38 paediatric nursing July vol 18 no 6

continuing professional deveiopment

The neonatal energy trianglePart 1: Metabolic adaptation

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

SummaryThe first part of this two part series on the neonatal energy triangle gives a generaloverview of the transition period during the first six to ten hours of life. Although allelements of the triangle, hypothermia, hypoglycaemia and hypoxia, are interlinkedthis first part of the series describes the normal metabolic adaptation at birth andthe difficulties involved in recognising and treating hypoglycaemia. In the secondpart of the series the two other elements of the triangle, hypoxia and hypothermia,will be addressed.

AuthorMarion Aylott RSCN, MA CertEd is Lecturer in Child Health Nursing, School of

Nursing & Midwifery, University of Southampton

KeywordsNeonates, 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 tointroduce the neoiiiital energy triangle{sec Figure 1) a conceptual frameworkwhich can be used for the early care of thepreterm baby on admission to the neonatalunit (NNU). The focus is the transitionperiod ofthe Hrst six to ten hours oflife. The transition period is more thansimply a period of time, it is a process ofphysiological change for the newborn babythat begins in iitcro as the fetus preparesfor transition from intrauterine placenta!support to extrauterine self-maintenance.

The neonatal energy triangle providesa framework which presents a logical yetintegrated physiological overview of thethree most common difficulties encounteredby the pretertn baby in this period. These are

the 3Hs; hypothermia, hypoglycaemia andhypoxia. The 3Hs can each have detrimentalphysiological effects independently (Wenet al 20041. However, the consequential oraccumulating impact of short falls in allthree, unless interrupted will invariably leadto serious developmental unpairment ordeath {Wen ct al 2004).

Neonatal care is discussed witb tbeexpectation that the reader already has asound grasp of the principles of neonatalcare. After reading these two articles andundertaking the exercises within them yoLishould be able to:• Describe mechanisms of glucose

homeostasis, respiratory adaptation andtherniostasis in the preterm hab\

• Summarise how the mechanisms aboveinter-rclate with each other

• Analyse the main aims of assessment inthe neonatal transition period

• Identify and prioritise care delivery withinthe first six to 12 hours of admission

• With reference to hypothermia,hypoglycaemia and hypoxla explain theimportance of a holistic and integratedcare approach in the arrangement of care.

IntroductionThe fetus prepares for transition mainlyin the third trimester by storing glycogen,producing catecholamines and depositingbrown fat (Boxwell 2000). The preterm babyis less prepared and is therefore challengedby the physiological adaptations requiredfor extra-uterine life. Much has been writtenabout neonatal hypoxia, hypothermia andhypoglycaemia since clinicians first cameto recognise them as important factors inneonatal morbidity and mortality more than50 years ago (Verklan and Walden 2004).This neonatal literature, possibly for the

paediatric nursing July vol 18 no 6 3 9

FIGURE 1

Neonatal energy triangle

Hypothermia

purpose of simplicity, largely concentrateson these factors individually and in isolationfrom each other. However, this is anartificial division that can inhibit timely andappropriate care.

An appropriate knowledge base toenable nurses to anticipate and preventproblems should include integrative neonataiphysiology. If this is not possible, the nursemust have the ability to detect problemsas early as possible and act appropriately.Nurses are expected to enhance theirapplication of clinical knowledge by using anevidence-based approach to improve patientoutcomes as part of continuing professionaldevelopment (DH 2000). The nurse must,therefore, be able to bring together allthe pieces of a clinical puzzle to ensurecomprehensive, clinically excellent andcompassionate care.Now do Time out 1

Physiological adaptation toextra-uterine lifeThermal and glycaemic stability, togetherwith effortless respiration, are criticalphysiological functions that are closelyrelated. Body temperature, glucose andoxygen levels are physiological variablesthat are precisely controlled by the bodyin health. Just as adequate oxygen andglucose are essential to cellular metabolism,appropriate body temperature is criticalto the function of enzymatic systemsregulating cellular function (Thomas 1994).Neonatal hypoglycaemia, hypothermia andhypoxia are not pathological conditionsthemselves. They are features of illness or

a failure to adapt from the fetal state ofcontinuous transplacental glucose, warmthand oxygen consumption to the extrauterineenvironment and pattern of intermittentnutrient supply. These variables are closelyinter-related to the successful transition fromuterine to extra-uterine life and survival.

Normal metabolic adaptation at birthAt birth the neonate^" glucose level is 70per cent of the mother's serum glucose(Cornblath and Ichord 2000). With theloss of continuous maternal glucose source(via the placenta), the neonate must assumecontrol of glucose homeostasis and maintainit through the intermittent feed cycle thatensues postnatally, while still ensuring anadequate supply of fuel for the brain andother organs. This metabolic adaptation atbirth involves mobilisation of glycogen stores(glycogenolysis), hepatic synthesis of glucosefrom substrates (gluconeogenesis) andproduction of alternative cerebral energy.

