This document discusses the infant of a diabetic mother. It begins with an introduction stating that diabetes is a common complication of pregnancy and risks to the infant have decreased but still exist. It then covers pathophysiology, epidemiology, complications, management, and prognosis. Key points include: fetal macrosomia is a risk; hypoglycemia is common due to hyperinsulinemia; other risks include hypocalcemia, hypomagnesemia, and congenital heart defects. Management involves monitoring glucose and electrolytes along with imaging tests. Treatment focuses on maintaining normal glucose during labor and delivery along with early breastfeeding to prevent hypoglycemia. Prognosis is generally good but neurodevelopmental risks exist if maternal glucose control was

1. Infant of diabetic
mother
Yassin AlSaleh
Dr.Sameer AlAbdi

2. ‫بسم ا الرحمن‬
‫الرحيم‬
‫) هو الذ ي‬
‫وُ ا َ َّ ي يِ‬
‫يصوركم ف ي‬
‫وُ ا َ رِّ وُ وُ ف ْ ي يِ‬
‫ف ْ ا َ ي يِ ا َ ف ْ ا َ‬
‫ال ا َرحمام كيف‬
‫ا َ ا َ‬
‫ا َ ا َ‬
‫يشماء ل ا َ إ ي يِلهـه إ ي يِل َّ‬
‫وُ ا َ ف ْ ا َ ي يِ وُ‬
‫هو العزيز‬
‫الحكيم(‬
‫ف ْ ا َ ي يِ وُ‬
‫سورة آل عمران‬

3. Objectives
•
•
•
•
•
•
Introduction
Pathophysiology
Epidemiology
Complications
Management
Prognosis

4. Introduction
• Diabetes is the most common
medical complication of pregnancy.
• Fetal and neonatal mortality rates
were as high as 65%.
• nowadays nearly 30-fold decrease
in morbidity and mortality rates.
• there is still an increased risk of
complications.

5. Definitions
Gestational diabetes mellitus (GDM):
any abnormal glucose intolerance that begins or is
first recognized during pregnancy using glucose
tolerance test.

7. Pathophysiology

8.  estrogen and progesterone
beta-cell hyperplasia
 insulin (hyper insulinism)
 human placental lactogen
 lipolysis in the mother
 glycerol and fatty acids
preserving the glucose and aminoacid for the fetus
Glucose and amino acids traverse the placental membrane
Before 20 weeks' gestation, fetal islet
cells are incapable of responding,
subjecting the fetus to unchecked
hyperglycemia (IUGR)
before 9 week (malformation)*
After 20 weeks' gestation, the fetus
responds to hyperglycemia with
pancreatic beta-cell hyperplasia and 
insulin levels (macrosomia).(TTN)
(birth injure) (cardiomegally)
 fetal basal metabolic rate and oxygen consumption
 erythropoieten production polycythemia. (thrombocytopnia) (stroke)
redistributes iron  organs iron deficient ( heart and Neurodevelop)
 insulin levels inhibit the maturational effect of cortisol on the lung (RDS)

9. Incidence
incedince of diabetis among
pregnant from May-Dec 2008
1791 total life birth
8.90%
91.10%
• 3-10% of
pregnancies are
involved.
• in KAH 8.9%
• Of these, 80%
are related to
GDM.

10. incedince of IDM among the admitted baby from
2003-2008 total 1772
330
19%
1442
81%

11. Mortality
• Major congenital malformations are
found in 5-9% of affected infants.
• the stillbirth and perinatal mortality
rate is 5 times the rate in the general
population.
• neonatal mortality rates 15 times
• infant mortality rates are 3 times .

12. Complications

13. Complication
•
•
•
•
•
•
•
•
Fetal macrosomia
Fetal congenital malformations
Impaired fetal growth
Pulmonary disease
Metabolic and electrolyte abnormalities
Hematologic problems
Cardiovascular anomalies
Congenital malformations

14. Fetal macrosomia
• large for gestational age
macrosomia :
• as birth weight greater
than the 90th percentile
or above 4000 g.
What is the most appropriate
pathophysiologic definition of term
macrosomic IDM?

