paediatric nursing July vol 18 no 6

38

continuing professional deveiopment

The neonatal energy triangle

Part 1: Metabolic adaptation
PN906 Marion Aylott (2006) The neonatal energy triangle. Part 1: Metabolic adaptation
Paediatric Nursitig. 18,6,38-42. Date of acceptance: 21 April 2006.

Summary
The first part of this two part series on the neonatal energy triangle gives a general
overview of the transition period during the first six to ten hours of life. Although all
elements of the triangle, hypothermia, hypoglycaemia and hypoxia, are interlinked
this first part of the series describes the normal metabolic adaptation at birth and
the difficulties involved in recognising and treating hypoglycaemia. In the second
part of the series the two other elements of the triangle, hypoxia and hypothermia,
will be addressed.

Author
Marion Aylott RSCN, MA CertEd is Lecturer in Child Health Nursing, School of
Nursing & Midwifery, University of Southampton

Keywords
Neonates, Thermoregulation, Metabolism, Physiology
These keyv^ords are based on tlie subject headings from the British Nursing Index.
This article has been subject to double-blind review. For related articles and author
guidelines visit our online archive at www.paediatric nursing.co.uk and search using
the keywords.

Aim and intended learning outcomes

The aim of this two part article is to
introduce the neoiiiital energy triangle
{sec Figure 1) a conceptual framework
which can be used for the early care of the
preterm baby on admission to the neonatal
unit (NNU). The focus is the transition
period ofthe Hrst six to ten hours of
life. The transition period is more than
simply a period of time, it is a process of
physiological change for the newborn baby
that begins in iitcro as the fetus prepares
for transition from intrauterine placenta!
support to extrauterine self-maintenance.
The neonatal energy triangle provides
a framework which presents a logical yet
integrated physiological overview of the
three most common difficulties encountered
by the pretertn baby in this period. These are

the 3Hs; hypothermia, hypoglycaemia and

hypoxia. The 3Hs can each have detrimental
physiological effects independently (Wen
et al 20041. However, the consequential or
accumulating impact of short falls in all
three, unless interrupted will invariably lead
to serious developmental unpairment or
death {Wen ct al 2004).
Neonatal care is discussed witb tbe
expectation that the reader already has a
sound grasp of the principles of neonatal
care. After reading these two articles and
undertaking the exercises within them yoLi
should be able to:
Describe mechanisms of glucose
homeostasis, respiratory adaptation and
therniostasis in the preterm hab\
Summarise how the mechanisms above
inter-rclate with each other
Analyse the main aims of assessment in
the neonatal transition period
Identify and prioritise care delivery within
the first six to 12 hours of admission
With reference to hypothermia,
hypoglycaemia and hypoxla explain the
importance of a holistic and integrated
care approach in the arrangement of care.
Introduction
The fetus prepares for transition mainly
in the third trimester by storing glycogen,
producing catecholamines and depositing
brown fat (Boxwell 2000). The preterm baby
is less prepared and is therefore challenged
by the physiological adaptations required
for extra-uterine life. Much has been written
about neonatal hypoxia, hypothermia and
hypoglycaemia since clinicians first came
to recognise them as important factors in
neonatal morbidity and mortality more than
50 years ago (Verklan and Walden 2004).
This neonatal literature, possibly for the

paediatric nursing July vol 18 no 6

39

FIGURE 1
Neonatal energy triangle

Hypothermia

a failure to adapt from the fetal state of

continuous transplacental glucose, warmth
and oxygen consumption to the extrauterine
environment and pattern of intermittent
nutrient supply. These variables are closely
inter-related to the successful transition from
uterine to extra-uterine life and survival.
Normal metabolic adaptation at birth

purpose of simplicity, largely concentrates

on these factors individually and in isolation
from each other. However, this is an
artificial division that can inhibit timely and
appropriate care.
An appropriate knowledge base to
enable nurses to anticipate and prevent
problems should include integrative neonatai
physiology. If this is not possible, the nurse
must have the ability to detect problems
as early as possible and act appropriately.
Nurses are expected to enhance their
application of clinical knowledge by using an
evidence-based approach to improve patient
outcomes as part of continuing professional
development (DH 2000). The nurse must,
therefore, be able to bring together all
the pieces of a clinical puzzle to ensure
comprehensive, clinically excellent and
compassionate care.
Now do Time out 1
Physiological adaptation to
extra-uterine life

