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MOTHER
Page 1
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:
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EPIDEMIOLOGY
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Page 4
PATHOPHYSIOLOGY
PROGRESSIVE INSULIN
RESISTANT
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Page 5
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.
Page 6
WHITE CLASSIFICATION
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Page 7
CLASSIFYING AND DIAGNOSING DIABETES
IN PREGNANCY
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DETECTION OF DIABETES IN MOTHER
Page 10
• There is a current movement to
move to a single diagnostic test ,
consisting of a 75 gm , 2 hour GTT.
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Page 11
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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Page 12
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Page 13
DEFINITE DIAGNOSIS
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Page 14
RISK OF COMPLICATIONS
Page 15
COMPLICATIONS AT
DELIVERY
• Premature delivery
• Perinatal asphyxia
• Birth injury
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Page 16
FETAL EFFECTS OF MATERNAL
HYPERGLYCEMIA
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Page 17
CONGENITAL ANOMALIES
Page 18
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
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Page 19
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Page 20
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,
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Page 21
Cardiac Anomalies
Page 22
Neurologic
CNS anomalies
Anencephaly and spina bifida occur 12-20x
more frequently in IDMs
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Page 23
Anencephaly and Caudal Regression
Syndrome
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Page 24
Sacral Agenesis
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Page 25
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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Page 26
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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Page 27
• 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
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catecholamines,
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Page 29
Macrosomia
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Page 30
Prevention of Macrosomia
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Page 31
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,
Page 33
Neonatal Effects
Page 34
METABOLIC
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Page 35
IUGR OR MACROSOMIA:
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Page 36
LGA and SGA babies
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Page 37
HYPOGLYCEMIA
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Page 38
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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Page 39
IV Glucose Administration
• Symptomatic infant
• Low blood glucose level after entral
feeding
• Infant <2 kg
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Page 40
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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Page 41
INFANT NOT INSEVERE DISTRESS
Page 42
TREATMENT
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Page 43
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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Page 44
Metabolic
Page 45
RESPIRATORY DISTRESS IN IDMS
ETIOLOGY:
• RDS
• HCM
• TTNB
• Polycythemia
• Pneumonia
• Pneumothorax
• Diaphragmatic hernia
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Page 46
DIAGNOSIS
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Respiratory
Page 48
RDS
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Page 49
Respiratory
Page 50
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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Page 51
Hypertrophic Cardiomyopathy
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Page 52
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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Page 53
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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Page 55
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
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sludging, ischemia, and infarction of internal
organs Page 56
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
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Page 57
Birth Injury
Page 58
Birth Injuries
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OBSTETRIC COMPLICATION
• Preeclempsia
• Polyhydromnios
• Ketoacidosis
• Abnormal labour
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Page 60
EVALUATION AND MONITORING OF IDM
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Page 62
MANAGEMENT OF DM DURING PREGNANCY
Page 64
• 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.
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Page 65
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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Page 66
Prognosis
Page 67
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