15. • it was more accurate to adopt the
BW of 4000g as a practical
definition of full-term macrosomic
IDM rather than the definition with
BW90th percentile.
Hakam Yaseen2/2001.

16. Fetal macrosomia
• Fetal macrosomia is observed in
26% of IDMs and in 10% of NON
DM.
• Macrosomia occurs among all
classes of diabetic pregnancies
except those with vasculopathy .
• typically appear large and plethoric,
with excessive fat accumulation in
the abdominal and scapular regions,
and visceromegaly.

17. Fetal macrosomia
• Macrosomia in IDMs is associated
with disproportionate growth,
resulting in an increased ponderal
index.
• disproportionate macrosomic infants
were more likely to have
hyperbilirubinemia , hypoglycemia,
and acidosis.
• fetal macrosomia may occur despite
maternal euglycemia.

18. Fetal macrosomia
•
•
•
•
birth injury:
shoulder dystocia.
brachial plexus injury;
clavicular or humeral
fractures.
• Cephalohematoma.
• subdural hemorrhage.
• facial palsy

19. • The newborn of the diabetic
mother complicated with shoulder
dystocia does not appear to be at
an increased risk for perinatal
morbidity compared with the
newborn of the non-diabetic
mother.
Levy A, 2006 Jan

20. SGA IUGR
– Impaired fetal growth may occur in
as many as 20% of diabetic
pregnancies, compared to a 10% .
– Maternal vascular disease is the
common cause of impaired fetal
growth.
– has been associated with “too tight”
control.

21. Premature delivery
• Spontaneous premature labor occurs
more frequently in diabetic
pregnancies
• Causes:
• Poor glycemic control.
• associated high rate of urinary tract
infections.
• Maternal preeclampsia.

22. Pulmonary disease
• an increased risk of respiratory
distress syndrome particularly in
those ≤ 38 weeks .
• In contrast, fetal lung maturation may
occur early in diabetic pregnancies
complicated by vasculopathy .
• transient tachypnea of the newborn.
• persistent pulmonary hypertension of
the newborn.
• Pnumothorax.

24. Metabolic Hypoglycemia
– Definition: blood glucose levels below 40
mg/dL (2.2 mmol/L)
• Seminars in Fetal Neonatal Medicine 14
(2009) 106–110
• This level is defined as a plasma glucose
concentration of 1.7–2.0 mmol/L or less for
healthy term newborns during the first 24 h after
birth.
• Beyond 24 h of age the threshold is defined as a
plasma glucose concentration of 2.2–2.8
mmol/L or less.

25. Metabolic Hypoglycemia
– Hypoglycemia is caused by
hyperinsulinemia due to hyperplasia of
fetal pancreatic beta cells consequent to
maternal-fetal hyperglycemia.
– Because the continuous supply of
glucose is stopped after birth, the
neonate develops hypoglycemia
because of insufficient substrate.
– Strict glycemic control during pregnancy
decreases but does not abolish the risk
of neonatal hypoglycemia .

26. Metabolic Hypoglycemia
– Hypoglycemia may present within
the first few hours .
– may persist for as long as one
week.
– Or the neonate is asymptomatic.
– such symptoms as jitteriness,
irritability, poor feeding, weak cry,
hypotonia, or frank seizure activity.

27. Metabolic / Hypocalcemia
– definition: total serum calcium
concentration of less than 7 mg/dL (1.8
mmol/L) or an ionized calcium value of
less than 4 mg/dL (1 mmol/L )
– Hypocalcemia is thought to be caused
by the lower parathyroid hormone (PTH)
level.
– symptoms may include jitteriness or
seizure.
– In term infant ,self resolving no need to
tratment.

