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Thermoregulation and Hypoglycemia in the Neonate

April Davidson, RNC-NIC

Cold Stress: Does it really matter?

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Cold Stress: YES, It really does matter!

Gain an understanding of:

• Infants at increased risk for hypothermia

• The normal physiologic response to cold stress                   for term and preterm infants

• Environmental factors affecting temperature management

• Mechanisms of heat gain and loss

• Heat sources and thermoregulation guidelines

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What is Neutral Thermal Temperature?

The body temperature at which an individual’s oxygen use and energy expenditure are minimized

Knobel, 2014

Goal of Thermoregulation

Maintain correct body temperature (NTE) range in order to:•Maximize metabolic efficiency•Reduce oxygen consumption•Reduce calorie expenditure• Knobel, 2014

Body temperature in the newborn infant

• NORMAL – 36.5 to 37.5˚C (97.7 –99.5˚F)

• Cold Stress 36.0 to 36.4˚C (96.8 – 97.6 ˚F)• Cause for concern

• Moderate hypothermia 32 –35.9˚C (89.6-96.6˚F)• Danger, warm infant

• Severe hypothermia – below 32˚C (89.6 ˚F)• Outlook grave, skilled care

urgently needed Weber, 2000

Classification of

hypothermia is based on

core temperature

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Physiology of Neonatal Heat Production • Brown fat functions as a site of

heat production• This conversion of brown fat to

heat requires oxygen and glucose

• Cold stimulates sympathetic response and norepinephrine is released

• Norepinephrine release results in fatty acid oxidation

• The production of heat occurs during oxidation

Verklan & Walden, 2010

Cold Consequences = Hypoglycemia• Metabolic rate increases to produce heat• Glycogen stores and blood glucose are

exhausted• Hypoglycemia results Knobel, 2014

Cold Consequences = Acidosis

• During cold stress, brown fat is converted to heat and free fatty acids

• Fatty acids and lactic acid accumulate • Metabolic acidosis develops• Acidosis causes vasoconstriction of the

pulmonary beds which leads to hypoxemia• Increases risk for PPHN in the term and near

term infantKnobel, 2014

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Cold Consequences = Hypoxia

• During cold stress extra oxygen is needed for heat production

• Cold infant with normal lungs = increase RR for increased O2 needs

• Cold infant with lung pathology = may not be able to maintain oxygenation for brain/body

• Increasing respiratory distress:–Grunting & retracting–Nasal flaring & tachypneaKnobel, 2014

Hypothermia increases morbidity and mortality

• Metabolic Acidosis• Hypoglycemia• Neurological complications• Altered LFTs, clotting disorders• Death

There is an important relationship between maintainingadequate oxygenation, temperature and blood glucose

levels. A change in one affects the other.Verklan & Walden, 2010

Knobel, 2014

Since Hypothermia increases morbidity and mortality, it is a priority!

In terms of ABC’s think:A-AirwayB-BreathingC-Circulation

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Why Are Infants At Greater Risk for Thermoregulation

Problems?

Infants at Risk for Hypothermia*Preterm/low birth weight*Small for gestational age*Prolonged resuscitation*Acutely ill*Open abdominal/body wall defects*Hypotonia from sedatives, analgesics,

paralytics, or anesthetics

Kenner & Lott, 2006

Preterm Infant Risk Factors

• Large surface area-to-bodymass ratio

• Decreased subcutaneous fat/little brown fat• Greater body water content• Immature skin leading to evaporative water and

heat losses• Poorly developed metabolic mechanism for

responding to thermal stress• Super imposed illness/RDS related to

prematurity Karlsen, 2006

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Preterm Infant Risk Factors

• Delivery Room Issues–Wet skin and wet linen–Cool room temperature–Blockage of heat source by personnel – Invasive procedures (umbilical lines/intubation)

–Cold bed, cold hands and cold equipment–Emergency deliveries = less preparation–Priority on resuscitation efforts often placed above temperature maintenance

Karlsen, 2006

Maintenance of normal body temperature is priority for ALL infants

Routine care

activities which

conserve infant’s

body heat include:

•Removing wet linen•Bundling in warm

blankets•Placing skin-to-skin

on mother’s chest•Covering head with

a hat•Dressing in clothes

Methods of Neonatal Heat LossKarlsen, 2006

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COLD STRESSKnobel, 2014 –Toper & Honeyfield, 2009

IN CONCLUSION…….

• Keeping healthy babieswarm is an instinctualbehavior for caregivers • Preventing cold stress in sick or premature infants can be challenging and is often lost among the myriad of stabilization needs

MAKE THERMOREGULATION A PRIORITY

Gain an understanding of:

• Infants at increased risk for hypoglycemia

• Factors affecting neonatal glucose homeostasis

• Treatment guidelines for monitoring and managing neonatal hypoglycemia

• Review of umbilical venous catheter placement for high dextrose concentration infusions

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Preparation for birth!• Fetal plasma glucose is 60 – 80% of the maternal level.

• The fetus stores glucose in the form of glycogen (liver, heart, lung, and skeletal muscle).

• Most of the glycogen is made and stored in the 3rd trimester

Rozance, 2016

Preparation for birth!• The fetus has limited ability to convert

glycogen to glucose and must rely upon placental transfer of glucose to meet energy needs.

• When the infant is born, the cord is cut and so is the major supply of glucose!

Rozance, 2016

Preparation for birth!• Transition from fetus

to newborn is ahuge energy drain

• The newborn is required to meet increased metabolic demands while changing the energy source from a placenta-supplied source to an external food source.

