Professional Documents
Culture Documents
Outline of Lecture
1. Understand the biochemical basics of glucose
homeostasis
2. Understand relationship between maternal and fetal
glucose metabolism and normal physiologic changes
that occur post-natally
3. Review neonatal hypoglycemia data, including recent
literature and AAP position statement March, 2011
4. Discuss development and implementation of
Northwestern Memorial Hospital policy on hypoglycemia
Energy
Consumed
Generated
Generated
Gluconeogenesis
Glycogenolysis
**(adult norms)
://physicianjobster.com/physician-guidelines/homeostasis-diagram-of-insulin-and-glucagon-in-controlling-blood-glucose/
http
Glycolysis
http://en.wikipedia.org/wiki/Glycolysis
Coenzyme yield
2 NADH
Source of ATP
Phosphorylation of glucose
and fructose 6-phosphate
uses two ATP from the
cytoplasm.
Substrate-level
phosphorylation
Oxidative phosphorylation
2 NADH
Oxidative phosphorylation
Glycolysis
preparatory
phase
ATP yield
-2
2
Krebs cycle
6 NADH
2 FADH2
Total yield
18
4
38 ATP
Substrate-level
phosphorylation
Oxidative phosphorylation
Oxidative phosphorylation
Lactate
Pyruvate
Amino acids
Glycerol
Propionate
Glutamine
Amino Acids
Depleted
glycogen
stores
Catabolism of
muscle proteins
Amino Acids
Glucogenic:
Ketogenic:
Carbon skeletons make
fatty acids
leucine, lysine
Isoleucine, phenylalanine,
threonine, tryptophan,
tyrosine
Fatty Acids
Glycerol
Glycerol
Glycogen
Outline of Lecture
1. Understand the biochemical basics of glucose
homeostasis
2. Understand relationship between maternal and fetal
glucose metabolism and normal physiologic changes
that occur postnatally
3. Review neonatal hypoglycemia, including recent
literature and AAP position statement March, 2011
4. Discuss development and implementation of
Northwestern Memorial Hospital policy on hypoglycemia
2nd half
Maternal stores mobilized to
meet babys needs
Surge of anti-insulin factors
Human placental
lactogen, progesterone,
estrogen
Pregnant women have higher
blood glucose levels than
nonpregnant women (fasted)
Pregnancy becomes a
diabetogenic-like state
Maternal glucose provides majority of glucose for fetus via facilitated diffusion
Fetus can use alternate substrates if necessary, but depends entirely on
maternal supply and placental transfer of glucose, amino acids, free fatty
acids, ketones, and glycerol for energy needs.
Normal lower limit of fetal glucose concentration remains around 3 mmol/L
(54 mg/dL) over most of gestation, particularly after 20 weeks
Enzymes for gluconeogenesis are present by the third month of gestation, but
there is almost no fetal glucose production under normal conditions
NICHD Report, 2009
Immediately Postnatally
Glucose cut off
Fetal glucagon, epinephrine,
and cortisol increase; insulin decreases
Promote glycogenolysis
Stimulate gluconeogenesis
Glucose Turnover
I have a
big head
to body
ratio
Premature Neonate
6-8 mg/kg/min
Full-term Neonate
4-6 mg/kg/min
Adult
2-3 mg/kg/min
LGA
Outline of Lecture
1. Understand the biochemical basics of glucose
homeostasis
2. Understand relationship between maternal and fetal
glucose metabolism and normal physiologic changes
that occur post-natally
3. Review neonatal hypoglycemia, including recent
literature and AAP position statement March, 2011
4. Discuss development and implementation of
Northwestern Memorial Hospital policy on hypoglycemia
Neonatal Hypoglycemia
Etiology
Clinical manifestations
Laboratory features
Approach to therapy (NICHD workshop report)
Potential sequelae
Etiology of Hypoglycemia
Inadequate
Production
Excessive Use
COLD STRESS
Limited glycogen
Hyperinsulinism
SGA
Prematurity
IDM
Glycogen storage
Beckwith-Wiedeman
disease
Nesidioblastosis
Limited gluconeogenesis
Erythroblastosis Fetalis
Inadequate substrate
(have b-cell hyperplasia)
SGA
Exchange transfusion
Inborn errors
Maternal medications
Asphyxia
Chlorpropamide
Benzothiazides
B-sympathomimetics
Malpositioned umbilical
catheters
Other
LGA
Sepsis
Polycythemia
Hyperviscosity
syndrome
Congenital
hypopituitarism
Multiple sources
Clinical Manifestations
Jitteriness
Tremors
Apnea
Cyanosis
Limpness/ lethargy
Seizures
None
Laboratory Features
Glucose concentrations in whole
blood 10-15% lower than in plasma
Glucose oxidation by erythrocytes
can cause falsely low levels
Glucometers tend to be less
accurate at lower levels
Full work-up of persistent
hypoglycemia extensive
pH, insulin, cortisol
ketones, FFA, lactate, pyruvate,
