Infant of dm

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INFANT OF DIABETIC
MOTHER
Presenter: Dr Samiul Ahsan Hussain Modrator : Dr Pranita Kalita
PGT in Paediatrics Proffesor and HOD
Dept of paediatrics
SMCH

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INTRODUCTION
• Diabetes is the most common endocrinal
disorder during pregnancy.
• Yet pregnancy does not have a significant
impact on the presence of diabetes.
COMPARED TO CONTROL:
• The risk of serious birth injury is doubled
• Likelihood of CS is tripled and
• Incidence of NICU admission is
quadrupled.

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EPIDEMIOLOGY
• WHO has predicted that between 1995
and 2025, there will be a 35% increase in
the worldwide prevalence of diabetes .
• Moreover, women born in Asian countries
display the highest prevalence of
Gestational Diabetes Mellitus (GDM), with
up to 17% of women likely to develop
GDM, in comparison to 4% of European
and white American women

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EPIDEMIOLOGY
• Frequency: 3-10% of pregnant
women have diabetes
– 88% have gestational diabetes
– 12% have known diabetes
• 35% with Type I diabetes
• 65% with Type II diabetes

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PATHOPHYSIOLOGY
PROGRESSIVE INSULIN RESISTANT

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• Mother’s insulin turnover rate is increased during pregnency due to
proteolytic degradation of insulin by the placenta and opposing effect of
placental prolactin , progesterone and cortisol.
• Placental steroid and peptide hormone production (estrogens,
progesterone) rises linearly throughout the second and third trimesters,
resulting in a progressively increasing tissue resistance to maternal insulin
action.
• Progressive maternal insulin resistance requires a significant augmentation
in pancreatic insulin production (more than two fold nonpregnant levels)
during feeding to maintain euglycemia. Twenty-four–hour mean insulin
levels are 30% higher in the third trimester than in the non pregnant state.
• If pancreatic insulin output is not adequately augmented, hyperglycemia and
then fetal hyperglycemia result. The severity of hyperglycemia and its timing
depend on the relative inadequacy of insulin production.

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WHITE CLASSIFICATION

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CLASSIFYING AND DIAGNOSING DIABETES
IN PREGNANCY

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DETECTION OF DIABETES IN MOTHER
• Screening of GDM : done between 24-28
weeks gestation by 50 gm, 1 hour glucose
challenge.
• Result: ≥140 mg/dl is positive
• Diagnostic: 100 gm , 3 hour oral glucose
tolerance test(GTT)
• Positive result: 2 or more elevated value in
GTT

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• There is a current movement to move to a
single diagnostic test , consisting of a 75
gm , 2 hour GTT.

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SCREENING
• Risk factors for GDM should be assessed at the initial
prenatal visit.
• Factors that should lead to a first-trimester glucose
challenge test are listed in next slide.

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DEFINITE DIAGNOSIS

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RISK OF COMPLICATIONS
• Depends on degree of glucose control
• White’s classification system helps predict
perinatal mortality
• Higher risk for complications to the fetus in
mothers with pre-gestational diabetes than with
gestational diabetes
– i.e. increased risk for congenital anomalies, future obesity,
and diabetes
• Higher risk of complications during pregnancy
when diabetic
– i.e. preeclampsia 2x more common in diabetic pregnancies
vs. normal pregnancies

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COMPLICATIONS AT DELIVERY
• Premature delivery
• Perinatal asphyxia
• Birth injury

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FETAL EFFECTS OF MATERNAL
HYPERGLYCEMIA

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CONGENITAL ANOMALIES
• normoglycemic pregnancy the risk of a major birth defect is 1% to
2%.
• pregestational diabetes :fourfold to eightfold higher risk.
• The typical defects and their frequency of occurrence, noted in a
prospective study of infants with major malformations are listed in
next slide.
• There is no increase in birth defects among offspring of diabetic
fathers, nondiabetic women, or women in whom gestational
diabetes develops after the first trimester.

