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NEWBORN OF A DIABETIC MELITUS
MOTHER
MIRITI M.D
MASTER OF CLINICAL MEDICINE; ACCIDENTS AND
EMERGENCY
MCM/2017/73494
FACILITATORS: DR SIMBA
DR MBURUGU
Objectives
• Introduction
• Definitions
• Epidemiology
• Pathophysiology
• Clinical Manifestations
• Work up & Management
• Prognosis
Introduction
• Women with diabetes in pregnancy (type 1, type
2, and gestational) are at increased risk for
adverse pregnancy outcomes.
• Adequate glycemic control before and during
pregnancy is crucial to improving outcome.
• Diabetic mothers have a high incidence of
polyhydramnios, preeclampsia, pyelonephritis,
preterm labor, and chronic hypertension;
• Their fetal mortality rate is greater than that of
nondiabetic mothers especially after 32 wk of
gestation.
•Fetal loss throughout pregnancy is associated with
poorly controlled maternal diabetes (especially
ketoacidosis) and congenital anomalies.
•Most infants born to diabetic mothers are large
for gestational age.
•If the diabetes is complicated by vascular disease,
infants may be growth restricted, especially those
born after 37 wk of gestation.
•The neonatal mortality rate is >5 times that of
infants of nondiabetic mothers and is higher at all
gestational ages and in every birthweight for
gestational age category.
Definitions
• Gestational diabetes mellitus (GDM):
any abnormal glucose intolerance that begins or is first
recognized during pregnancy using glucose tolerance
test.
• Type 1 diabetes mellitus, also known as juvenile
diabetes or insulin-dependent diabetes, is a chronic
condition in which the pancreas produces little or no
insulin.
• Type 2 diabetes mellitus, also known as adult-onset or
noninsulin-dependent diabetes, is a chronic condition
that affects the way your body metabolizes sugar
(glucose), characterized by high blood sugar, insulin
resistance, and relative lack of insulin.
Epidemiology
• Harmful effects of maternal diabetes recognized
more than 100 years ago.
• Since development of specialized maternal, fetal,
and neonatal care for women with diabetes and
their offspring; a nearly 30 fold decrease in
morbidity and mortality has been noted.
• Currently worldwide 3-10% of pregnancies affected
by abnormal glucose regulation and control.
• Majorly GDM about 80-88%.
• For the preexisting diabetes (about 12-20%); type 1
accounts for about 35%, while type 2 about 65%
Infants born to mothers with glucose
intolerance are at an increased risk of
morbidity and mortality related to the
following:
•Respiratory Distress
•Growth abnormalities (LGA/ SGA)
•Hyperviscosity secondary to Polycythemia
•Congenital malformations
•Hypocalcemia
•Hypomagnesemia
•Iron abnormalities
Pathophysiology
• The probable pathogenic sequence is that maternal
hyperglycemia causes fetal hyperglycemia, and the
fetal pancreatic response leads to fetal
hyperinsulinemia; fetal hyperinsulinemia and
hyperglycemia then cause increased hepatic glucose
uptake and glycogen synthesis, accelerated
lipogenesis, and augmented protein synthesis.
• Hyperinsulinism and hyperglycemia produce fetal
acidosis, which may result in an increased rate of
stillbirth.
•Separation of the placenta at birth suddenly interrupts
glucose infusion into the neonate without a proportional
effect on the hyperinsulinism thus hypoglycemia and
attenuated lipolysis may develop during the 1st few hr
after birth.
•Hyperinsulinemia has been documented in infants of
mothers with gestational diabetes and in those of
mothers with insulin-dependent diabetes (diabetic
mothers) without insulin antibodies.
• The former group also has significantly higher fasting
plasma insulin levels than normal newborns do despite
similar glucose levels; they also respond to glucose with
an abnormally prompt elevation in plasma insulin and
assimilate a glucose load more rapidly.
•After arginine administration, they also have an
enhanced insulin response and increased
disappearance rates of glucose in comparison with
normal infants.
•In contrast, fasting glucose production and utilization
rates are diminished in infants of mothers with
gestational diabetes.
•The lower free fatty acid levels in infants of mothers
with insulin-dependent diabetes reflect their
hyperinsulinemia.
•With good prenatal diabetic control, the incidence of
macrosomia and hypoglycemia has decreased.
