so they go into hypoglycemia.
• Hypocalcemia = Its exact cause is not clear, but
may be due to diminished production of
parathormone.
7. CLINICAL MANIFESTATIONS IN
THE BABY.
• Hypomagnesemia. = may be due to increased losses of
magnesium in the urine of diabetic Mothers.
• Hyperbilirubinemia = may be due to the break down of
Hb from collection of blood in cephal hematoma which
is usual in the delivery of large babies.
• Respiratory distress = Since insulin blocks induction of
enzyme system, this may explain lower production of
surfactant leading to RDS.
• Difficult labour.
• Sometimes there may be failure of neural tubeclosure ,
ASD , VSD , Coarctation of aorta , skeletal abnormalities
, GIT abnormalities etc.
9. MANAGEMENT OF I.D.M.
• Start feeds and increase the volume and frequency of
feeds
• In symptomatic cases ; Dextrose 10% , 2ml/kg I.V as
bolus ( if hypoglycemic seizures , then administer
4ml/kg) followed by infusion of Dextrose 10% , 6 to 8
mg/kg/minute.
• Repeat RBS every 30 minutes.
• Slowly wean off IV fluids once RBS value is stable.
• If atleast two normal values are obtained, decrease the
infusion rate by2mg/kg/minute Q6H. A more rapid
decrease in rate is accepted if the baby tolerates oral
feeds.
10. MANAGEMENT OF I.D.M.
• If hyperglycemia persists even with 12 mg/kg/minute of
Dextrose , other causes of hyperglycemia are considered (
persistent insulinemic hypoglycemia of infancy – PHHI ,
shock, hypothermia etc . ) .
Inj. Glucagon 300mcg/kg/day IV or IM can be
administered.
• Managing electrolyte abnormalities
- If hypocalcemia = Inj. 10% Calcium gluconate slowly
and cautiously.
- If hypomagnesemia = Inj. Magnesium Sulfate 0.5 to
2.5ml/kg of 5% Magnesium sulfate IV over one hour.
• Management of respiratory distress = Assisted ventilation
, Surfactant therapy.
• Managing cardiovascular complications.