pathophysiology , complications , management of IDM

1. 8 /2017

2. INFANT OF DIABETIC
MOTHER
DR.SAYED ISMAIL
PROFESSOR OF PEDIATRICS
ALAZHAR UNIVERISITY

3. IDM , FT , LGA Wt 5.75kg CS ,BG 21 , BABY GIRL A/G 4/8

4. OBJECTIVES
• Discuss briefly the effects of maternal Diabetes
on the Fetus
• Review the morbidities encountered in an IDM
• Discuss the management of an IDM
• How we can prevent the complications of IDM
• Discuss the prognosis for an IDM

5. IDM - Definitions
• Any offspring of a gestational or insulin dependent diabetic
woman
• Diabetes- WHO –Classification:-
1. Type 1- insulin dependent
2. Type 2 – insulin resistance
3. Gestation Diabetes Mellitus***- Impaired Glucose
Tolerance during pregnancy
4. other rare types of DM ( CF , drug-induced DM.)

6. Pathophysiology of gestational diabetes mellitus. During pregnancy, insulin resistance is
increased due to production of placental hormones that antagonize insulin action. when
insulin release is inadequate, hyperglycemia occurs (gestational diabetes mellitus) and an
excess amount amount of glucose is transferred via the placenta to the embryo. Neither
maternal nor embryo insulin crosses the placenta.

7. INCIDENCE
• 3% to 10% of pregnancies
are complicated by abnormal
glycemic control.
• Of these, 80% are caused by
gestational diabetes mellitus

8. Infant of the Diabetic Mother – perinatal
mortality
• Maternal mortality decreased from
50 to 9 %
• Fetal and neonatal mortality rates
decreased from 65/100 to
20/1000
• Congenital malformations remain
high

9. PATHOPHYSIOLOGY
• Most, but not all, of the fetal and
neonatal sequelae of diabetes during
gestation are a function of maternal
glycemic control

10. PATHOPHYSIOLOGY

11. Effects of Poor glycemic control in pregnant
diabetic women
• major birth defects
• spontaneous abortions
Maternal hyperglycemia
In the first trimester
during fetal
organogenesis
• Hyperinsulinemia
• macrosomia
Maternal hyperglycemia
in the second and third
trimesters, resulting in.

12. IDM -Early Pregnancy
Diabetic Embryopathy
(Hyperglycemic embryo)
Risk for Congenital
Malformations

13. Glucose Control and Malformations
MALFORMATION RATES BY LEVEL Of MATERNAL
HEMOGLOBIN A1c
6.9 or less  0 %
7.0-8.5  5.1 %
8.6 or greater  22.4 %

14. Congenital anomalies of diabetic
embryopathy
–Central nervous system
–Cardiac malformations
–Renal , urinary
–GI tract anomalies
–Skeletal anomalies

15. CNS anomalies
• Neural tube defects
– Anencephaly
– Meningomyelocele
• Hydrocephaly
• Holoprosencephaly

16. Diabetic Embryopathy
• Midline facial defects
• Facial microsomia
• microtia/anotia
Diabetes in 10.3% 1.4% of control
mothers

17. Cardiac anomalies
• Cardiac functional abnormalities are present in up
to 30% of IDMs
– intraventricular septal hypertrophy and
cardiomyopathy
– Transposition of great vessels
– Coarctation of the aorta
– Atrial & Ventricular septal defects
– Dextrocardia
– Single ventricle, hypoplastic left heart
– Patent ductus arteriosus

18. GI anomalies
• GI: Small Left Colon Syndrome
• Bowel atresia
• Bowel dysmotility
(feeding intolerance)

19. Skeletal Anomalies
• Caudal Dysplasia or Regression SD
– Rare disorder (1/25000)
– The most specific malformation related
to diabetes 200-400 times more often
in IDMs
– Sacral agenesis with hypoplastic pelvis
– Usually with other malformations like:
femoral hypoplasia, extrophy of the
bladder, and club foot

20. Sacral Agenesis Caudal Regression

21. Diabetic Embryopathy
PREVENTION :
• TIGHT GLYCEMIC CONTROL
• Folic Acid/ Vitamin intake

22. IDM - Late Pregnancy
Fetal and Neonatal Complications
• Poor late control (Hyperglycemic fetus)
 Risk for Hyperinsulinemia (growth factor)

24. Fetal and Neonatal Complications
of Hyperinsulinemia
–Macrosomia
–Hypoglycemia
–Polycythemia/hyperbilirubinemia
–Renal vein thrombosis
–Cardiomyopathy
–RDS

25. • LGA
– Birth weight > 4 kg or ˃ 90th
percentile for gestational
age
• Occurs in 20-60% IDM
• Physical findings
– Increased adipose tissue
– Disproportionate
head/shoulder ratio
– Plethoric
– Large placenta & cord
Macrosomia

26. Macrosomia
Complications associated with delivery
• Birth trauma
– Shoulder dystocia
– Brachial plexus injury
– Fractured clavicle
– Visceral hemorrhage
– Birth Asphyxia
– Risks associated with C/Section and
operative vaginal deliveries (vacuum
extraction, forceps, etc.)