Thermal and glycaemic stability, together

with effortless respiration, are critical
physiological functions that are closely
related. Body temperature, glucose and
oxygen levels are physiological variables
that are precisely controlled by the body
in health. Just as adequate oxygen and
glucose are essential to cellular metabolism,
appropriate body temperature is critical
to the function of enzymatic systems
regulating cellular function (Thomas 1994).
Neonatal hypoglycaemia, hypothermia and
hypoxia are not pathological conditions
themselves. They are features of illness or

At birth the neonate^" glucose level is 70

per cent of the mother's serum glucose
(Cornblath and Ichord 2000). With the
loss of continuous maternal glucose source
(via the placenta), the neonate must assume
control of glucose homeostasis and maintain
it through the intermittent feed cycle that
ensues postnatally, while still ensuring an
adequate supply of fuel for the brain and
other organs. This metabolic adaptation at
birth involves mobilisation of glycogen stores
(glycogenolysis), hepatic synthesis of glucose
from substrates (gluconeogenesis) and
production of alternative cerebral energy.
After cord clamping, the neonate's
blood glucose concentration falls reaching
its lowest point at one to two hours. At
this point hepatic glycogen stores are
depleted and glycogenolysis is replaced
by gluconeogenesis so that even though
glucose concentration is low, the brain is
not fuel deficient. The neonate defends itself
against hypoglycaemia by decreasing insulin
production while simultaneously increasing
giucagon, epinephrine, growth hormone and
cortisol secretion. These hormones work
together as counter-regulatory hormones
(Sunehag and Haymond 2002). They
oppose the effect of insulin and therefore
cause increased hepatic glucose output by
other means. This comes initially from the
breakdown of fatty stores due to lower
insulin and decreased giucagon.
During hypoglycaemia other substrates
such as ketone bodies, lactate, glycerol
and amino acids can also be converted by
glycolysis to pyruvate, enter the citric acid
cycle and produce adenosine triphosphate
(ATP), thus serving as an energy source
for the brain (Ward Platt and Deshpande
2005). These events increase lipolysis and
ketone bodies which become available
as an alternative fuel which in turn
compete to inhibit glucose use (see Figure
2) (Noerr 2001). The neonate, therefore,
gradually mobilises glucose to meet energy

Reflecting on your
own practice, mind tnap
the first things you assess
when evaluating the preterm
baby oti admission. For this
exercise you might find it useful
to use the system you are familiar
with e.g. Airway, Breathing,
Circulation.

paediatric nursing July vol 18 no 6

40

continuing professional development

neonates based on a meta-analysis of study

findings in the review. You will note that the
values related to age ofthe neonate reflects
the physiology as described above.
In summary, postnatal metabolic
adaptation in the full-term neonate is
characterised by vigorous ketogenesis.
Impaired metabolic adaptation

Glucose control in the preterm infant

Post natal
conditions

Prevailing conditions
pre-birth

Homeostasis

TABLE 1

Table 1: Definition of
hypoglycaemia in term, healthy
infant (Hewitt efo/2005)
Age of Neonate
(hours)
0-3
3-6
6-24
24-48
>48

Definition of
hypoglycaemia
(mmol/l)
<2.0

<L4
<L7
<2.2
<2.5

requirements hy secreting glucagon and

catechulnmines iind suppressing insulin
release which causes blood glucose levels to
rise physiologically at three to four hours
of age (Hawdoii et al 2000). Transient
neonatal hypoglycaemia is physiologically
self-limiting in healthy term newborns
as they adapt to extrauterine lite after
abrupt cessation ofthe maternal glucose
supply at birth. It was concluded in a
systematic review by Hewitt ct al (2005)
that healthy full term infants do not require
routine blood glucose monitoring. Table 1
demonstrates a consensus opinion ofthe
normal values of blood glucose level for

