Professional Documents
Culture Documents
Objectives
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Definitions
Gestational:
●GDM A1 – Impaired glucose tolerance: diet
controlled
●GDM A2 – medication tx
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GDM Incidence
by Race/Ethnicity in CA 2005
▪ California 5.88 GDM per 100 deliveries
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▪ Asphyxia
▪ Birth injury
▪ Cardiomyopathy
▪ Caudal regression
▪ Congenital anomalies
▪ Double outlet right ventricle
▪ Heart failure
▪ Hyperbilirubinemia
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Teratogenesis
▪ Process by which congenital malformations are produced in an
embryo or fetus
▪ Congenital malformations account for approx. 50% of perinatal
deaths in IDMs
▪ Mechanism not well understood
▪ Abnormal metabolic environment is teratogenic
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Teratogenesis
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Slide 11
Diabetic Embryopathy
Diabetic Fetopathy
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Maternal Hyperglycemia
▪ Maternal hyperglycemia results in fetal
hyperglycemia
• glucose readily crosses through the placenta
• Insulin does not
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Slide 16
2 figure it out
Tanya Hatfield, 6/25/2018
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Fetal hyperinsulinemia
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1. Growth
▪ Poor maternal glycemic control predicts neonatal
macrosomia
▪ > 95%-tile considered abnormal
▪ IDM generally have increased fat mass so will have
higher weight than length and head circumference
percentiles
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Growth-Macrosomia
▪ Infants with BW ≥4000gms or >90%tile, with
excess fat accumulation in abdominal and
scapular regions, along with visceromegaly
Growth-Macrosomia
▪ Occurs in >25% of diabetic pregnancies and puts babies at risk for
birth injuries
▪ Disproportionate growth: higher chest-to-head and shoulder-to-
head ratios
▪ More likely to have hyperbilirubinemia, hypoglycemia, acidosis,
respiratory distress, shoulder dystocia, brachial plexus injury
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▪ SGA
▪ BW <10th percentile
▪ May occur in up to 20% of diabetic pregnancies
▪ Associated with pregnant mothers with renal, retinal or cardiac
diseases
▪ More likely to deliver SGA, premature, poor fetal outcome, fetal
distress, or fetal death
Growth-Metabolic Imprinting
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Growth-Metabolic Imprinting
Growth-Metabolic Imprinting
▪ Pima Indian Studies
• 45% of offspring of mothers with GDM develop Type 2
diabetes btwn 20 and 24 years of age (1988)
• In follow-up study more than 2/3 of offspring of mothers
with GDM developed Type 2 diabetes by 34 years of
age (2000)
▪ Thought to stem from exposure to hyperglycemia
and increased insulin secretion leading to
abnormal glucose uptake and utilization in
peripheral tissue, especially muscle
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2. Glucose Metabolism
▪ The fetus glucose concentration is proportional to
maternal concentrations and measures about 70-80%
of maternal levels
▪ Almost all of this comes from facilitated diffusion
across the placenta
▪ Glycogen stored in liver, heart, lung and skeletal
muscle
• Glycogen content slowly increases during first two
trimesters
• Majority made and stored in the liver during the
third trimester
Glucose Metabolism
▪ IDM infant undergoes sudden interruption of
glucose delivery, which when accompanied by
high neonatal insulin levels results in neonatal
hypoglycemia
▪ Up to 50% of IDMs experience significant
hypoglycemia after birth
▪ Nadir in blood glucose usually occurs between 1
and 3 hours of life
▪ Hyperinsulinemia may persists up to 72 hours
and may last up to 1 week
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5. Cardiovascular Issues
▪ Hypertrophic cardiomyopathy
• caused by fat and glycogen deposition into myocardial
cells causing thickening of intraventricular septum with
reduction in the size of ventricular chambers
• results in potential obstructed left ventricular outflow
• infants often asymptomatic but 5-10% have respiratory
distress or signs of poor cardiac output
• usually transient and resolves as plasma insulin levels
normalize
• Symptomatic infants recover after 2-3 weeks of supportive
care and ECHO findings resolve within 6 to 12 months
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5. Cardiovascular Issues
▪ Hypertrophic cardiomyopathy
Cardiovascular
▪ Other defects associated with IDM:
• TGA
• VSD, ASD
• Coarctation of the aorta
• Single ventricle, hypoplastic left ventricle
