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

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Presentation on theme: "The Infant of the Diabetic Mother Maureen L. Tate LTC MC February, 2003."— Presentation transcript:

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

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

3 Introduction l Discovery of insulin l Understanding of pathophysiology of diabetes l Improved preconception counseling  maternal mortality50% 9%  fetal mortality 21% 2%

4 Introduction  morbidity not as striking l 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 l Overall incidence---5 to 9% –2-3 fold higher than general population –Predominantly with IDDM l Malformations of CNS seen most often l Diversity-No malformation considered pathognomonic

7 Congenital Malformations l 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/ Kitzmiller12/ Greene23/ Ballard19/ Simpson11/ Kitzmiller13/ Gabbe19/2607.3

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

11 Congenital Malformations l 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 Congenital Malformations l Hyperglycemia l Hyperketonemia l Oxygen-Free Radicals

13 Hyperglycemia Specific ultrastructural changes l Decreased embryo size l 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 l Dose and time dependent l Post implantation rat embryo 100% teratogenic dose 950 mg/dl D-glucose Day 10primary neural tube defect Day 11cardiac defects Day 12no defects

16 Hyperketonemia  -hydroxybutyrate –Dose related –Time-of-exposure related –Synergism with glucose u minimally teratogenic doses of both metabolites l Long-term neurodevelopmental abnormalities

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

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

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

20 Congenital Malformations: The Laundry List

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

22 Caudal Regression Syndrome l 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 l Transposition + VSD l Ventricular septal defect l Coarctation + VSD or PDA l Atrial septal defect l Hypertrophic Cardiomyopathy

24 Congenital Malformations Renal l Hydronephrosis l Renal agenesis l Ureteral duplication

25 Congenital Malformations GI l Duodenal atresia l Anorectal atresia l 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? A B

29 What perinatal and neonatal complications should you anticipate?

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

31 l Hypertrophic Cardiomyopathy l Polycythemia l Hyperbilirubinemia l Hypocalcemia Perinatal and Neonatal Complications

32 Disorders of Fetal Growth

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

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

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

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

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

38 Hypoglycemia l Risk Factors –Prematurity –Birth asphyxia –Cesarean section –Disorders of fetal growth –Stimulation of the fetal pancreas u Pedersen Hypothesis

39 Hypoglycemia l Pedersen Hypothesis –Maternal hyperglycemia –Fetal hyperglycemia –Fetal  -cell hyperplasia –Neonatal hyperinsulinemia

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

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

42 Hypoglycemia Diagnosis l Test within minutes of admission l Glucose < 40 confirm with serum glucose l Do not delay treatment pending results

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

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

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

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

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

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

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

51 Hypertrophic Cardiomyopathy l Treatment of heart failure –Propranolol –decreases HR and dynamic outflow obstruction –Digoxin----contraindicated –reduces LV volume –increase dynamic outflow obstruction –exacerbates heart failure

52 Septum

53 Polycythemia l Respiratory distress l Cardiac failure l Decreased renal function l Renal vein thrombosis l Necrotizing enterocolitis l CNS damage l Hypoglycemia l Hypocalcemia l Hypomagnesemia l Hyperbilirubinemia

54 Hyperbilirubinemia l Prematurity l Polycythemia l Birth trauma –Injuries to abdominal viscera –Cephalhematoma –Bruising

55 Summary l Diabetes in pregnancy poses significant risk to both mother and fetus l Overpowering effects that extend from the time of conception through post natal development

56 Summary l Biochemical basis for teratogenicity l Disorders of growth and metabolism lead to considerable morbidity and mortality l Role of the obstetrician –significantly reduce morbidity and mortality u preconception counseling u attention to maternal glucose control

57 l Role of the Pediatrician –Understand the fetal metabolic consequences of maternal diabetes –Anticipate and treat complications

58 Maui Sunset


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