27. Birth Injuries due to macrosomia

28. IDM may also be SGA in advanced diabetes complicated
with renal and cardiac disease

29. Hypoglycemia
Symptoms
• Jitteriness 81%
• Seizures 58%
• Apnea/cyanosis 47%
• Irritability 41 %
• Hypotonia 26%
• Poor feeding
• Hypothermia
• None
Defintition: Blood glucose <40 mg/dL
Usually presents at ½-2 hours of life
Incidence: up to 50% of IDM

31. Hypoglycemia
Treatment
If stable give early feedings
If not able to feed:
D10%W 2mL/kg (slow IVP)
plus
Continuous IV infusion of
D10%W at 80-100 mL/kg/day
Use glucagon in extreme
cases
Follow blood glucose with
frequent Chemstrips

32. Hyperbilirubinemia
• Definitions: Elevated indirect
(unconjugated) bilirubin >10mg/dL in
term infant,
• Incidence in IDM 20-40%
• Pathophysiology
– Increased bilirubin production
• Polycythemia
• Liver immaturity

33. Hyperbilirubinemia
• Prevention
– Early, adequate
breastfeeding
– Good hydration and stooling
• Treatment:
– Adequate hydration and
nutrition
– Phototherapy
– Exchange transfusion

34. Polycythemia
• Polycythemia, defined as central hemoglobin concentrations more than 20 g/dL
and hematocrit levels more than 65%,
• Present in 20% to 30% of IDMs at birth
• Due to bone marrow stimulation (high erythropoietin levels) from hypoxia
• Signs and symptoms
– Plethora
– Jitteriness
– Tachypnea
– Cyanosis (general or circumoral)
– Oliguria
– Poor feeding
– Lethargy/seizures
• Screening: shortly after birth. And on a daily basis for 3 days

35. Polycythemia
• Treatment
– Hydration
– Partial exchange transfusion
• Common complications
– Hyperbilirubinemia
– Renal vein thrombosis
– Hypertension
– persistent pulmonary hypertension
– Necrotizing enterocolitis

36. IDM -Cardiomyopathy
• Cardiomyopathy with ventricular
hypertrophy and outflow tract
obstruction may occur in as many as
30% of IDMs
• CHF in 5%
Treatment: supportive therapy and
beta blockers

37. Perinatal Hypoxia
• May lead to fetal death or neonatal asphyxia
• May result from complicated labor and delivery
– Placental insufficiency (vascular disease, pre eclampsia)
– Maternal ketoacidosis
– Prolonged labor due to Macrosomia
– Meconium Aspiration
– Polycythemia

38. Respiratory Distress
• Transient Tachypnea of Newborn (delayed
lung fluid clearance)
• Aspiration of meconium or amniotic fluid
• Prematurity
• Respiratory Distress Syndrome

39. Respiratory Distress Syndrome
RDS (delayed lung maturity), higher risk than non IDMs.
This increased risk persists until approximately 38 weeks’ gestation.

40. Respiratory Distress Syndrome
• surfactant from
decreased steroids due to
insulin
• Prevention: Check for lung maturity with
presence of PG and L:S ratio >2
• Treatment:
– Surfactant
– Assisted support and ventilation
– Supplemental oxygen
lecithin/sphingomyelin (L/S) ratio exceeds 2:1 and phosphatidylglycerol is more than 3% in amniotic fluid samples

41. Hypocalcemia/Hypomagnesemia
• Incidence: 50 % IDM
• Secondary to transient hypoparathyroid function
• Related to severity of maternal diabetes
• Develops in first 3 days

42. Hypocalcemia/Hypomagnesemia
• Symptoms:
– Irritability
– Jitteriness
– Apnea
– Lip smacking
– Tongue thrusting
• Laboratory Tests
– Calcium
– Ionized CA
– Magnesium
• Treatment
– Transfer to Neonatal Intensive Care Unit
– Calcium gluconate
– Magnesium sulfate

43. IDM - Neurologic Dysfunction
• Jitteriness
• Irritability
• Increased or Decreased
tone
• Seizures
• Poor feeding
• Due to:
– Chronic and/or acute
hypoxia
– Immaturity
– Hypoglycemia
– Hypocalcemia
– Polycythemia/strokes
– Delivery trauma
– Iron deficiency