• Pulmonic stenosis
• Pulmonary valve atresia
• DORV
• Truncus Arteriosus
• Tricuspid Atresia
• PDA
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6. Hematologic Changes
Hematologic Changes
▪ Hyperviscosity
• ↑ risk of vascular sludging, ischemia, seizures,
necrotizing enterocolitis, renal vein thrombosis,
infarction of vital organs
• Pulmonary vascular bed sludging can lead to PPHN
▪ Low iron stores
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7. Birth Trauma
▪ Shoulder dystocia
• occurs in 1/3 of IDMs that are macrosomic
▪ Cephalhematoma
▪ Brachial plexus injury
▪ Erb’s palsy
▪ Facial nerve palsy
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8. Neurologic Issues
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Neurologic Malformations
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Neurodevelopmental outcome
▪ Outcome of infants of well-controlled diabetic mothers
appear similar to that of normal infants
▪ Poorly controlled may result in developmental
abnormalities
• Head circumference at 3 years of age negative
correlated with HbA1c levels during pregnancy
• Smaller H.C. associated with poorer intellectual
performance
9. GI/GU Issues
▪ GI Anomalies
• Situs inversus
• atresias (duodenal, anorectal)
• small left colon syndrome
• Imperforate anus
▪ GU Anomalies:
• Ureteral duplication
• Renal agenesis
• Hydronephrosis
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Glucose Utilization
Glucose Homeostasis
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Glucose Homeostasis
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▪ Adaptation response
▪ Increase in plasma glucagon
▪ Decrease in plasma insulin
▪ Mobilization of glucose and fatty acids from glycogen
and triglyceride deposits
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What is Hypoglycemia?
▪ NO UNIVERSAL DEFINITION
▪ Operational threshold is defined as that
concentration of plasma or whole blood glucose at
which clinicians should consider intervention, based
on the evidence currently available in literature
• This threshold is currently believed to be a blood
glucose value of less than 40 mg/dL (plasma
glucose less than 45 mg/dL).
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Clinical Hypoglycemia
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Incidence of Hypoglycemia
Etiology of Hypoglycemia
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Etiology of Hypoglycemia
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Suckling Ketogenesis
▪ Ketones are an alternative fuel for
the brain during a fast or periods of
hypoglycemia
▪ Produced from breakdown of fatty
acids in the colostrum (high fat
content), peaks on 3rd day
▪ Response is blunted with formula
▪ May protect newborn brain for
injurious affects of hypoglycemia
(Hawdon, Ward Platt, & Aynsley-Green, 1992)
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Anaerobic glycolysis
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Etiology of
Hypoglycemia ↑metabolism
Cold Stress…
Anaerobic
↑glucose
metabolism
Cold stress
↑ O2
Hypoxemia
consumption
↑ respiratory
rate
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Perinatal Asphyxia…
▪ What group of babies are at higher risk of
perinatal asphyxia? Shoulder dystocia?
IDM babies!!
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Hypoglycemia is Associated with Increased Risk for Brain Injury and Adverse
Neurodevelopmental Outcome in Neonates at Risk for Encephalopathy
• Hypoglycemia (glucose <46) seen in the first 24 hours after birth
in 16% of the cohort.
• After adjusting for potential confounders of early perinatal distress
and need for resuscitation
• Neonatal hypoglycemia was associated with:
• 3.72-fold increased odds of corticospinal tract injury
(P = .047)
• 4.82-fold increased odds of worsened neuromotor score
(P = .038)
• Lower cognitive and language score on the Bayley Scales of
Infant Development (P = .015).
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Neonatal Management
▪ Prior to delivery:
• Assess need for neonatal resuscitation based on
GA, anticipated BW, presence of a congenital
anomaly or labor complications/mode of delivery
▪ After delivery:
• Routine care:
‒ warm/dry/stim, clearing airway, rapid assessment
and examination to identify congenital anomalies
‒ Glucose monitoring per unit policy
‒ Routine newborn care
Neonatal Management
- Further evaluation:
‒ Cyanosis/resp distress: assess for cardiac and
respiratory disease
▪ CXR
▪ Pre/post ductal oxygen saturations
▪ 4 limb BP
▪ EKG
▪ ECHO
‒ Bilirubin, hematocrit checks
‒ Electrolytes in symptomatic infants
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Physical Assessment
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Dude!