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Pathogenesis
• exact mechanisms unknown.
• But reduced levels of arachidonic acid and myo-inositol and accumulation of
sorbitol and trace metals in the embryo have been demonstrated in animal
models (Pinter et al, 1986).
• Fetal hyperglycemia may promote excessive formation of oxygen radicals in
the mitochondria of susceptible tissues, leading to the formation of
hydroperoxides, which inhibit prostacyclin. The resulting overabundance of
thromboxanes and other prostaglandins may then disrupt vascularization of
developing tissues.
• Prevention
• Because the critical period for teratogenesis is the first 3 to 6 weeks after
conception, normal glycemic control must be instituted before pregnancy to
prevent these birth defects.

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Cardiac
• Cardiac Anomalies
– Poor diabetic control in the 1st
trimester is
associated with an increased risk of congenital
malformations
– 2/3 of congenital anomalies are cardiovascular
or CNS related.
– Common cardiac anomalies: Transposition of
the great arteries, ASD, VSD, aortic coarctation

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Cardiac Anomalies
Transposition of the great
arteries

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Neurologic
CNS anomalies
Anencephaly and spina bifida occur 12-20x more frequently
in IDMs
Caudal Regression Syndrome: incomplete development of
the lumbar and sacral vertebrae
 occurs 200x more frequently in IDMs
 spectrum of structural defects possible
 associated with neurologic impairment due to involvement
of distal spine (i.e. incontinence, decreased growth and
movement of legs)

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Anencephaly and Caudal Regression
Syndrome

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Sacral Agenesis

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Macrosomia
• Common Definition:
Infant with Bwt >4000 or
birth weight > 90th
percentile .
• IDMs have increased fat
cells and fat cell
hypertrophy.
• Excess non-fatty tissue in
shoulders and scapular
areas.

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MACROSOMIA
• it occurs in 15% to 45% of diabetic pregnancies.
• Pathophysiology
• Pedersen (1952) hypothesized that maternal
hyperglycemia stimulates fetal hyperinsulinemia, which
in turn mediates acceleration of fuel utilization and
growth. The features of the abnormal growth in diabetic
pregnancy include excessive adipose deposition,
visceral organ hypertrophy, and acceleration of body
mass accretion

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• In addition, in diabetic pregnancies:
• If maternal glucose levels surge excessively after a meal, the consequent
fetal hyperglycemia is accompanied by fetal pancreatic beta-cell hyperplasia
and hyperinsulinemia.
• Fetal hyperinsulinemia, lasting only episodically for 1 to 2 hours, has
detrimental consequences for fetal growth and well-being, in that it
• (1) promotes storage of excess nutrients, resulting in macrosomia, and
• (2) drives catabolism of the oversupply of fuel, using energy and depleting
fetal oxygen stores.
• Episodic fetal hypoxia stimulated by episodic maternal hyperglycemia leads
to an outpouring of adrenal catecholamines, which in turn causes
hypertension, cardiac remodeling, and cardiac hypertrophy.

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Macrosomia- Complications
• Birth Injuries- Brachial
Plexus injury, Fracture
Clavicle or Humerus,
Facial n. injury,
Cephalhematoma.
• Shoulder Dystocia (2-4
fold more)
• Hypoglycemia
• Increased risk for
asphyxia
• Increased recurrence risk
in mother.

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Macrosomia

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Prevention of Macrosomia
• Measures that promote consistent
maternal euglycemia may prevent
macrosomia.

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Fetal Hypoxic Stress
• Episodic maternal hyperglycemia promotes a fetal
catabolic state in which oxygen depletion occurs. Several
fetal metabolic adaptive responses to this episodic
hypoxia occur. For example,
• Stimulation of erythropoietin, red cell hyperplasia, and
elevation in fetal hematocrit. Polycythemia can lead to
poor circulation and postnatal hyperbilirubinemia.
• Profound episodic hyperglycemia in the third trimester
causing severe fetal hypoxic stress has been theorized
as the cause of sudden intrauterine fetal demise in
poorly controlled diabetes.