•Although hyperinsulinism is probably the main
cause of hypoglycemia, the diminished
epinephrine and glucagon responses that occur
may be contributing factors.
•Congenital anomalies correlate with poor
metabolic control during the periconception
and organogenesis periods and may be the
result of hyperglycemia-induced teratogenesis.
•Chronic fetal hypoxia, indicated by elevated
amniotic fluid erythropoietin values, is
associated with increased fetal and neonatal
morbidity.
Large, plump, plethoric infant of a mother with gestational
diabetes.
Source: Figure 107-2 Nelson Textbook of pediatrics 20th Edition (Black& white)
Clinical Manifestations
• Neonates large and plump as a result of increased
body fat and enlarged viscera, with puffy, plethoric
facies resembling that of patients who have been
receiving corticosteroids.
• May be of normal or low birthweight, particularly if
they are delivered before term or if their mothers
have associated vascular disease.
• Hypoglycemia develops in approximately 25-50%
of infants of diabetic mothers and 15-25% of
infants of mothers with gestational diabetes, but
only a small percentage of these infants become
symptomatic.
NEONATAL HYPOGLYCEMIA
• Level of blood glucose low enough to cause symptoms
•CNS/autonomic: jitteriness, tremors, convulsions,
limpness, lethargy, eye-rolling, diaphoresis, hypothermia,
high-pitched cry
• RESPIRATORY: cyanosis, tachypnea, apnea
•CVS: pallor, cardiac failure/arrest
•GI/nutrition: feeding difficulty
*note: 1. All inter-related! 2. Symptoms can be seen
with other diagnoses, so always keep a differential in
mind, consider other diagnoses if glucose administration
does not improve symptoms
Source: Canadian Pediatric Society (CPS) Position
Statement: 2015
•The infants tend to be jittery, tremulous, and hyper
excitable during the 1st 3 days after birth, although
hypotonia, lethargy, and poor sucking may also occur.
•They may have any of the diverse manifestations of
hypoglycemia. Early appearance of these signs is
more likely to be related to hypoglycemia, and their
later appearance to hypocalcaemia;
these abnormalities may also occur together.
•Perinatal asphyxia may produce similar signs.
Hypomagnesemia may be associated with
the hypocalcaemia. These manifestations may also
occur in the absence of hypoglycemia, hypocalcaemia,
and asphyxia.
Clinical manifestations: Respiratory
• Respiratory Distress Syndrome (RDS)
– Occurs more frequently in IDMs
– Hyperinsulinemia causes delayed maturation of surfactant
synthesis
Diabetic moms likely to go into premature labor hence greater
risk of having immature lungs at birth
• 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
Clinical Features- Cardiovascular Sys
• 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, causing
thickening of interventricular septum &/or ventricular walls
• 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
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)
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
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
– Hyperviscosity in vasculature can cause sludging, ischemia,
and infarction of internal organs
• 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
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:
-Cephalhematoma
-Facial bruising
-Facial nerve injuries
Work-Up and Management
• Follow blood sugars
• If SGA or LGA, also check hematocrit
• Further work-up and management depends on
patient’s clinical presentation and physical exam
– Hypoglycemia – early feeding or IVFs with dextrose
– Symptomatic electrolyte abnormalities – replete
electrolytes
– Respiratory distress – Cardiopulmonary support, CXR/echo
to search for cause
– Hyperbilirubinemia – phototherapy
– Polycythemia – IVF hydration or exchange transfusion
– Neuro/GI/GU anomalies – imaging studies, specialist
consult
Prognosis
• Morbidity and mortality lessen with adequate
diabetes control during pregnancy
• If diabetes is poorly controlled, there is a higher risk
of neurodevelopment deficits
• The risk of CP and epilepsy is increased
• The risk of childhood obesity, diabetes, and
metabolic syndrome is increased
REFERENCES
• Canadian Pediatric Society (CPS) Position Statement
on Neonatal Hypoglycaemia: 2015
• Harris DL, Weston PJ, Harding JE: Incidence of
neonatal hypoglycemia in babies identified as at
risk, J Pediatr 161:787–791, 2012.
• Nelson Textbook of Pediatrics 20th Edition, Chapter
107.
