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
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.