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Neonatal Effects
Seen in 0.6% to 4% of diabetic
pregnancies

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METABOLIC

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IUGR OR MACROSOMIA:
– Mothers with poorly controlled diabetes and
renal, cardiovascular, retinal disease (class F)
are more likely to have a premature and/or
IUGR baby
– Macrosomia is due to the direct effects of
hyperinsulinemia

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LGA and SGA babies

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HYPOGLYCEMIA
• glucose <40 mg/dl
– 30-40% of IDMs have hypoglycemia
– Usually occurs in 1 to 2 hours of life
– Secondary to persistent hyperinsulinemia while
transplacental glucose supply has stopped
– S/S: lethargy, hypotonia, tremors, seizures,
apnea, tachypnea, shock, cynosis

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TREATMENT
1) Asymtomatic infants with normal blood
glucose level:
a)”Well” IDM: bottle or gavage feeding with
dextrose 10%(5ml/kg) at or before 1 hour
of age.
b) Feed hourly for three or four feeding until
stable sugar level.
c) Switched to formula feeding if feeding
are 2 hour apart or more.

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IV Glucose Administration
• Symptomatic infant
• Low blood glucose level after entral
feeding
• Infant <2 kg

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INFANT WITH SEVERE DISTRESS
• e.g. seizure or respiratory compromise
• 2-4 ml/kg of 25% dextrose in water at a
rate of 1 ml/min/kg.
• Followed by continuous infusion 4-8 mg
glucose /kg/min

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INFANT NOT INSEVERE DISTRESS
• 200 mg of glucose per kg body weight
(2ml/kg of 10% dextrose) over 2 to 3
minutes.
• In difficult cases : HYDROCORTISONE
(5mg/kg day IM in two divided doses)
• If hypoglycemia last more than 7 days
consider other causes.

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TREATMENT

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Metabolic
• Hypocalcemia: Ca <7 mg/dl
_ 22% of IDM
– Usually occurs in first 24-72 hours of life
– Thought to be due to low PTH in infant
– Delay in usual postnatal rise of parathyroid hormone
– or vitamin D antagonism at the intestinal level from
eleveted cortisol and hyperphosphatemia that is due to
tissue catabolism.
– S/S: asymptomatic with self resolution or jitteriness,
tachypnea, seizures/tetany, lethargy, apnea

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Metabolic
• Hypomagnesemia: Mg <1.5 mg/dl
– Occurs in 40% of IDMs
– Thought to be from increased renal losses in
diabetic mother
– Usually transient and asymptomatic
– May need to treat if also hypocalcemic
– Because hypocalcemia may not respond until
the hypomagnesemia is treated.

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RESPIRATORY DISTRESS IN IDMS
ETIOLOGY:
• RDS
• HCM
• TTNB
• Polycythemia
• Pneumonia
• Pneumothorax
• Diaphragmatic hernia

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DIAGNOSIS
• Blood gas analysis
• Blood culture with spinal fluid examination
and culture: when infection is a possibility
• CXR
• Electrocardiogram/Echocardiogram

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Respiratory
• Respiratory Distress Syndrome (RDS)
– Occurs more frequently in IDMs
– Hyperinsulinemia blocks cortisol induction of
lung maturation.
– Diabetic mothers are more likely to go into
premature labor and delivery, which puts infants
at an even greater risk of having immature
lungs at birth

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RDS

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Respiratory
• Transient Tachypnea of the Newborn (TTN)
– Occurs more frequently in IDMs because of risk
factors associated with having diabetes:
Prematurity Macrosomia
Birth asphyxia Polycythemia
Increased likelihood of c-section
– Caused by delayed resorption of fetal lung fluid,
mild pulmonary immaturity, and mild surfactant
deficiency
– Usually resolves by 72 hours of life

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Cardiac
• Hypertrophic cardiomyopathy
– Most infants are asymptomatic, but 5-10% have
respiratory distress, other signs of poor cardiac
output, or heart failure
– Usually resolves by 6 months of age
– Thought to be caused by hyperinsulinemia,
which increases fat and glycogen deposition
into myocardial cells, causes thickening of
interventricular septum &/or ventricular walls

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Hypertrophic Cardiomyopathy

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GI and GU
• GI anomalies
– Situs inversus, atresias, small left colon
syndrome: presents like Hirschsprung disease,
but innervation of the bowel is normal, inability
to pass meconium resolves spontaneously
• GU anomalies
– Renal agenesis and other urinary tract
abnormalities, renal vein thrombosis.

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SMALL LEFT COLON SYNDROME
• Small left colon syndrome presents as
generalized abdominal distension
because of inability to pass meconium.
• Managed by enemas with meglumine
diatrizoate (gastrograffin) or half normal
saline(5ml/kg) and glycerine suppositories.