• Rozance PJ, Hay WW Jr: Neonatal hypoglycemia—
answers, but more questions, J Pediatr 161:775–
776, 2012.

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Newborn of a diabetic melitus mother

  • 1. NEWBORN OF A DIABETIC MELITUS MOTHER MIRITI M.D MASTER OF CLINICAL MEDICINE; ACCIDENTS AND EMERGENCY MCM/2017/73494 FACILITATORS: DR SIMBA DR MBURUGU
  • 2. Objectives • Introduction • Definitions • Epidemiology • Pathophysiology • Clinical Manifestations • Work up & Management • Prognosis
  • 3. Introduction • Women with diabetes in pregnancy (type 1, type 2, and gestational) are at increased risk for adverse pregnancy outcomes. • Adequate glycemic control before and during pregnancy is crucial to improving outcome. • Diabetic mothers have a high incidence of polyhydramnios, preeclampsia, pyelonephritis, preterm labor, and chronic hypertension; • Their fetal mortality rate is greater than that of nondiabetic mothers especially after 32 wk of gestation.
  • 4. •Fetal loss throughout pregnancy is associated with poorly controlled maternal diabetes (especially ketoacidosis) and congenital anomalies. •Most infants born to diabetic mothers are large for gestational age. •If the diabetes is complicated by vascular disease, infants may be growth restricted, especially those born after 37 wk of gestation. •The neonatal mortality rate is >5 times that of infants of nondiabetic mothers and is higher at all gestational ages and in every birthweight for gestational age category.
  • 5. Definitions • Gestational diabetes mellitus (GDM): any abnormal glucose intolerance that begins or is first recognized during pregnancy using glucose tolerance test. • Type 1 diabetes mellitus, also known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin. • Type 2 diabetes mellitus, also known as adult-onset or noninsulin-dependent diabetes, is a chronic condition that affects the way your body metabolizes sugar (glucose), characterized by high blood sugar, insulin resistance, and relative lack of insulin.
  • 6. Epidemiology • Harmful effects of maternal diabetes recognized more than 100 years ago. • Since development of specialized maternal, fetal, and neonatal care for women with diabetes and their offspring; a nearly 30 fold decrease in morbidity and mortality has been noted. • Currently worldwide 3-10% of pregnancies affected by abnormal glucose regulation and control. • Majorly GDM about 80-88%. • For the preexisting diabetes (about 12-20%); type 1 accounts for about 35%, while type 2 about 65%
  • 7. Infants born to mothers with glucose intolerance are at an increased risk of morbidity and mortality related to the following: •Respiratory Distress •Growth abnormalities (LGA/ SGA) •Hyperviscosity secondary to Polycythemia •Congenital malformations •Hypocalcemia •Hypomagnesemia •Iron abnormalities
  • 8. Pathophysiology • The probable pathogenic sequence is that maternal hyperglycemia causes fetal hyperglycemia, and the fetal pancreatic response leads to fetal hyperinsulinemia; fetal hyperinsulinemia and hyperglycemia then cause increased hepatic glucose uptake and glycogen synthesis, accelerated lipogenesis, and augmented protein synthesis. • Hyperinsulinism and hyperglycemia produce fetal acidosis, which may result in an increased rate of stillbirth.
  • 9.
  • 10. •Separation of the placenta at birth suddenly interrupts glucose infusion into the neonate without a proportional effect on the hyperinsulinism thus hypoglycemia and attenuated lipolysis may develop during the 1st few hr after birth. •Hyperinsulinemia has been documented in infants of mothers with gestational diabetes and in those of mothers with insulin-dependent diabetes (diabetic mothers) without insulin antibodies. • The former group also has significantly higher fasting plasma insulin levels than normal newborns do despite similar glucose levels; they also respond to glucose with an abnormally prompt elevation in plasma insulin and assimilate a glucose load more rapidly.
  • 11. •After arginine administration, they also have an enhanced insulin response and increased disappearance rates of glucose in comparison with normal infants. •In contrast, fasting glucose production and utilization rates are diminished in infants of mothers with gestational diabetes. •The lower free fatty acid levels in infants of mothers with insulin-dependent diabetes reflect their hyperinsulinemia. •With good prenatal diabetic control, the incidence of macrosomia and hypoglycemia has decreased.