I’mWill
you be my
Hungry
bodyguard?
TOO!!!
Erb’s Palsy
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Plethoric Baby
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▪ Jitteriness/tremors
▪ Sweating
▪ Irritability
▪ Tachypnea
▪ Pallor
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Neuroglycopenic symptoms
▪ Seizures
▪ Hypotonia
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▪ Apnea
▪ Bradycardia
▪ Cyanosis
▪ Hypothermia
▪ NO SYMPTOMS AT ALL
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Jittery Infant
▪ http://med.stanford.edu/newborns/professional-
education/photo-gallery/neuro-
reflexes.html#jittery_movements
Seizing Infant
▪ http://med.stanford.edu/newborns/professional-education/photo-
gallery/neuro-reflexes.html#seizure_activity
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Glucose testing
▪ Point of care testing
▪ iStat
▪ Plasma glucose concentration
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Diagnosis
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▪ Insert chart
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Management of Hypoglycemia
▪ Important to have unit policy and procedure
▪ Enteral
• breastfeeding
• donor breast milk
• dextrose water
• formula
• dextrose gel
▪ Parenteral
• D10W bolus 2ml/kg
• Start D10W at 80ml/kg/day
Management of Hypoglycemia
▪ Recheck glucose within 30 minutes after
intervention
▪ If glucose does not improve, may need to bolus
again and increase IV rate and/or dextrose
concentration
▪ May need to consider central access if requires
concentration exceeds D12.5W
▪ Do not use D25W, D50W or large volume
boluses as this creates rebound hypoglycemia
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Management of Hypoglycemia
▪ Weaning IV infusions: when BG levels have been
stable for 12-24 hours, Begin decreasing IV
infusion by 1-2 ml/hr q 3-4 hours if BG > 50-
60mg/dL.
▪ Further testing should be done in infants who
continue to require glucose infusions at rates
exceeding 8-10mg/kg/min to maintain normal
glucose levels beyond 1st week of life
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UCSF NC2
(Northern CA Neonatology Consortium)
▪ Representatives from multiple northern
California hospitals
▪ Meet quarterly to recommend consensus
statements on neonatal conditions
▪ Consensus statements available on UCSF
website
▪ Statements include:
▪ Hypoglycemia
▪ Hyperbilirubinemia
▪ Early onset sepsis
▪ Soon… Apnea of prematurity
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Oral Sucrose
Legal Implications
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Case Study I
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Case study
▪ C/S for intolerance of labor:
‒ Birthweight 4065 gm
‒ Infant profoundly cyanotic after birth.
‒ Echocardiogram reveals transposition of the
great arteries (TGA).
▪ Questions to ask:
• Why was she induced?
• How significant is A1C in 3rd trimester?
• Why were the lungs immature?
• What caused the TGA?
Case Study II
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Case Study
Case Study
▪ CUA: 6.92/82/-18.5
▪ Initial BG 92 HR 160 RR 66
▪ HS blood gases attempted but clotted
▪ 7.05/40/-19 via HS @ 3 HOL
▪ BG 38 @ 3 HOL
▪ 2 ml/kg D10W bolus followed by infusion of D10W
@ 80 ml/kg/d
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Case Study
Case Study
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Brain Care
Legal Implications
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Legal Implications
▪ In one review of neonatal litigation cases from 2
years, 37 % of the cases dealt with neonatal
hypoglycemia.
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In summary…
▪ Neonatal hypoglycemia remains a controversial
topic, as no literature defines what blood glucose
is too low, for how long, and at what level or time
does irreversible neurodevelopmental injury
occur
▪ Clinical consensus and guidelines recommend
levels that symptomatic and at-risk infants
should be treated
▪ Dextrose/glucose gels are potentially providing a
new management approach for hypoglycemia,
while promoting exclusive breastfeeding
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References
▪ Ashwal, E. Hod, M. Gestational diabetes mellitus: Where are we now?, Clin Chim
Acta (2015), http://dx.doi.org/10.1016/j.cca.2015.01.021
▪ Barker, D. J., Osmond, C., Forsen, T. J., Kajantie, E., & Eriksson, J. G. (2005).