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Small Left Colon Syndrome

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HEMATOLOGIC
• Polycythemia
– Intervention required when central hematocrit >
65 with symptoms or >70 when asymptomatic
– Occurs in 13-33% of IDMs
– Related to hypoxia in utero -> stimulates
erythropoietin, which increases RBC production
– May be due to reduced oxygen delivery
secondary to elevated HbA1
– Hyperviscosity in vasculature can cause
sludging, ischemia, and infarction of internal
organs

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HEMATOLOGIC
• Hyperbilirubinemia
– Occurs in 11-29% of IDMs
– Risk factors include:
• Prematurity
• Birth injury resulting in bruising or cephalohematoma
• Polycythemia causing increased hemolysis and
release of bilirubin
• Decreased RBC life span because of less
deformable cell membranes, possibly related to
glycosylation of erythrocyte cell membrane.

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Birth Injury
Macrosomia puts infant at risk for injuries
during delivery
Shoulder dystocia can lead to:
 Clavicular and/or humeral fractures
 Brachial plexus injuries
Traumatic delivery or need for vacuum/forceps
assistance can lead to:
 Cephalohematomas
 Facial bruising
 Facial nerve injuries

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Birth Injuries

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OBSTETRIC COMPLICATION
• Preeclempsia
• Polyhydromnios
• Ketoacidosis
• Abnormal labour

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EVALUATION AND MONITORING OF IDM
• Assess at birth: APGAR
• Supportive care: provide warmth, suction
and oxygen as needed.
• Blood glucose checked at
1,2,3,6,12,24,26 and 48 hours
• Hematocrit levels are checked at 1 and 24
hours
• Calcium levels are checked if thee infant
appears jittery or sick
• Bilirubin levels if jaundiced.

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MANAGEMENT
Preconception Management
• Preconception counseling and a detailed medical risk
assessment are recommended for all women with overt
diabetes as well as for those with a history of gestational
diabetes in a previous pregnancy.
• The significant effects on the maternal and neonatal
complications of diabetic pregnancy cannot be realized
until meticulous preconception metabolic control is
achieved in all women contemplating pregnancy

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MANAGEMENT OF DM DURING PREGNANCY
• A) Specific management of pregnancy
• 1)Diabetic control: is achieved with
nutritional modification, exercise, and
medication, with traditional goals of fasting
glucose conc <95mg/dl and postprandial
values <140 mg/dl for 1st
hour and 120
mg/dl for 2 hours.
• b)Recently OHG agent glyburide has been
shown to be effective in the management
of GDM.
• c) Insulin Therapy

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• 2) First trimester Testing:
• a) Measurement of glycosylated hemoglobin:
reflects ambient glucose during organogenesis.
• b)USG: accurate dating of the pregnancy
• c)Ophthalmologic examination:
• d)Renal function:24-hour urine collection for
protein excretion and creatinine clearance.
• e)Thyroid function test:
• f) Nuchal translucency

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• 2)Second trimester Testing:
• a) Maternal screening for neural tube defects is
performed between 15 and 19 weeks gestation.
(10×)
• b) Fetal echo and USG for detecting structural
abnormility.
• c)CVS or Amneocentesis: karyotyping
• 3) Third trimester Testing:
• a) Monthly USG examination for fetal growth
measurement.
• b) Weekly fetal survillance.

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MANAGEMENT OF LABOUR AND
DELIVERY
• Delivery is planned for 39 to 40 weeks.
• Non emergent delivery before 39 week ,
go for FLM test
• a) lecithine-sphingomyelin ratio greater
than 3.5:1
• b) positive amniostat(Phosphotidylglycerol
present)
• c) Saturated Phosphatidylcholine (SPC)
greater than 1000 micro gm/dl

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Prognosis
• Morbidity and mortality lessen with
adequate diabetes control during
pregnancy
• If diabetes is poorly controlled, there is
a higher risk of neurodevelopmental
deficits
• The risk of CP and epilepsy is
increased
• The risk of childhood obesity, diabetes,
and metabolic syndrome is increased

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THANK YOU
THANK YOU

Infant of dm

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