  • 12. •Although hyperinsulinism is probably the main cause of hypoglycemia, the diminished epinephrine and glucagon responses that occur may be contributing factors. •Congenital anomalies correlate with poor metabolic control during the periconception and organogenesis periods and may be the result of hyperglycemia-induced teratogenesis. •Chronic fetal hypoxia, indicated by elevated amniotic fluid erythropoietin values, is associated with increased fetal and neonatal morbidity.
  • 13. Large, plump, plethoric infant of a mother with gestational diabetes. Source: Figure 107-2 Nelson Textbook of pediatrics 20th Edition (Black& white)
  • 14. Clinical Manifestations • Neonates large and plump as a result of increased body fat and enlarged viscera, with puffy, plethoric facies resembling that of patients who have been receiving corticosteroids. • May be of normal or low birthweight, particularly if they are delivered before term or if their mothers have associated vascular disease. • Hypoglycemia develops in approximately 25-50% of infants of diabetic mothers and 15-25% of infants of mothers with gestational diabetes, but only a small percentage of these infants become symptomatic.
  • 15. NEONATAL HYPOGLYCEMIA • Level of blood glucose low enough to cause symptoms •CNS/autonomic: jitteriness, tremors, convulsions, limpness, lethargy, eye-rolling, diaphoresis, hypothermia, high-pitched cry • RESPIRATORY: cyanosis, tachypnea, apnea •CVS: pallor, cardiac failure/arrest •GI/nutrition: feeding difficulty *note: 1. All inter-related! 2. Symptoms can be seen with other diagnoses, so always keep a differential in mind, consider other diagnoses if glucose administration does not improve symptoms Source: Canadian Pediatric Society (CPS) Position Statement: 2015
  • 16.
  • 17. •The infants tend to be jittery, tremulous, and hyper excitable during the 1st 3 days after birth, although hypotonia, lethargy, and poor sucking may also occur. •They may have any of the diverse manifestations of hypoglycemia. Early appearance of these signs is more likely to be related to hypoglycemia, and their later appearance to hypocalcaemia; these abnormalities may also occur together. •Perinatal asphyxia may produce similar signs. Hypomagnesemia may be associated with the hypocalcaemia. These manifestations may also occur in the absence of hypoglycemia, hypocalcaemia, and asphyxia.
  • 18. Clinical manifestations: Respiratory • Respiratory Distress Syndrome (RDS) – Occurs more frequently in IDMs – Hyperinsulinemia causes delayed maturation of surfactant synthesis Diabetic moms likely to go into premature labor hence greater risk of having immature lungs at birth • 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
  • 19. Clinical Features- Cardiovascular Sys • 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, causing thickening of interventricular septum &/or ventricular walls • 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
  • 20. 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)
  • 21. 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
  • 22. 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 – Hyperviscosity in vasculature can cause sludging, ischemia, and infarction of internal organs • 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
  • 23. 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: -Cephalhematoma -Facial bruising -Facial nerve injuries
  • 24. Work-Up and Management • Follow blood sugars • If SGA or LGA, also check hematocrit • Further work-up and management depends on patient’s clinical presentation and physical exam – Hypoglycemia – early feeding or IVFs with dextrose – Symptomatic electrolyte abnormalities – replete electrolytes – Respiratory distress – Cardiopulmonary support, CXR/echo to search for cause – Hyperbilirubinemia – phototherapy – Polycythemia – IVF hydration or exchange transfusion – Neuro/GI/GU anomalies – imaging studies, specialist consult
  • 25.
  • 26. Prognosis • Morbidity and mortality lessen with adequate diabetes control during pregnancy • If diabetes is poorly controlled, there is a higher risk of neurodevelopment deficits • The risk of CP and epilepsy is increased • The risk of childhood obesity, diabetes, and metabolic syndrome is increased
  • 27. REFERENCES • Canadian Pediatric Society (CPS) Position Statement on Neonatal Hypoglycaemia: 2015 • Harris DL, Weston PJ, Harding JE: Incidence of neonatal hypoglycemia in babies identified as at risk, J Pediatr 161:787–791, 2012. • Nelson Textbook of Pediatrics 20th Edition, Chapter 107. • Rozance PJ, Hay WW Jr: Neonatal hypoglycemia— answers, but more questions, J Pediatr 161:775– 776, 2012.