44. Long Term Prognosis of IDM
IDMs are at increased risk for delayed motor and cognitive
development if suffer
Birth asphyxia
Hypoxemia
Hypo- or hyperglycemia,
Acidosis,
Iron deficiency.
Risk of Developing Insulin Dependent DM
. Diabetic mother 2%
. Diabetic father 6%

45. Develpomental delayNormal child

46. Role of Obstetrician
• Preconception counselling
• Good maternal glucose control
Role of Paediatrician
• Anticipate, monitor
• Treat complications
The IDM needs to be
supported since
conception

47. Workup for IDM
• CBC count
• Glucose (serum or whole-blood)
• Magnesium ,Calcium
• Bilirubin level
• Arterial blood gas
• Chest radiography
• Abdominal, pelvic, or lower extremity radiography
– When caudal dysplasia is present,
• Cardiac echocardiography
• Barium enema
– Infants with feeding intolerance, abdominal distention, nonbilious emesis, or poor passage of
meconium may require a barium enema. Indwelling vascular lines (peripheral, umbilical, or
central)
• Noninvasive blood gas monitoring using transcutaneous electrodes (PaO2 and PaCO2) and
oximeters (O2% saturation) has greatly reduced the need for invasive, indwelling catheters.
However, indwelling lines are often needed early in the course of cardiorespiratory disease.

48. Transfer, Consultations, and Follow-Up
• (IDMs) having congenital anomalies, heart disease, or significant
respiratory illness may require transfer to a tertiary care neonatal
intensive care unit (NICU) for continued care and access to
subspecialists. Because of the frequency with which cardiac
problems occur in IDMs, early consultation with a pediatric
cardiologist often is necessary. Other consultations depend on
which other congenital malformations or complications are
present.
• Basic outpatient care should consist of routine well-baby care
provided by the infant's general pediatrician. Additional follow-up
by consultant subspecialists depends on the neonatal clinical
problems and their resolution.

49. Summary
• Maternal hyperglycemia in the first trimester time of
conception, during fetal organogenesis result in major
birth defects and spontaneous abortions
• Diabetic embryopathy can be prevented by control of
diabetes BEFORE CONCEPTION

50. References
[1] Kicklighter SD. Infant of diabetic mother. Emedicine October 26, 2001. Available at www.
emedicine.com/ped/topic485.htm. Accessed February 25, 2004.
[2] Widness JA. Fetal risks and neonatal complications of diabetes mellitus and metabolic and
endocrine disorders. In: Brody SA, Ueland K, editors. Endocrine disorders in pregnancy. Norwalk
(CT): Appleton-Lang; 1989. p. 273– 97.
[3] Pedersen J. The pregnant diabetic and her newborn. 2nd edition. Baltimore: Williams and Wilkins;
1977.
[4] Kalhan SC, Parimi PS, Lindsay CA. Pregnancy complicated by diabetes mellitus. In: Fanaroff
AA, Martin RJ, editors. Neonatal-perinatal medicine: diseases of the fetus and infant. 7th edition.
Philadelphia: Mosby; 2002. p. 1357– 62.
[5] Georgieff MK. Therapy of infants of diabetic mothers. In: Burg FD, Ingelfinger JR, Wald ER,
Polin RA, editors. Current pediatric therapy. 15th edition. Philadelphia: WB Saunders; 1995.
p. 793– 803.
[6] Creasy RK, Resnik R. Intrauterine growth restriction. In: Creasy RK, Resnick R, editors. Maternal-
fetal medicine. 4th edition. Philadelphia: WB Saunders; 1999. p. 569– 84.
[7] Fee B, Weil WM. Body composition of a diabetic offspring by direct analysis. Am J Dis Child
1960;100:718–9.
[8] Wagner RK, Nielsen PE, Gonik B. Controversies in labor management: shoulder dystocia.
Obstet Gynecol Clin North Am 1999;26(2):371– 83.
[9] Lucas MJ. Medical complications of pregnancy: diabetes complicating pregnancy. Obstet Gynecol
Clin North Am 2001;28(3):513– 36.
[10] Milley JR, Papacestas JS, Tabats BD. Effect of insulin on uptake of metabolic substrates by the
sheep fetus. Am J Physiol 1986;251:E349– 59.
[11] Philipps AF, Porte PJ, Strabinsky S, Rosenkranz TS, Ray JR. Effects of chronic fetal hyperglycemia
upon oxygen consumption in the ovine uterus and conceptus. J Clin Invest 1984;74:
279– 87.