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Prepared By: Dr. Shaju Edavana
 Introduction
 Pathophysiology
 Epidemiology
 Complications
 Management
 Diabetes - most common medical
complication of pregnancy
 Still an increased risk of complications
 Any abnormal intolerance that begins or is
first recognized during pregnancy using
glucose tolerance test
 Using 100 mg glucose load
 Two or more of the plasma glucose
concentration must be met for the diagnosis.
 Insulin level inhibit the maturational effect of
control on the lungs (RDS)
Gestational age Pathophysiology
Before 9 weeks Malformation
Before 20 weeks fetal islet cells are incapable of responding
hyperglycemia leading to IUGR.
After 20 weeks Fetus responds to hyperglycemia with
pancreatic beta cell hyperplasia and insulin
levels.
Seen in 3-10 % of pregnancies
In Kuwait incidence of Diabetes is high
23 % of population are diabetic-
35% type 1 and 65% type 2
 Major congenital malformations are found in
5-9 % of affected infants
Affected Group Mortality Rates
Still birth and perinatal 5 times more than general
population
Neonates 15 times
Infants 3 times
 Fetal macrosomia
 Fetal congenital malformation
 Impaired fetal growth
 Pulmonary disease
 Metabolic and electrolyte abnormalities
 Haematological problems
 Cardiovascular abnormalities
 Congenital malformations
 Large for gestational age
 Birth weight more than 90th percentile or
above 4000 gm
 More likely to have hyperbilirubinemia,
hypogycemia and acidosis
 Birth injury, shoulder dystocia
 Brachial plexus palsy and Subdural
haemorrhage
 Facial palsy
 Impaired Fetal growth (associated with ‘Too
tight control’ )
 Maternal vascular disease
is the common cause of
impaired fetal growth
 Poor glycaemic control
 Associated with high risk of UTI and
maternal preeclampsia
 Increased number of Respiratory Distress
Syndrome
 More incidence of TTN, PPHN and
pneumothorax
 In contrast, Fetal lung maturation may occur
in diabetic pregnancies complicated by
vasculopathy
 Blood glucose level less than 2.6 mmol/L
 Caused by hyper insulinemia due to hyperplacia of Fetal
pancreatic beta cells
 Neonate develops hypoglycaemia - continuous supply of
glucose is stopped after birth
 Strict glycaemic control decreases but does not abolish the risk
 Symptoms –
• Jitteriness
• Irritability
• Poor feeding
• Weak cry
• Hypotonia
• Seizure
 Definition → total serum calcium < 1.8 mmol/L
or ionized calcium < 1 mmol/L
 Caused by lower PTH level
 Symptoms → jitteriness or seizures
 Definition → serum magnesium
concentration less than 0.75 mmol/L
 Mechanism is increased urinary loss
secondary to diabetes
 Prematurity may be a contributing factor
 Hypocalcaemia may not respond to
treatment until the hypomagnesaemia is
corrected.
 65% of all IDMs demonstrate abnormalities of
iron metabolism at birth
 Iron deficiency increases an infants risks for
neuro-developmental abnormalities
 Haematocrit more than 65%
 Plethoric appearance, sluggish capillary refill
or respiratory distress
 Excess red blood cells precursors lead to
hyperbilirubinemia or thrombocytopenia.
 Hypertrophic cardiomyopathy with intra
ventricular hypertrophy may occur in 50% of IDM
 Infants are often asymptomatic, but 5 to 10%
have respiratory distress or sign of heart failure
 Symptomatic infants typically recover after 2-3
weeks of supportive care
 VSD
 TGA
 PDA
 Caudal Regression Syndrome → structural
defects of caudal region → 200 times more
frequent
 Severe form is known as Sirenomelia or Mermaid
Syndrome
 Risk of Spinabifida →20 times higher
 Anencephaly → 13 times
 Microcephaly, holoprosencephaly
 Renal → hydronephrosis, renal agnesis,
ureteral duplication
 GI → duodenal or anorectal atresia, Small
Left Colon Syndrome (presents as transient
inability to pass meconium, lower bowel
obstruction)
 Unilateral micro-opthalmia
 Bilateral Microtia
 Cleft Palate
 Micro Penis
 Unilateral Cryptorchidism
 Bilateral Radial Hypoplasia
 Unilateral Polydactyly
 Bifid Tongue
 Single Umbilical Artery
 Investigation
1. CBC
2. RBS
3. ABG
4. Calcium
5. Magnesium
6. Chest X-ray
7. Abdominal X-ray
8. Echo
9. Barium Enema
 Periconception control
 HbA1C – maintain 7% -tight glycemic control
and avoid pre-eclampsia
 Intervention is required if:
1. plasma value < 36 mg/dL or 2 mmol/L
2. infant develop symptoms
3. glucose level does not increase after feeding
 Target glucose level 45 mg/dL or 2.5 mmol/L
 Profound hypoglycaemia requires IV therapy
with hydrocortisone
 Immediate IV therapy with 2-4 ml/Kg in
symptomatic infants
 Maintain continuous infusion of 6-8 mg/Kg/min
 If the follow-up glucose level remains low,
dextrose infusion increase by 2 mg/kg/min
 Maintain 80-100 ml/kg/day
 If infant requires dextrose concentration more
than 12.5% insert central line
 Early breast feeding- colustrum as well as
breast milk provides generous concentration
of glucose
 Monitor plasma glucose routinely
 Adequate enteral feeding
 Cardiologic screening
 Excellent prognosis
Management of Diabetes in Pregnancy and Infants
Management of Diabetes in Pregnancy and Infants

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Management of Diabetes in Pregnancy and Infants

  • 1. Prepared By: Dr. Shaju Edavana
  • 2.  Introduction  Pathophysiology  Epidemiology  Complications  Management
  • 3.  Diabetes - most common medical complication of pregnancy  Still an increased risk of complications
  • 4.  Any abnormal intolerance that begins or is first recognized during pregnancy using glucose tolerance test  Using 100 mg glucose load  Two or more of the plasma glucose concentration must be met for the diagnosis.
