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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

The Infant of the Diabetic Mother

Maureen L. Tate LTC MC

February, 2003

maternal diabetes
Maternal Diabetes
  • Harmful effects on the fetus recognized over 100 years ago
  • GDM----3 to 10 %
  • IDDM --0.1 to 0.3 %
introduction
Introduction
  • Discovery of insulin
  • Understanding of pathophysiology of diabetes
  • Improved preconception counseling

1964 1984

¯ maternal mortality 50% 9%

¯ fetal mortality 21% 2%

introduction4
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
congenital malformations
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
congenital malformations7
Congenital Malformations
  • No increase in major congenital malformations among offspring of
    • Diabetic fathers
    • Prediabetic women
    • GDM after first trimester
slide8
Suggests that glycemic control during embryogenesis is the main factor in the origin of malformations
slide9
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

congenital malformations10
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 %

congenital malformations11
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

congenital malformations12
Hyperglycemia

Hyperketonemia

Oxygen-Free Radicals

Congenital Malformations
hyperglycemia
Hyperglycemia

Specific ultrastructural changes

  • Decreased embryo size
  • Yolk sac malformations
    • sparse, patchy, non-uniform capillaries
    • ¯ rough ER, ribosomes, and mitochondria
    • abnormal transport of nutrients
hyperglycemia14
Hyperglycemia

Other consequences:

  • Arachadonic acid deficiency
  • Accumulation of sorbitol
  • Deficiency of myo-inositol

associated with CNS malformations

maternal hyperglycemia
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

hyperketonemia
Hyperketonemia
  • b-hydroxybutyrate
    • Dose related
    • Time-of-exposure related
    • Synergism with glucose
      • minimally teratogenic doses of both metabolites
  • Long-term neurodevelopmental abnormalities
fetal hyperglycemia
Fetal Hyperglycemia
  • 1-2 hours of fetal hyperglycemia can have detrimental effects
  •  insulin secretion
    • Storage of excess nutrients  macrosomia
    • Post natal hypoglycemia
fetal hyperglycemia18
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
oxygen free radicals
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
congenital malformations21
Congenital Malformations

Skeletal/CNS

  • Caudal regression syndrome

not considered pathognomonic

occurs 600x more frequently among IDDM

  • Neural tube defects
  • Microcephaly
slide22
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

congenital malformations23
Congenital Malformations

Cardiac

  • Transposition + VSD
  • Ventricular septal defect
  • Coarctation + VSD or PDA
  • Atrial septal defect
  • Hypertrophic Cardiomyopathy
congenital malformations24
Congenital Malformations

Renal

  • Hydronephrosis
  • Renal agenesis
  • Ureteral duplication
congenital malformations25
Congenital Malformations

GI

  • Duodenal atresia
  • Anorectal atresia
  • Small left colon syndrome
slide26
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.
slide27
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.
slide30

Perinatal and Neonatal Complications

  • Disorders of fetal growth
  • Intrauterine and perinatal asphyxia
  • Hypoglycemia
  • Respiratory distress syndrome
perinatal and neonatal complications
Perinatal and Neonatal Complications
  • Hypertrophic Cardiomyopathy
  • Polycythemia
  • Hyperbilirubinemia
  • Hypocalcemia
macrosomia
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
macrosomia34
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
intrauterine growth restriction
Intrauterine Growth Restriction
  • Incidence reported as high as 20 %
  • Contributing factors:
    • Maternal vascular disease
    • Hypertension
    • Intrauterine infection
    • Chromosomal abnormalities
intrauterine growth restriction36
Intrauterine Growth Restriction
  • Oligohydramnios
  • Hypoxia
  • Fetal distress
  • Asphyxia
  • Intrauterine and neonatal death
birth asphyxia
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
hypoglycemia
Hypoglycemia
  • Risk Factors
    • Prematurity
    • Birth asphyxia
    • Cesarean section
    • Disorders of fetal growth
    • Stimulation of the fetal pancreas
      • Pedersen Hypothesis
hypoglycemia39
Hypoglycemia
  • Pedersen Hypothesis
    • Maternal hyperglycemia
    • Fetal hyperglycemia
    • Fetal b-cell hyperplasia
    • Neonatal hyperinsulinemia
hypoglycemia40
Hypoglycemia
  • Maternal glucose interrupted at parturition
  • Neonatal hyperinsulinemia results in neonatal hypoglycemia
  • Suppression of FFA
  • Decreased glycogenolysis
  • Decreased response to glucagon and catecholamines
signs of hypoglycemia
Tremors

Jitteriness

Irritability

Lethargy

Apnea

Cyanosis

Hypothermia

Weak or high pitched cry

Poor feeding

Seizures

Signs of Hypoglycemia
hypoglycemia42
Hypoglycemia

Diagnosis

  • Test within 30-60 minutes of admission
  • Glucose < 40 confirm with serum glucose
  • Do not delay treatment pending results
hypoglycemia43
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.
respiratory distress syndrome
Respiratory Distress Syndrome
  • Risk:
    • 3 to 5 times the risk in the non-diabetic population
  • Contributing Factors:
    • Prematurity
    • Maternal glycemic control
respiratory distress syndrome45
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
respiratory distress syndrome46
Respiratory Distress Syndrome
  • 1980 to present---reported risk is equal to the non-diabetic population in series of women with good glycemic control
hypertrophic cardiomyopathy
Hypertrophic Cardiomyopathy
  • IDDM and GDM with poor glycemic control
  • Incidence 20 to 30 %
  • Manifestation of generalized organomegally
  •  catecholamines
    • hypertension, cardiac remodeling and hypertrophy
hypertrophic cardiomyopathy48
Hypertrophic Cardiomyopathy
  • LV and RV hypertrophy
  • Asymmetric ventricular septal hypertrophy
  • Valves and great vessels normal
hypertrophic cardiomyopathy49
Hypertrophic Cardiomyopathy
  • Variable RV outflow obstruction
  • LV outflow obstruction
    • asymmetric septal hypertrophy
    • proximity of the anterior leaflet of the MV to the septum
hypertrophic cardiomyopathy50
Hypertrophic Cardiomyopathy
  • Natural history
    • Transient; resolution by 6 to 12 months
    • Most infants asymptomatic
    • Heart failure occurs in 5 to 10%
hypertrophic cardiomyopathy51
Hypertrophic Cardiomyopathy
  • Treatment of heart failure
    • Propranolol
        • decreases HR and dynamic outflow obstruction
    • Digoxin----contraindicated
        • reduces LV volume
        • increase dynamic outflow obstruction
        • exacerbates heart failure
polycythemia
Respiratory distress

Cardiac failure

Decreased renal function

Renal vein thrombosis

Necrotizing enterocolitis

CNS damage

Hypoglycemia

Hypocalcemia

Hypomagnesemia

Hyperbilirubinemia

Polycythemia
hyperbilirubinemia
Hyperbilirubinemia
  • Prematurity
  • Polycythemia
  • Birth trauma
    • Injuries to abdominal viscera
    • Cephalhematoma
    • Bruising
summary
Summary
  • Diabetes in pregnancy poses significant risk to both mother and fetus
  • Overpowering effects that extend from the time of conception through post natal development
summary56
Summary
  • Biochemical basis for teratogenicity
  • Disorders of growth and metabolism lead to considerable morbidity and mortality
  • Role of the obstetrician
    • significantly reduce morbidity and mortality
      • preconception counseling
      • attention to maternal glucose control
slide57
Role of the Pediatrician
    • Understand the fetal metabolic consequences of maternal diabetes
    • Anticipate and treat complications