Infant of a Diabetic Mother - PowerPoint

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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
   Improved preconception counseling
                            1964        1984
     maternal mortality    50%         9%
     fetal mortality       21%         2%
                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
What is the etiology of
congenital malformations
associated with diabetes?
    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 Malformations

   No increase in major congenital
    malformations among offspring of
    – Diabetic fathers
    – Prediabetic women
    – GDM after first trimester
Suggests that glycemic
control during embryogenesis
is the main factor in the origin
of malformations
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 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 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 Malformations
 Hyperglycemia
 Hyperketonemia
 Oxygen-Free   Radicals
              Hyperglycemia
Specific ultrastructural changes
   Decreased embryo size
   Yolk sac malformations
     sparse, patchy, non-uniform capillaries
      rough ER, ribosomes, and mitochondria
     abnormal transport of nutrients
           Hyperglycemia

Other consequences:
– Arachadonic acid deficiency
– Accumulation of sorbitol
– Deficiency of myo-inositol
  associated with CNS malformations
        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
   b-hydroxybutyrate
    – Dose related
    – Time-of-exposure related
    – Synergism with glucose
          minimally teratogenic doses of both metabolites
   Long-term neurodevelopmental
    abnormalities
            Fetal Hyperglycemia

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

   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
Malformations:
 The Laundry List
      Congenital Malformations
Skeletal/CNS
   Caudal regression syndrome
    not considered pathognomonic
    occurs 600x more frequently among IDDM
   Neural tube defects
   Microcephaly
                               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 Malformations
Cardiac
   Transposition + VSD
   Ventricular septal defect
   Coarctation + VSD or PDA
   Atrial septal defect
   Hypertrophic Cardiomyopathy
    Congenital Malformations

Renal
   Hydronephrosis
   Renal agenesis
   Ureteral
    duplication
       Congenital Malformations

GI
   Duodenal atresia
   Anorectal atresia
   Small left colon
    syndrome
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.
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.
Which baby is the infant of the diabetic mother?




            A                      B
What perinatal
 and neonatal
 complications
  should you
  anticipate?
      Perinatal and Neonatal
           Complications

 Disorders of fetal growth
 Intrauterine and perinatal asphyxia
 Hypoglycemia
 Respiratory distress syndrome
    Perinatal and Neonatal
         Complications
 Hypertrophic Cardiomyopathy
 Polycythemia
 Hyperbilirubinemia
 Hypocalcemia
Disorders of Fetal Growth
               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
                    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

 Incidence reported as high as 20 %
 Contributing factors:
    –   Maternal vascular disease
    –   Hypertension
    –   Intrauterine infection
    –   Chromosomal abnormalities
Intrauterine Growth Restriction
 Oligohydramnios
 Hypoxia
 Fetal distress
 Asphyxia
 Intrauterine and neonatal
  death
                    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
   Risk Factors
    –   Prematurity
    –   Birth asphyxia
    –   Cesarean section
    –   Disorders of fetal growth
    –   Stimulation of the fetal pancreas
            Pedersen Hypothesis
              Hypoglycemia

   Pedersen Hypothesis
    –   Maternal hyperglycemia
    –   Fetal hyperglycemia
    –   Fetal b-cell hyperplasia
    –   Neonatal hyperinsulinemia
                  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           Cyanosis
   Jitteriness       Hypothermia
   Irritability      Weak or high
   Lethargy           pitched cry
   Apnea             Poor feeding
                      Seizures
               Hypoglycemia
Diagnosis
   Test within 30-60 minutes of admission
   Glucose < 40 confirm with serum glucose
   Do not delay treatment pending results
                   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
   Risk:
    – 3 to 5 times the risk in the non-diabetic
      population
   Contributing Factors:
    – Prematurity
    – Maternal glycemic control
    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 Syndrome

 1980 to present---reported risk
 is equal to the non-diabetic
 population in series of women
 with good glycemic control
     Hypertrophic Cardiomyopathy
   IDDM and GDM with poor glycemic control
   Incidence 20 to 30 %
   Manifestation of generalized organomegally
    catecholamines
    – hypertension, cardiac remodeling and
      hypertrophy
Hypertrophic Cardiomyopathy
 LV and RV hypertrophy
 Asymmetric ventricular septal
  hypertrophy
 Valves and great vessels normal
      Hypertrophic Cardiomyopathy

   Variable RV outflow obstruction
   LV outflow obstruction
    – asymmetric septal hypertrophy
    – proximity of the anterior leaflet of the MV to
      the septum
       Hypertrophic Cardiomyopathy
   Natural history
    – Transient; resolution by 6 to 12 months
    – Most infants asymptomatic
    – Heart failure occurs in 5 to 10%
    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
Septum
                Polycythemia
   Respiratory distress       CNS damage
   Cardiac failure            Hypoglycemia
   Decreased renal            Hypocalcemia
    function
                               Hypomagnesemia
   Renal vein thrombosis
   Necrotizing                Hyperbilirubinemia
    enterocolitis
     Hyperbilirubinemia
 Prematurity
 Polycythemia
 Birth   trauma
  – Injuries to abdominal viscera
  – Cephalhematoma
  – Bruising
             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
                      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
   Role of the Pediatrician
    – Understand the fetal metabolic
      consequences of maternal diabetes
    – Anticipate and treat complications
Maui Sunset

				
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