  • 5.  Insulin level inhibit the maturational effect of control on the lungs (RDS) Gestational age Pathophysiology Before 9 weeks Malformation Before 20 weeks fetal islet cells are incapable of responding hyperglycemia leading to IUGR. After 20 weeks Fetus responds to hyperglycemia with pancreatic beta cell hyperplasia and insulin levels.
  • 6. Seen in 3-10 % of pregnancies In Kuwait incidence of Diabetes is high 23 % of population are diabetic- 35% type 1 and 65% type 2
  • 7.  Major congenital malformations are found in 5-9 % of affected infants Affected Group Mortality Rates Still birth and perinatal 5 times more than general population Neonates 15 times Infants 3 times
  • 8.  Fetal macrosomia  Fetal congenital malformation  Impaired fetal growth  Pulmonary disease  Metabolic and electrolyte abnormalities  Haematological problems  Cardiovascular abnormalities  Congenital malformations
  • 9.  Large for gestational age  Birth weight more than 90th percentile or above 4000 gm  More likely to have hyperbilirubinemia, hypogycemia and acidosis  Birth injury, shoulder dystocia  Brachial plexus palsy and Subdural haemorrhage  Facial palsy
  • 10.  Impaired Fetal growth (associated with ‘Too tight control’ )  Maternal vascular disease is the common cause of impaired fetal growth
  • 11.  Poor glycaemic control  Associated with high risk of UTI and maternal preeclampsia
  • 12.  Increased number of Respiratory Distress Syndrome  More incidence of TTN, PPHN and pneumothorax  In contrast, Fetal lung maturation may occur in diabetic pregnancies complicated by vasculopathy
  • 13.  Blood glucose level less than 2.6 mmol/L  Caused by hyper insulinemia due to hyperplacia of Fetal pancreatic beta cells  Neonate develops hypoglycaemia - continuous supply of glucose is stopped after birth  Strict glycaemic control decreases but does not abolish the risk  Symptoms – • Jitteriness • Irritability • Poor feeding • Weak cry • Hypotonia • Seizure
  • 14.  Definition → total serum calcium < 1.8 mmol/L or ionized calcium < 1 mmol/L  Caused by lower PTH level  Symptoms → jitteriness or seizures
  • 15.  Definition → serum magnesium concentration less than 0.75 mmol/L  Mechanism is increased urinary loss secondary to diabetes  Prematurity may be a contributing factor  Hypocalcaemia may not respond to treatment until the hypomagnesaemia is corrected.
  • 16.  65% of all IDMs demonstrate abnormalities of iron metabolism at birth  Iron deficiency increases an infants risks for neuro-developmental abnormalities
  • 17.  Haematocrit more than 65%  Plethoric appearance, sluggish capillary refill or respiratory distress  Excess red blood cells precursors lead to hyperbilirubinemia or thrombocytopenia.
  • 18.  Hypertrophic cardiomyopathy with intra ventricular hypertrophy may occur in 50% of IDM  Infants are often asymptomatic, but 5 to 10% have respiratory distress or sign of heart failure  Symptomatic infants typically recover after 2-3 weeks of supportive care  VSD  TGA  PDA
  • 19.  Caudal Regression Syndrome → structural defects of caudal region → 200 times more frequent  Severe form is known as Sirenomelia or Mermaid Syndrome  Risk of Spinabifida →20 times higher  Anencephaly → 13 times  Microcephaly, holoprosencephaly
  • 20.  Renal → hydronephrosis, renal agnesis, ureteral duplication  GI → duodenal or anorectal atresia, Small Left Colon Syndrome (presents as transient inability to pass meconium, lower bowel obstruction)
  • 21.  Unilateral micro-opthalmia  Bilateral Microtia  Cleft Palate  Micro Penis  Unilateral Cryptorchidism  Bilateral Radial Hypoplasia  Unilateral Polydactyly  Bifid Tongue  Single Umbilical Artery
  • 22.  Investigation 1. CBC 2. RBS 3. ABG 4. Calcium 5. Magnesium 6. Chest X-ray 7. Abdominal X-ray 8. Echo 9. Barium Enema
  • 23.  Periconception control  HbA1C – maintain 7% -tight glycemic control and avoid pre-eclampsia
  • 24.  Intervention is required if: 1. plasma value < 36 mg/dL or 2 mmol/L 2. infant develop symptoms 3. glucose level does not increase after feeding  Target glucose level 45 mg/dL or 2.5 mmol/L  Profound hypoglycaemia requires IV therapy with hydrocortisone
  • 25.  Immediate IV therapy with 2-4 ml/Kg in symptomatic infants  Maintain continuous infusion of 6-8 mg/Kg/min  If the follow-up glucose level remains low, dextrose infusion increase by 2 mg/kg/min  Maintain 80-100 ml/kg/day  If infant requires dextrose concentration more than 12.5% insert central line
  • 26.  Early breast feeding- colustrum as well as breast milk provides generous concentration of glucose  Monitor plasma glucose routinely  Adequate enteral feeding  Cardiologic screening  Excellent prognosis