Trajectories of growth among children who have coronary events as adults. The New
England Journal of Medicine, 353(17), 1802-1809.
▪ Barnes-Powell, L. L. (2007). Infants of diabetic mothers: The effects of hyperglycemia
on the fetus and neonate. Neonatal Network : NN, 26(5), 283-290.
▪ Bardenheier, B., Elixhauser, A., Imperatore, G., Devlin, H., Kuklina, E., Geiss, L., &
Correa, A. (2012). Variation in Prevalence of Gestational Diabetes Mellitus Among
Hospital Discharges for Obstetric Delivery Across 23 States in the United States.
Diabetes Care, 36(5), 1209-1214. doi: 10.2337/dc12-0901
▪ Cornblath, M., Hawdon, J. M., Williams, A. F., Aynsley-Green, A., Ward-Platt, M. P.,
Schwartz, R., et al. (2000). Controversies regarding definition of neonatal
hypoglycemia: Suggested operational thresholds. Pediatrics, 105(5), 1141-1145.
▪ Cowett, R. M., & Loughead, J. L. (2002). Neonatal glucose metabolism: Differential
diagnoses, evaluation, and treatment of hypoglycemia. Neonatal Network : NN, 21(4),
9-19.
▪ Esakoff, T. F., Cheng, Y. W., Sparks, T. N., & Caughey, A. B. (2009). The association
between birthweight 4000 g or greater and perinatal outcomes in patients with and
without gestational diabetes mellitus. American Journal of Obstetrics and Gynecology,
References
▪ Garg, M., & Devaskar, S. U. (2006). Glucose metabolism in the late preterm infant.
Clinics in Perinatology, 33(4), 853-70; abstract ix-x.
▪ Harris, D. L., Weston, P. J., & Harding, J. E. (2012). Incidence of neonatal
hypoglycemia in babies identified as at risk. The Journal of Pediatrics,
▪ Hatfield, L., Schwoebel, A., & Lynyak, C. (2011). Caring for the infant of a diabetic
mother. MCN.the American Journal of Maternal Child Nursing, 36(1), 10-16.
▪ Hay, W. W.,Jr. (2012). Care of the infant of the diabetic mother. Current Diabetes
Reports, 12(1), 4-15.
▪ Hay, W. W.,Jr, McGowan, J. E., Kalhan, S., Adamkin, D., Hawdon, J. M., Williams, A.
F., et al. (2008). How low can I go? the impact of hypoglycemia on the immature brain.
Pediatrics, 122(6), 1411-2; author reply 1412.
▪ Hay, W. W.,Jr, Raju, T. N., Higgins, R. D., Kalhan, S. C., & Devaskar, S. U. (2009).
Knowledge gaps and research needs for understanding and treating neonatal
hypoglycemia: Workshop report from eunice kennedy shriver national institute of child
health and human development. The Journal of Pediatrics, 155(5), 612-617.
▪ Kaaja, R. (2009). Vascular complications in diabetic pregnancy. Thrombosis Research,
123 Suppl 2, S1-3.
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References
▪ Laptook, A., & Jackson, G. L. (2006). Cold stress and hypoglycemia in the late
preterm ("near-term") infant: Impact on nursery of admission. Seminars in
Perinatology, 30(1), 24-27.
▪ Maayan-Metzger, A., Lubin, D., & Kuint, J. (2009). Hypoglycemia rates in the first
days of life among term infants born to diabetic mothers. Neonatology, 96(2), 80-85.
▪ Milcic, T. L. (2008). Neonatal glucose homeostasis. Neonatal Network : NN, 27(3),
203-207.
▪ Nold, J., & Georgieff, M.K. (2004). Infants of diabetic mothers. Pediatric Clinics of
North America, 51, 619-637.
▪ Riskin, A. Infant of a diabetic mother, Post, TW (Ed), UpToDate, Waltham, MA, 2014.
▪ Rozance, P. J., & Hay, W. W. (2006). Hypoglycemia in newborn infants: Features
associated with adverse outcomes. Biology of the Neonate, 90(2), 74-86.
▪ Rozance, P. J., & Hay, W. W.,Jr. (2012). Neonatal hypoglycemia-answers, but more
questions. The Journal of Pediatrics
Questions?
Thank you!!
Tanya.Hatfield@ucsf.edu
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