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The Infant of the Diabetic Mother

The Infant of the Diabetic Mother. Maureen L. Tate LTC MC February, 2003. Maternal Diabetes. Harmful effects on the fetus recognized over 100 years ago GDM----3 to 10 % IDDM --0.1 to 0.3 %. Introduction. Discovery of insulin Understanding of pathophysiology of diabetes

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The Infant of the Diabetic Mother

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  1. The Infant of the Diabetic Mother Maureen L. Tate LTC MC February, 2003

  2. Maternal Diabetes • Harmful effects on the fetus recognized over 100 years ago • GDM----3 to 10 % • IDDM --0.1 to 0.3 %

  3. Introduction • Discovery of insulin • Understanding of pathophysiology of diabetes • Improved preconception counseling 1964 1984 ¯ maternal mortality 50% 9% ¯ fetal mortality 21% 2%

  4. Introduction • ¯ morbidity not as striking • 4 to 5 fold decrease morbidity • d/o of fetal growth and birth trauma • intrauterine and perinatal asphyxia • polycythemia • hyperbilirubinemia • cardiomyopathy • postnatal metabolic disturbances

  5. What is the etiology of congenital malformations associated with diabetes?

  6. Congenital Malformations • Overall incidence---5 to 9% • 2-3 fold higher than general population • Predominantly with IDDM • Malformations of CNS seen most often • Diversity-No malformation considered pathognomonic

  7. Congenital Malformations • No increase in major congenital malformations among offspring of • Diabetic fathers • Prediabetic women • GDM after first trimester

  8. Suggests that glycemic control during embryogenesis is the main factor in the origin of malformations

  9. Incidence of major malformations among women without preconception counseling SOURCE n % 1993 Willhoite 8/123 6.4 1991 Kitzmiller 12/110 10.9 1991 Greene 23/432 7.4 1984 Ballard 19/196 9.7 1983 Simpson 11/142 7.7 1978 Kitzmiller 13/137 9.5 1977 Gabbe 19/260 7.3

  10. Congenital Malformations Impact of Pre-conception Counseling • Kitzmiller (1991) Pre-conception counseling 1.2 % Referred at 6-30 weeks EGA 10.9 % • Willhoite (1993) Pre-conception counseling 1.6 % No pre-conception counseling 6.5 %

  11. Congenital Malformations • Freinkel 1980 Fuel Mediated Teratogenesis--exposure of the embryo to an abnormal metabolic environment during the initial stages of embryogenesis results in abnormal development of the embryo

  12. Hyperglycemia Hyperketonemia Oxygen-Free Radicals Congenital Malformations

  13. Hyperglycemia Specific ultrastructural changes • Decreased embryo size • Yolk sac malformations • sparse, patchy, non-uniform capillaries • ¯ rough ER, ribosomes, and mitochondria • abnormal transport of nutrients

  14. Hyperglycemia Other consequences: • Arachadonic acid deficiency • Accumulation of sorbitol • Deficiency of myo-inositol associated with CNS malformations

  15. Maternal Hyperglycemia • Dose and time dependent • Post implantation rat embryo 100% teratogenic dose 950 mg/dl D-glucose Day 10 primary neural tube defect Day 11 cardiac defects Day 12 no defects

  16. Hyperketonemia • b-hydroxybutyrate • Dose related • Time-of-exposure related • Synergism with glucose • minimally teratogenic doses of both metabolites • Long-term neurodevelopmental abnormalities

  17. Fetal Hyperglycemia • 1-2 hours of fetal hyperglycemia can have detrimental effects •  insulin secretion • Storage of excess nutrients  macrosomia • Post natal hypoglycemia

  18. Fetal Hyperglycemia • Drives catabolism of the oversupply of nutrients • depletes fetal O2 stores  episodic fetal hypoxia •  catecholamines • hypertension, cardiac remodeling and hypertrophy •  erythropoiesis  polycythemia • poor circulation and hyperbilirubinemia

  19. Oxygen-Free Radicals • Result of glucose metabolism • Increased lipid peroxidation • direct effect on DNA • imbalance between prostaglandins and prostacyclins • Rat embryo—superoxide dismutase shown to be protective against malformations

  20. Congenital Malformations:The Laundry List

  21. Congenital Malformations Skeletal/CNS • Caudal regression syndrome not considered pathognomonic occurs 600x more frequently among IDDM • Neural tube defects • Microcephaly

  22. Caudal Regression Syndrome • Spectrum of malformation • cessation of growth of rostral portion of spinal cord • abnormal neural, muscular, skeletal and vascular components Caudal Regression with limbs intact but malformed Sirenomelia Absence of hind limbs, external genitalia, anus and rectum; Potter sequence secondary renal agenesis

  23. Congenital Malformations Cardiac • Transposition + VSD • Ventricular septal defect • Coarctation + VSD or PDA • Atrial septal defect • Hypertrophic Cardiomyopathy

  24. Congenital Malformations Renal • Hydronephrosis • Renal agenesis • Ureteral duplication

  25. Congenital Malformations GI • Duodenal atresia • Anorectal atresia • Small left colon syndrome

  26. Mrs. J is 32 YO, G1P0 who is currently in labor and has been pushing for two hours. You are called to the delivery secondary to fetal distress. While waiting in the DR you learn that the prenatal tests were unremarkable except for glucose testing that led to the dx of GDM. Maternal glucose control was poor during the past few weeks with average glucoses > 120 and insulin was rx.