Rozance, 2016

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AfterBirth…..• Glucose Utilization is 4-6 mg/kg/min• At birth infant’s glucose is ~70% of mothers• 2-4 hours after birth, glucose declines to as low

as ~30mg/dl• Intrinsic metabolic transition starts infant’s own

glucose homeostasis• Until exogenous glucose source is provided, the

hepatic glucose output serves as glucose sourceBarnes, 2007

Glucose Homeostasis• Controlled primarily by insulin and glucagon• Adrenaline, cortisol, and growth hormone also

play a roll• Insulin stimulates the liver to store glucose as

glycogen (decrease blood glucose)• Glucagon stimulates glycogenolysis and

gluconeogenesis (increase blood glucose)• During periods of low glucose intake, fatty acids

can be broken down into ketone bodies (alternate fuel source body/brain)

Barnes, 2007

Risk Factors for Hypoglycemia

• Preterm infants (less than 37 weeks)• Infant’s of a diabetic mother (all types)• LGA• SGA• IUGR• Infant’s with RDS, HIE, or other illness• Poor breastfeeding infants• Cold stressed infants Karlsen, 2006

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Categories of Hypoglycemia Risk

• Inadequate Glycogen

• Increased Utilization of Glucose

•Excessive Insulin

Inadequate Glycogen

• Glycogen stores increase rapidly in the last month of the 3rd trimester

• Preterm infants are born before this occurs. • SGA/IUGR: Chronically stressed infants have

higher metabolic demands and decreased glycogen stores

• Post-mature: increasedmetabolic demand &glycogen use

Karlsen, 2006

Increased Utilization of Glucose

• Sick/Stressed infants*Increase in metabolic demand*Rapid hypoglycemia*Double impact when preterm, SGA/IUGR, or IDM

Karlsen, 2006

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Excessive Insulin• Maternal hyperglycemia = fetal hyperglycemia• Fetal hyperglycemia = hyperinsulinemia • Fetal hyperinsulinemia = increased glycogen

synthesis and storage in the liver and increased fat synthesis (Macrosomia) .

• Cord clamping interrupts the transplacental glucose supply without an effect on infant’s insulin production=

HYPERINSULINEMIABarnes, 2007

Excessive Insulin

What is Normal???• Defining a normal glucose level remains

controversial –50 – 110 mg/dl (Karlsen, 2006)–> 40 mg/dl (Verklan & Walden, 2010)–> 30 term, > 20 preterm (Kenner & Lott, 2004)

–> 45 mg/dl (Cowett, R. as cited by Barnes-Powell, 2007)

Barnes, 2007

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What does the AAP tell us?• No recommendation for a specific normal-

Usually defined as less than 40-45mg/dl• Best Practice = have a practical guide for

screening and management • Early identification of at risk infants with

measures to prevent hypoglycemia despite the absence of a consistent definition of hypoglycemia in the literature.

Postnatal Glucose Homeostasis in Late Preterm and Term Infants. Pediatrics, 2011

MONITORING• Serum glucose level

is the gold standard• Bedside glucose levels are for screening• Do not wait for serum level before providing

treatment• Monitor at LEAST hourly until glucose level has

stabilized• Know YOUR hospital policy for monitoring

infants at risk for hypoglycemiaPediatrics, 2011

Most hospital policies are based on:Screening and Management of Postnatal Glucose in Late

Preterm/SGA/IDM/LGA Infants (Pediatrics 2011)

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Signs and Symptoms of Hypoglycemia

Hypoglycemia Treatment • Oral feedings as tolerated, if well baby • If glucose is very low or the infant is not able

to feed orally:– 2ml/kg of D10W IV bolus SIVP followed by IV infusion – IV infusion of D10W at 80-100 ml/kg/day– Follow up screenings within 30 minutes– If unable to stabilize glucose consider: Repeat D10W bolus 2 ml/kg Increasing IV rate Increase glucose concentrationKarlsen, 2006Barnes, 2007

Umbilical Venous CatheterKarlsen, 2006

• Utilize when desired glucose concentrations exceed D12.5W

• #3.5 French for infants less than 1500 grams• #5.0 French for infants greater than 1500 grams

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Umbilical Venous Catheter

Umbilical Venous Catheter

• The tip should be positioned in the IVC at the level of thediaphragm.

• Must be removed ifinadvertently placedin the hepatic system

www.radiologyassistant.comKarlsen, 2006

THANK YOU

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QUESTIONS

REFERENCES

Barnes-Powell, L. (2007). Infants of Diabetic Mothers: The effects of hyperglycemia on the fetus and neonate. Neonatal Network, 26(5) p. 283-289.

Topper, E. P. & Honeyfield, M. E. (2009). Physical assessment of the newborn: A comprehensive approach to the art of physical examination. (4th ed.). Santa Rosa: NICU INK.

Knobel R. (2014). Fetal and Neonatal Thermal Physiology. Newborn & Infant Nursing Reviews. Vol. 14, Issue 2, June 2014, Pages 45-49.

Rozance PJ, Hay WW. New approaches to management of neonatal hypoglycemia. Matern Health Neonatol Perinatol. 2016;2:3. Published 2016 May 10. doi:10.1186/s40748-016-0031-z

REFERENCES

Karlsen, K. (2006) The S.T.A.B.L.E. Program. Pre-transport/Post-resuscitation Stabilization Care of /sick Infants, Guidelines for Neonatal Healthcare Providers. 5th

Edition.Kenner, C., Lott, J. (2004). Neonatal Nursing Handbook.

Elsevier.Postnatal Glucose Homeostasis in Late-Preterm and Term Infants

Pediatrics Mar 2011, 127 (3) 575-579; DOI: 10.1542/peds.2010-3851

Verklan, M. T., & Walden, M. (2010). Core curriculum for neonatal intensive care nursing (4th ed.). St.Louis: Saunders.

Weber, R. (2000). Neonatal Thermoregulation. Retrieved from Www.continuingeducation.com/nursing/thermoreg/coldstress.htm