28. Metabolic / Hypo magnesium
– Definition:serum magnesium
concentration less than 1.5 mg/dL (0.75
mmol/L
– The mechanism is increased urinary
loss secondary to diabetes.
– Prematurity may be a contributing
factor.
– the hypocalcemia may not respond to
treatment until the hypomagnesemia is
corrected .

29. Iron deficiency
– 65% of all IDMs demonstrate
abnormalities of iron metabolism at
birth.
– Iron deficiency increases an infant's risk
for neurodevelopmental abnormalities.

30. Hematologic /Polycythemia
• Definition: hematocrit of more than
65 percent.
• ruddy appearance, sluggish capillary
refill, or respiratory distress.
• Hyperviscosity increases the risk for:
• stroke
• Seizure
• necrotizing enterocolitis
• renal vein thrombosis.

31. Hematologic /Thrombocytopenia
• Thrombocytopenia: because of an
excess of red blood cell precursors
within the bone marrow .

32. Hyperbilirubinemia
• Excessive red cell
hemolysis, leads to elevated
bilirubin levels.
• Polycythemia and
prematurity also are
contributing factors

33. Cardiomyopathy
• Hypertophic Cardiomyopathy with
intraventricular hypertrophy may occur in as
many as 50% of these infants.
• Infants often are asymptomatic, but 5 to 10
percent have respiratory distress or signs of
heart failure.
• Symptomatic infants typically recover after
two to three weeks of supportive care.
• echocardiographic findings resolve within 6
to 12 months.

35. Congenital
malformations

36. Congenital malformations
– Some speculate that may arise from
an insult to the developing
mesoderm and cephalic neural crest
cells.
– Metabolic disturbances, such as
hyperglycemia, hypoglycemia, and
hypoxia, also may be involved.
– Glucose-induced free radicals of
oxygen also have been implicated.
– CVS and CNS are the most
common.

37. Cardiovascular
– These infants are at an increased risk of
congenital heart defects.
– VSD
– TGA

38. • Abu-Sulaiman RM, 2006
• The most common echocardiographic findings were patent
ductus arteriosus (PDA; 70%), patent foramen ovale (68%),
atrial septal defect (5%), small muscular ventricular septal
defect (4%), mitral valve prolapse (2%), and pulmonary
stenosis (1%). Hypertrophic cardiomyopathy (HCMP) was
observed in 38% of cases, mainly hypertrophy of the
interventricular septum. Severe forms of CHD encountered
were D-transposition of great arteries, tetralogy of Fallot,
and hypoplastic left heart syndrome (1% each)..
• Overall incidence of congenital heart disease was 15% after
excluding PDA and HCMP. Maternal IDDM is a significant
risk factor for CHD. Careful evaluation and early diagnosis
of CHD in this high-risk group are highly indicated. There is
a need for development of prenatal screening programs for
CHD in our population.

39. • Infant of diabetic mother presents a high risk for
cardiac involvement, either cardiac congenital
malformations (27% of cases) or acquired cardiac
pathology-hypertrophic cardiomyopathy (71% of
cases) which justifies early cardiologic screening
for all of these newborns in presence or absence
of cardiac suffering signs or symptoms.
Early Human Development, November 2008

40. nervous systems
• the risk of anencephaly
is 13 times higher.
• the risk of spina bifida
is 20 times higher.
• microcephaly,
holoprosencephaly.

41. Caudal regression syndrome
• also referred to as caudal
agenesis, sacral
dysgenesis, or caudal
dysplasia sequence.
• occurs approximately 200
times more frequently in
IDMs than in other infants.
• 600 times more frequently
among IDDM
• The syndrome consists of a
spectrum of structural
defects of the caudal region,

42. Caudal regression syndrome
• severe form called
sirenomelia (Mermaid
syndrome).
• is a lethal abnormality.

43. others
• Renal (eg,
hydronephrosis, renal
agenesis, ureteral
duplication).
• gastrointestinal (eg,
duodenal or anorectal
atresia, small left colon
syndrome)

44. small left colon syndrome
• a transient inability to
pass meconium .
• presents as lower
bowel obstruction.
• Diagnosis is made by
barium enema and
history of maternal
diabetes.