  27. Delivery of the body is delayed secondary to shoulder dystocia. Your initial assessment of the infant includes poor resp effort, cyanosis, and HR 80. After the initial steps of resuscitation including 45 sec. of FM PPV the infant responds and is transferred to the baby suite for further evaluation.

  28. Which baby is the infant of the diabetic mother? B A

  29. What perinatal and neonatal complications should you anticipate?

  30. Perinatal and Neonatal Complications • Disorders of fetal growth • Intrauterine and perinatal asphyxia • Hypoglycemia • Respiratory distress syndrome

  31. Perinatal and Neonatal Complications • Hypertrophic Cardiomyopathy • Polycythemia • Hyperbilirubinemia • Hypocalcemia

  32. Disorders of Fetal Growth

  33. Macrosomia • Birth Weight > 4000 g or > 90th %-ile • Incidence 15 to 45% among IODM • Increased rate of C-section • Birth Trauma • shoulder and body dystocia • brachial plexus injury • facial nerve injury • asphyxia • abdominal trauma

  34. Macrosomia • Insulin and insulin-like growth factors • Primary growth factors for the fetus • Abnormal adipose deposition • Visceral organ hypertrophy and hyperplasia • Acceleration of skeletal growth • Increased levels of lipids, ketones, and amino acids also stimulate insulin secretion

  35. Intrauterine Growth Restriction • Incidence reported as high as 20 % • Contributing factors: • Maternal vascular disease • Hypertension • Intrauterine infection • Chromosomal abnormalities

  36. Intrauterine Growth Restriction • Oligohydramnios • Hypoxia • Fetal distress • Asphyxia • Intrauterine and neonatal death

  37. Birth Asphyxia • Incidence • 20 TO 30% • Primary Risk factors: • Prematurity • Fetal growth disorders • Maternal vascular disease • Peripartum maternal hyperglycemia • Drives catabolism of the oversupply of nutrients • depletes fetal O2 stores  episodic fetal hypoxia

  38. Hypoglycemia • Risk Factors • Prematurity • Birth asphyxia • Cesarean section • Disorders of fetal growth • Stimulation of the fetal pancreas • Pedersen Hypothesis

  39. Hypoglycemia • Pedersen Hypothesis • Maternal hyperglycemia • Fetal hyperglycemia • Fetal b-cell hyperplasia • Neonatal hyperinsulinemia

  40. Hypoglycemia • Maternal glucose interrupted at parturition • Neonatal hyperinsulinemia results in neonatal hypoglycemia • Suppression of FFA • Decreased glycogenolysis • Decreased response to glucagon and catecholamines

  41. Tremors Jitteriness Irritability Lethargy Apnea Cyanosis Hypothermia Weak or high pitched cry Poor feeding Seizures Signs of Hypoglycemia

  42. Hypoglycemia Diagnosis • Test within 30-60 minutes of admission • Glucose < 40 confirm with serum glucose • Do not delay treatment pending results

  43. Hypoglycemia • Management • Oral Feeding • IV bolus D10 (2cc/kg) over 2 to 5 min. • Continuous infusion D10 @ 6 to 8 mg/kg/min • Careful attention to total fluid administration • Increase glucose concentration • Resolution of hyperinsulinemia • 24 to 48 hrs.

  44. Respiratory Distress Syndrome • Risk: • 3 to 5 times the risk in the non-diabetic population • Contributing Factors: • Prematurity • Maternal glycemic control

  45. Respiratory Distress Syndrome • Hyperinsulinemia Decreases or Inhibits • Number of Type II pneumocytes • Choline uptake in Type II pneumocytes • Steroid-enhanced phospholipid synthesis • Number of lamellar bodies • Surfactant Protein A production

  46. Respiratory Distress Syndrome • 1980 to present---reported risk is equal to the non-diabetic population in series of women with good glycemic control

  47. Hypertrophic Cardiomyopathy • IDDM and GDM with poor glycemic control • Incidence 20 to 30 % • Manifestation of generalized organomegally •  catecholamines • hypertension, cardiac remodeling and hypertrophy

  48. Hypertrophic Cardiomyopathy • LV and RV hypertrophy • Asymmetric ventricular septal hypertrophy • Valves and great vessels normal

  49. Hypertrophic Cardiomyopathy • Variable RV outflow obstruction • LV outflow obstruction • asymmetric septal hypertrophy • proximity of the anterior leaflet of the MV to the septum

  50. Hypertrophic Cardiomyopathy • Natural history • Transient; resolution by 6 to 12 months • Most infants asymptomatic • Heart failure occurs in 5 to 10%

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