HypoglycaL-niia is the result ot inadequate

hepatic glucose production that cannot
meet peripheral demand or excessive insulin
production (Cowett and Longhead 2002).
The preterm baby is especially susceptible to
pathologic hypoglycaemia due to immature
glucose control mechanisms, decreased
glucose stores and a reduced availability
of alternative fuels such as ketone bodies.
Babies who are likely to have inadequate/
delayed feeding, inadequate glucose
stores or increased glucose utilisation
should be considered at particular risk
for hypoglycaemia. Preterm babies are
heavily dependent on adequate exogenous
glucose supply. Early institution of feeding
or intravenous dextrose is of paramount
importance for the preterm baby (Cornblath
Furthermore, concurrent neonatal
conditions such as hypoxia and hypothermia
where additional fuel is required to provide
energy, for the increased work of breathing
for example, hypoglycaemia may result from
rapid depletion of glycogen storage. Perhaps
the best way to visualise these interactions is
to draw an analogy with a simple pendulum.
Glucose homeostasis in a preterm infant can
be represented by a pendulum which swings
between factors that influence glucose
metabolism pre-birth and post birth.
The preterm baby has to work hard to
achieve a position of equilibrium and then
maintain euglycaemia. This is demonstrated
in Figure 3.
Therefore, it is recommended that
glucose monitormg should comnience as
soon as possible (usually within the Hrst 30
minutes of admission after birth) for these
'high risk' babies, and continue ar least
hourly thereafter until stable (Cornblath
and Schwartz 1993). However, this is
problematic as the definition of neonatal
hypoglycaemia in the preterm infant has
long courted controversy with definitive
values ranging from below 1 mmol/l to

paediatric nursing July vol 18 no 6

TABLE 2

^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ 1

'At risk' babies (Williams 2005)

Maternal

Diabetes (pre-gestational and

gestational)
Drug treatment (Beta blockers. oral
hypoglycaemic agents
Intrapartum glucose administration

Neonatal
problems

Preterm
Intrauterine growth retardation
Perinatal hypoxia-ischaeniia
Hypothermia
Infection
Polycythaeniia
Syndromes e.g. BeckwithWiedermann

41

'

FIGURE 4

^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ 1

Autonomic nervous system in neonate compared with child and adult

i _---'

^r

^ ^

^^^^^^

4 m m o l / l ( B o x w e l l 2 0 0 0 ) . Babies considered

Williams (2005) are shown in Table 2.

Babies with abnormal clinical signs, or

at risk of disordered metabolic adaptation,
will require blood glucose monitoring
and close observation. Table 3 lists the
abnormal clinical signs suggested in
most general neonatal textbooks. The
symptoms of hypoglycaemia reflect two
major physiological pathways. The first
is caused by activation of the sympathetic
nervous system, which causes symptoms oi
sweating, hypothermia, bounding pulses and
tachycardia for example. The second group
of symptoms is due to neuroglycopenia
which causes symptoms such as irritability,
lethargy, and muscle weakness.
These symptoms vary with the gestational
age of the newborn baby. It must be
remembered that the neonatal response to
stress is predominantly vagal through the
parasympathetic nervous system as opposed
to sympathetic in the child and adult (see
Figure 4).

Now do Time out 2

Now do Time out 3
Glucose is an essential nutrient for the brain.
Abnormally low levels have the potential
to produce long term neurological injury
(Mchta 1994, Kalhan and Riley 1996).
The term 'hypoglycaemia' refers to a low
blood glucose concentration {Hawdon et ul
1994). A 'normal range' for blood glucose
values in the neonate has not been properly
defined. However, it is known that values
are influenced by birthweight, gestational
age, feeding method and postnatal age
(Deshpande and Ward Platt 2005). There is
much controversy over the definition of the
minimum 'safe' blood glucose value, that
is, the value below which there is a risk of
long-term neurodevelopmental impairment
(Cornblath <f/a/2000).