45. Accompanying congenital
anomalies • unilateral microphthalmia.
•
•
•
•
•
•
•
•
bilateral microtia.
cleft palate.
micropenis .
unilateral cryptorchidism.
bilateral radial hypoplasia.
unilateral polydactyly.
bifid tongue.
Single umbilical artery

46. Management

47. Investigation
•
•
•
•
•
•
Glucose concentration.
Complete blood cell count.
Calcium concentration.
Magnesium concentration.
Bilirubin level.
Arterial blood gas.

48. Imaging
• Chest radiograph
– Adequacy of lung expansion, evidences
of focal or diffuse atelectasis, presence
of interstitial fluid, signs of free air in
pleural or interstitial spaces
– echocardiogram

49. Imaging
• Abdominal, pelvic, or lower extremity
radiographs
– Sacral agenesis
– hypoplastic femur.
– defects of the tibia and the fibula, flexion
contractures of the knee and hip, or
clubfoot.

50. Imaging
• Barium enema
– Infants with feeding intolerance,
abdominal distention, nonbilious
emesis, or poor passage of meconium .
– Radiologically: distal tapering of the
colon

52. Treatment
?
when
Hypoglycemia
electrolyte
respiratory
Cardiac

53. Before pregnancy
• Better periconception control would
result in better outcome.
• international recommendations for
pre-pregnancy control is glycated
haemoglobin of 7%.

54. During pregnancy
• tight glycaemic control.
• avoiding hypoglycaemia. particularly
in the first trimester and in those with
type 2.
• Pre-eclampsia should be controlled.
• Use of antioxident.
• Avoid the flatuation in glucose level.

55. • Fetal macrosomia may result from episodic
rather than sustained maternal
hyperglycaemia.Reduction in blood glucose
variability may improve outcome
Seminars in Fetal Neonatal Medicine
(2005)

56. around the labor
• Maintain maternal glucose level at
around 4.5–5.5 mmol/L during
delivery.(2009)
• Antenatal steroid.
• Mode of delivery.

57. • The metabolic and blood pressure
balance is dangerously disturbed
in such pregnancies by this
treatment.( Antenatal steroid)
Arch Pediatr. 2007

58. After delivery
• Early breast feeding.
• Avoid unnecessary glucocheck.
• cardiologic screening

59. • Establishing early breast-feeding is
paramount, since colostrum as well
as breast milk provides a generous
concentration of glucose
Mimouni F,. 1990
• It appears that one half of these
episodes can be successfully
treated with enteral feedings.
Leandro Cordero, 1998

60. • study drew attention to the observation
that, because there is a physiological fall in
blood glucose concentration after birth,
testing for hypoglycaemia too soon (i.e.
within 60 min of birth) may result in
identifying this physiological dip in the
blood glucose concentration and therefore
unnecessary intervention.
de Rooy L, Pediatrics 2002.

61. • Monitor routinely plasma glucose
(before feeding) at 2,4, 6, 12, 24 and 48
h after birth.
• Avoid blood glucose testing too early.
Term babies of diabetic mothers who
are otherwise well with no clinical
signs of hypoglycaemia should not
have blood glucose testing in the first
2 h after birth.
2009

62. Prognosis
• Prognosis is very good .
• Neurodevelopmental outcome
– infants of mothers with poor glucose
control during pregnancy are at highest
risk for neurodevelopmental deficits.

63. Prognosis
• Growth
– Some evidence
indicates that IDMs will
have obesity as they get
older.
• It might play a role in
the pathogenesis of
atherosclerosis in adult
life.
• Also in developing
diabetes.

65. Thank
you for
your
attention