ammonia, LFTs, urine organic acids,
serum amino acids
Approach to Therapy
Approach to Treatment
Controversial
What We Agree On
Year
Publication
Value (blood)
Srinivasan
1986
J Pediatrics
Stanley
1999
NEJM Editorial
<60
Ogata
2005
Averys
<40
Fanaroff and
Martin
<36
McGowan and
Hay
Handbook of
Neonatal Care
<36-40
2006
of normal healthy breastfed babies will have a blood glucose level< 36 in the 1st
24 hours. These same babies have higher circulating levels of ketones (Hawdon,
1992; Swenne, 1994)
Unclear When
Neuroimpairment Occurs
Unclear Whether Following
Operation Threshold
Prevents Adverse Sequelae
Year
Population
Outcome/ Conclusion
Burns
2008
Symptomatic
hypoglycemic
Lucas
1988
Salhab
2004
Hypoglycemic
Acidotic Infants
Duvanel
1999
Preterm SGA
infants,
Stenninger
1997
Hypoglycemic IDMs
compared to
nonhypoglycemic
non-IDMs
Neonatal hypoglycemia associated with a slightly higher incidence of longterm neurological dysfunction related to minimal brain dysfunction/deficits in
attention, motor control, and perception compared with non-hypoglycemic,
non-IDM control infants
Brand
2005
LGA infants
(not IDM)
Groenendaal
2006
LGA infants
(not IDM)
November, 2009
2009
November, 2009
Your Work
November, 2009
March 1, 2011
Abstract
Outline of Lecture
1. Understand the biochemical basics of glucose
homeostasis
2. Understand relationship between maternal and fetal
glucose metabolism and normal physiologic changes
that occur postnatally
3. Review neonatal hypoglycemia, including recent
literature and AAP position statement March, 2011
4. Discuss development and implementation of
Northwestern Memorial Hospital policy on hypoglycemia
At Risk Infants
IDM
LGA
Late preterm 34 36 6/7 weeks gestation
SGA
APGAR < 6 at 5 mins
Symptomatic infants are always screened
Congenital anomalies, antenatally diagnosed endocrine
disorders
Infants typically admitted to NICU where routine glucose monitoring is
performed
Symptomatic Infants
Infants with a glucose
of less than 50 are
transferred to NICU
Are not typically
forcefed, IV route
preferred
Bolus of 2 ml/kg D10,
followed by GIR of 5.6
mk/kg/min
< 50
<35
<35
< 35
<45
<45
35-50
>55
45-55
Duration of Screening
Risk factor
Birth time
Age of infant
30 mins
after 1st
feed
3hr
34-36 6/7
weeks or
SGA
LGA or
IDM
APGAR <
6 at 5 mins
6hr
9hr
21hr 24hr
Discontinue if last 3
readings were > 55
Implications on Breastfeeding
Previous policy more detrimental to
breastfeeding
Cut-off of 55 used even in 1st 4 hours
Volume of 10 ml/kg formula
recommended
Current policy has reduced admissions
Extensive educational efforts used to promote
breastfeeding and weaning of IVF without aggressive
supplementation in NICU
GIR weaned by 2 mg/kg/min each 6 hours
SNS, 30 ml
SNS, 10 ml
NICU-IVF
50 ml, 42 ml
Nursed 11x
in Newborn unit
Acknowledgements
Catherine Willows RN, BA, IBCLC
Samantha Schoenfelder, RN, MSN
Kathy Christoffel, MD, MPH
Gina Siggia, MSN, WHNP, C-EFM
Yasmin Khan, MD
Praveen Kumar, MD
Hospital Breastfeeding Council of
Metro Chicago
References
1.
2.
3.
4.
5.
6.
7.
8.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004559
https://www.abp.org/abpwebsite/certinfo/subspec/suboutlines/neon20
10.pdf
Hay WW Jr, et al Knowledge gaps and research needs for understanding
and treating neonatal hypoglycemia; workshop report from the Eunice
Kennedy Shriver NICHD, 2009
Avery, Fletcher, MacDonald, eds. 1999. Neonatology, Pathophysiology
and Management of the Newborn, 5th edition (Ed Ogatas chapter)
Fanaroff and Martin, eds. 2002. Neonatal-Perinatal Medicine, Diseases of
the Fetus and Infant, 7th edition
http://www.indstate.edu/thcme/mwking/home.html
http://physicianjobster.com/physician-guidelines/homeostasis-diagramof-insulin-and-glucagon-in-controlling-blood-glucose/
http://en.wikipedia.org/wiki/Glycolysis
References
9.
10.
11.
12.
13.
14.
References
15. Sunehag A, Gustafsson J, Ewald U. Glycerol carbon contributes to hepatic
glucose production during the first eight hours in health, term infants.
Acta Paediatr 1996;85:1339-43.
16. Sunehag A, Ewald U, Gustafsson J. Extremely preterm infants (<28 weeks)
are capable of gluconeogenesis from glycerol on their first day of life. Pediatr Res
1996;40:553-7.
17. Kalhan SC, Parimi P, Van Beek R, et al. Estimation of gluconeogenesis in
newborn infants. Am J Physiol 2001;281:E991-7.
18. Glucose Testing and Management of Neonatal Hypoglycemia,
Northwestern Memorial Hospital Protocol/Guideline, 2001
Others noted within text or see me!