INFANT OF DIABETICgggbcbvvfdgh MOTHER.pptx

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1. INFANT OF DIABETIC MOTHER DR. D. A. Y. MUDUWAN

2. IDM DEFINITION Any offspring of a gestational or insulin dependent diabetic woman

3. Type 1 diabetes (T1DM) Due to β-cell destruction, usually leading to absolute insulin deficiency. It is either immune mediated or idiopathic. Type 2 diabetes (T2DM) Range of predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance. Other specific types Genetic defects of the β-cell function, genetic defects in insulin action, diseases of the exocrine pancreas, endocrinopathies , drug or chemicalinduced , infections, uncommon forms of immune-mediated diabetes, other genetic syndromes sometimes associated with diabetes ( eg,Down , Klinefelter , Turner, Prader-Willi ). Gestational diabetesmellitus ( GDM ) Diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation met or exceeded:

4. Pathophysiology . Most of the problems with IDM are related to fetal hyperglycemia and the resulting increase in production of insulin by the fetal pancreas, which causes CHRONIC HYPERINSULINISM .

5. 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.

6. Complications according to time Poor control prior to conception, at the time of conception, and in early first trimester. Major congenital malformations, spontaneous early abortion, fetal growth restriction.

7. Poor control in the second trimester . Hypertrophic cardiomyopathy with septal hypertrophy, polyhydramnios , preeclampsia, placental insufficiency, Low intelligence quotient (IQ), pregnancy-induced hypertension, minor congenital anomalies, fetal loss, macrosomia .

8. Poor control in the third trimester. Macrosomia /large for gestational age ( LGA ) leading to cesarean delivery, birth trauma, fetal dystocia , Neonatal hypoglycemia, r espiratory distress syndrome, hypertrophic cardiomyopathy with septal hypertrophy, decreased oxygenation in the fetus, neonatal hypocalcemia , hypomagnesemia , hyperbilirubinemia , polycythemia / hyperviscosity , thrombocytopenia, intrauterine death.

9. Maternal hyperglycemia in labor. Hypoglycemia in the infant Poor Apgar scores. Long-term transgenerational effects. Obesity, diabetes, hypertension, kidney disease in children born to mothers with diabetes in pregnancy.

10. PATHOPHYSIOLOGY

11. Diabetic Embryopathy Hyperglycemia is thought to be the primary teratogen . It causes a deficiency of myoinositol , which is required in embryonic development. Other factors hypoglycemia, insulin, vascular disease, oxygen free radicals, hypoxia, fetal zinc depletion, low maternal magnesium, hormone imbalances, amino acid/ ketone abnormalities

12. 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 %

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

14. CNS anomalies Neural tube defects Anencephaly Meningomyelocele Hydrocephaly Holoprosencephaly

15. Diabetic Embryopathy Midline facial defects Facial microsomia microtia / anotia

16. 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

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

18. RENAL Renal agenesis ureteral duplication hydronephrosis .

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

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

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

24. Macrosomia /large for gestational age It is the result of biochemical events along the maternal hyperglycemia–fetal hyperinsulinemia pathway This occurs because increased glucose and amino acids from the mother cross the placenta into the infant and the infant produces an increase in insulin to compensate. Insulin is actually a growth hormone and causes accelerated fetal growth in the infant.

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 Defintition : Blood glucose <45 mg/ dL Usually presents at 1 -2 hours of life Incidence : up to 40% 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 delayed bilirubin clearance

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 surfactant from decreased steroids due to insulin 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

38. Hypocalcemia/ Hypomagnesemia Incidence: 50 % IDM Secondary to transient hypoparathyroid function Related to severity of maternal diabetes Develops in first 3 days Serum calcium levels are lowest at 24 to 72 hours

39. 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

40. 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

41. 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%

42. 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.

43. Management of the infant of a diabetic mother A. Initial evaluation. Upon delivery Look for any evidence of birth trauma and closely look for any major or minor malformations. blood glucose levels and a hematocrit may be obtained. The infant should be observedfor jitteriness, tremors, convulsions, apnea, weak cry, and poor sucking. A physical B. Over the first several hours after delivery should be screened for hypoglycemia and assessed for signs of respiratory distress. During the first 48 hours, observe for signs of jaundice and for renal, cardiac, neurologic, and gastrointestinal tract abnormalities.

44. C. Metabolic management Hypoglycemia Hypocalcemia Calcium therapy. Symptomatic infants should receive 10% calcium gluconate The hypocalcemia should respond in 3 to 4 days; until then, serum calcium levels should be monitored every 12 to 24 hours. magnesium sulfate

45. D. Management of cardiorespiratory problems Perinatal asphyxia. Close observation for fetal distress should continue throughout labor and delivery.. . Respiratory distress. Management of respiratory distress depends on the etiology. RDS , TTN , more common in the IDM . other causes ( eg , pneumonia or spontaneous pneumothorax ). Provide oxygen and ventilator support as needed initially.

46. Hypertrophic cardiomyopathy self-limited and usually resolves within 6 months. Therapy includes possible mechanical ventilation, maintenance fluids, and correction of hypoglycemia and hypomagnesemia ; short-acting β-blockers( esmolol , propranolol ). Digoxin or other positive inotropic agents are contraindicated can make the infant worse because of possible ventricular outflow obstruction and are only indicated if there is a decrease in cardiac contractility. Diuretics are not necessary unless there is fluid overload. If pulmonary hypertensionis present, inhaled nitric oxide should be considered.

47. Management of the infant of a diabetic mother E. Hematologic management Hyperbilirubinemia . Phototherapy exchange transfusion Polycythemia . fluids partial exchange transfusion

48. 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

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