Infant of diabetic mother

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:- Type 1- insulin dependent Type 2 – insulin resistance Gestation Diabetes Mellitus***- Impaired Glucose Tolerance during pregnancy 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

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

13. Glucose Control and Malformations MALFORMATION RATES BY LEVEL Of MATERNAL HEMOGLOBIN A 1c 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 PREVENTION PREVENTION PREVENTION

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

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

24. 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

25. 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.)

26. Birth Injuries due to macrosomia

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

28. 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

29. 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

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

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

32. 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

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

34. 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

35. 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

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

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

38. 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

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

40. 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

41. 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

42. 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%

43. Develpomental delay Normal child

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

45. 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 (PaO 2  and PaCO 2 ) and oximeters (O 2 % saturation) has greatly reduced the need for invasive, indwelling catheters. However, indwelling lines are often needed early in the course of cardiorespiratory disease.

46. 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.

47. 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

48. 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.