Early neonatal studies conducted by

Cornblath and Reisner (1965) determined
arbitrary theoretical definitions of
hypoglycaemia as; <1.1 mmol/l in preterm
infants irrespective of post natal age.
TABLE 3 ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ H However, tbe validity and reliability of
Clinical signs associated With
such a rigid definition of hypoglycaemia
hypoglycaemia
applicable to all neonates is questionable.
Change in level of
lethargy
Blood glucose concentrations represent a
consciousness
drowsiness
continuum, and a single value, like any
coma
single data item is unreliable and unlikely to
Changes in behaviour
irritability
represent a threshold of abnormality with
jitteriness
or without clinical signs of hypoglycaemia.
poor feeding
A single value only represents a point in
hypotonia
time representative of glycaemic status.
Changes in vital signs
yapnoea
In response to this challenge, many
bradycardia
Neonatologists have adopted a policy based
hypothermia
on pragmatic operational thresholds. For
sweating
bounding pulses
example, blood glucose concentrations

Apart from the

physiological causes
of hypoglycaemia in
the preterm baby there are
pathological conditions outside
the remit of this article which
cause either;
Disorders of excessive glucose
utilisation
Disorders of glucose underproduction
Access the World Health
Organization document
Hypoglycaemia atid the Newborn:
Review ofthe literature section
2.4 to identify and be able to
describe the most common causes
www.who.int/reproductive-health/
docs/hypoglycamia_newborn.htm

An area of medicolegal concern is the

infant/child who has
hypoglycaemia due to the
possibility of illicit exogenous
insulin administration. Access
the Clothier report (1994)
Independent inquiry relating
to deaths and injuries on the
children's ward at Grantham
and Kestevan General Hospital.
London, HMSO www.dh.gov.uk
(Clothier ef 0/1994).
You will note that this report was
a key influence in the promotion of
clinical supervision

paediatric nursing July vol 18 no 6

42

continuing professionai development

Answer tbe following

multiple choice
questions. All questions
and answers are developed from
the information within this article
I Most glycogen storage takes
place at what gestational age?

a. 24 weeks
b. 30 weeks
c. 34 weeks
2. After birth there is a decrease
in the blood level of which of the
following?
a. glucagon
b. epinephrine
c. insulin
3. Which of the following is a sign
of hypoglycaemia?
a. diuresis
b. hypothermia
c. respiratory acidosis
4. Which of the following infants
are at risk for hypoglycaemia?
(more than one answer)
a. Infant of diabetic mother
b. A jittery infant
c. SGA infant
d. 37 week gestation infant born to
a GBS positive mother
5. The level of hypoglycemia
resulting in serious sequelae is
well defined by scientific studies.
True/False

at which clinical interventions such as

adniinistrarion ot a dextrose bolus should
be given. Such policy often also employs a
'safety margin' based on 'risk". For example,
^1 policy may advise rh;it in the nutritional
management of normoglycacmia blood
yiucose levels will be miiintained above:
2.5mm<)l/l in a preterm infant
3.5mmol/l for those with theoretically
anticipated low ieveis of alternative fuels
such as the small for gcstational age infant
(Hawdon and W.ird Phitt 1994).
Such protocols reflect contemporary legal
Lidvice to move awiiy from precise universal
rmmerical definitions of continuous variables
towards a more flexible approach which
takes into account not only the plasma
glucose concentration but also the clinical
state ofthe neonate (Williams 2005).
Indeed Williams argues that as there is no
empirical basis to show that the preterm is
at any greater risk than their term healthy
counterparts to cerebral Injury secondary
to hypoglycaemia. This suggests that the
criteria for intervention should be based on
the presence of clinical symptoms. Thus.,
rhe 'symptomatic' baby with a serum blood
glucose <2.5mmol/l should receive 3m!/kg/
hour 10 per cent dextrose to increase the
blood glucose to >3.0mmol/l.

with other clinical conditions. This makes

them unreliable markers for hypoglycaemia.
Additionally, when present, these clinical
signs have been found to present at varying
blood glucose concentrations in different
babies., or may not be evident at all even
tbough the baby is experiencing severe
hypoglycaemia (Cornblath and Icbord 2000}.
Therefore, the nurse needs to determine
not only whicb biibies are at particular risk
and require routine testing of serum glucose
levels in order to provide a trend, hut also
be acutely mindful that changes in tone,
vital signs and level of consciousness may
or may not be present or reliable. This is
challenging. For example Parker ct al (1990)
researched the prevalence of 'jitteriness' and
its correlates in a study of term newborns.
They found that in 40 per cent of the 'jittery'
newborns, "jitteriness' was not attributable
to low serum glucose levels. Furthermore,
a liberal assessment is critically important
as the level of hypoglycaemia resulting in
serious sequelae is not defined by scientific
studies. This is further compounded by a
lack of accurate and precise methods of
testing at the cot-side.
Now do Time out 4

Most neonates, however, are free of

symptoms (Cornblatb et al 2000). Also,
the signs linked with hypoglycaemia are
nonspecific and may occur m conjunction

In the September Issue of Paediatric

Nursing the remaining elements of the
triangle, hypoxia and hypothermia, trill
he addressed.

References

Pedidtnc Endociinniogy. 6. 2,113-129.

Boxwell G (ed) (2000) Neonatal

Intensive Care Nursing. London,
Roiitlerigp

Cowett RM. Longhead JL (2002)

Neonatai glucose nietaboiism: differential
diagnoses, evaluation and treatment of
hypoglycemia. Neonatal Network. 21,
4,9-19.

Clothier C, MacDonald CA, Shaw DA

(1994) The Atlit inquiry: independent
inquiry relating to the deaths andinjuries
on the children's ward at Grantham and
Kesteven General Hospital during the
period February to April 1991. HMSO.
London.

Department of Health (2000) Tiie NHS

Plan London, DH

gestational age infants. Archives of

Disease in Childhood. 68, 262-268.

Thomas K (1994) Thermoregulation

Hewitt V ef ai (2005) Systematic
in iieonate'i Neonatal NetworJ<. 13,2,
review: Nursing and midwifery
management of hypoglycaemia in healthy
15-22
term neonafes. International Joumai of
Verktan M, Walden M (2004) Core
Evidence Based Healthcare. 3, 7.169-205, Curriciiium far Neonatai Intensive Care.

Deshpande S, Ward Platt M (2005)

The inyestigation and tnanagement
of neonatal hypoglycaemia. Seminars
in Fetal and Neonatal Medicine. 10, 4.
351-361.

Kalhan SC, Riley TF (1996)

Neiirosensory disorders. In: Kiiegnian
RM (Ed) Practical Strategies in Pediatric
Diagnosis and Therapy {2nd edition),
Phiiadelphia, WB Saimders. pp. 10371047

Hawdon JM et al (1994) Prevention and

nianagemetit of neonatal hypogiycaeniia.
Ardiives of Disease in Childhood. 70,1,
60-65,

Mehta A (1994) Prevention and

management of neonatal hypoglycaemia.
Archives of Disease in Chiidhood. 70,1,
54-59.

Cornhlath M. Ichord R (2000)

Hypoglycemia m the neonate. Seminars in
Perinatology. 24, 2.136-149.

Hawdon JM et al (2000) Controveriieb regarding definition of neonatal

hypcglycaemia: implications for neonatal
nursing. Joumai of Neonatal Nursing, b.
5,169-171,

Noerr B (2001) State of the science:

neonatal hypogiycemia. Advances in
Neonatai Care. l.\. A-21.

Cornblath M, Schwartz R (1993)

Hypoglycemia in the neon<ite. Journal of

Hawdon JM, Ward Platt MP (1993)

Metabolic adaptation in sniail for

Cornblath M, Reisner SH (1965)

Blood yiucoso in the neonate: clinical
significance, Tiie New England Journal of
Medicine. 111. 378-381,
Cornblath M et ai (2000) Controversies
regarding definition of neonatai
hypoglycemia: suggested operational
Pediatric;. 105,1141-1145,

Glucose extremes in newborn infants.

Clinics in Perinatology. 29, 2,245-260.

Parker S ef ai (1990) Jitteriness in

fuil-terni neonates: prevalence and
correlates. Pediatrics 85,1,17-23.
Sunehag AL, Haymond MW (2002)

London, Eiscvior.
Ward Piatt M, Deshpande S (2005)
Metabolic adaptation at birth. Seminars
in Fetal Neonatai Medicine. 10, 4,341350.
Wen SW, Smith G, Yang Q, Wallter M
(2004) Epidemiology of preterm birtii
and neonatal outcome. Seminars in
Neonatology. 9,6, 429-435,
Williams AF (2005) Neonatal
hypoglycaemia: clinical and legal aspects.
Seminars in Fetal Neonatai Medicine. 10,

4,363-368.
p'D'q'e>
D'qe

3 2
^ I

l7 ino aiuti 01SJ3MSUV