After cord clamping, the neonate'sblood glucose concentration falls reachingits lowest point at one to two hours. Atthis point hepatic glycogen stores aredepleted and glycogenolysis is replacedby gluconeogenesis so that even thoughglucose concentration is low, the brain isnot fuel deficient. The neonate defends itselfagainst hypoglycaemia by decreasing insulinproduction while simultaneously increasinggiucagon, epinephrine, growth hormone andcortisol secretion. These hormones worktogether as counter-regulatory hormones(Sunehag and Haymond 2002). Theyoppose the effect of insulin and thereforecause increased hepatic glucose output byother means. This comes initially from thebreakdown of fatty stores due to lowerinsulin and decreased giucagon.

During hypoglycaemia other substratessuch as ketone bodies, lactate, glyceroland amino acids can also be converted byglycolysis to pyruvate, enter the citric acidcycle and produce adenosine triphosphate(ATP), thus serving as an energy sourcefor the brain (Ward Platt and Deshpande2005). These events increase lipolysis andketone bodies which become availableas an alternative fuel which in turncompete to inhibit glucose use (see Figure2) (Noerr 2001). The neonate, therefore,gradually mobilises glucose to meet energy

Reflecting on yourown practice, mind tnapthe first things you assesswhen evaluating the pretermbaby oti admission. For thisexercise you might find it usefulto use the system you are familiarwith e.g. Airway, Breathing,Circulation.

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Glucose control in the preterm infant

Prevailing conditionspre-birth

Post natalconditions

Homeostasis

TABLE 1

Table 1: Definition ofhypoglycaemia in term, healthyinfant (Hewitt efo/2005)

Age of Neonate(hours)

Definition ofhypoglycaemia(mmol/l)

0-33-66-2424-48>48

<2.0<L4<L7<2.2<2.5

requirements hy secreting glucagon andcatechulnmines iind suppressing insulinrelease which causes blood glucose levels torise physiologically at three to four hoursof age (Hawdoii et al 2000). Transientneonatal hypoglycaemia is physiologicallyself-limiting in healthy term newbornsas they adapt to extrauterine lite afterabrupt cessation ofthe maternal glucosesupply at birth. It was concluded in asystematic review by Hewitt ct al (2005)that healthy full term infants do not requireroutine blood glucose monitoring. Table 1demonstrates a consensus opinion ofthenormal values of blood glucose level for

neonates based on a meta-analysis of studyfindings in the review. You will note that thevalues related to age ofthe neonate reflectsthe physiology as described above.

In summary, postnatal metabolicadaptation in the full-term neonate ischaracterised by vigorous ketogenesis.

Impaired metabolic adaptationHypoglycaL-niia is the result ot inadequatehepatic glucose production that cannotmeet peripheral demand or excessive insulinproduction (Cowett and Longhead 2002).The preterm baby is especially susceptible topathologic hypoglycaemia due to immatureglucose control mechanisms, decreasedglucose stores and a reduced availabilityof alternative fuels such as ketone bodies.Babies who are likely to have inadequate/delayed feeding, inadequate glucosestores or increased glucose utilisationshould be considered at particular riskfor hypoglycaemia. Preterm babies areheavily dependent on adequate exogenousglucose supply. Early institution of feedingor intravenous dextrose is of paramountimportance for the preterm baby (Cornblath

Furthermore, concurrent neonatalconditions such as hypoxia and hypothermiawhere additional fuel is required to provideenergy, for the increased work of breathingfor example, hypoglycaemia may result fromrapid depletion of glycogen storage. Perhapsthe best way to visualise these interactions isto draw an analogy with a simple pendulum.Glucose homeostasis in a preterm infant canbe represented by a pendulum which swingsbetween factors that influence glucosemetabolism pre-birth and post birth.The preterm baby has to work hard toachieve a position of equilibrium and thenmaintain euglycaemia. This is demonstratedin Figure 3.

Therefore, it is recommended thatglucose monitormg should comnience assoon as possible (usually within the Hrst 30minutes of admission after birth) for these'high risk' babies, and continue ar leasthourly thereafter until stable (Cornblathand Schwartz 1993). However, this isproblematic as the definition of neonatalhypoglycaemia in the preterm infant haslong courted controversy with definitivevalues ranging from below 1 mmol/l to

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TABLE 2 ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ 1'At r isk' babies (Williams 2005)

Maternal • Diabetes (pre-gestational andgestational)

• Drug treatment (Beta blockers. oralhypoglycaemic agents

• Intrapartum glucose administration

Neonatal • Pretermproblems • Intrauterine growth retardation

• Perinatal hypoxia-ischaeniia• Hypothermia• Infection• Polycythaeniia• Syndromes e.g. Beckwith-

Wiedermann

4 m m o l / l (Boxwel l 2000) . Babies considered

' FIGURE 4 ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ 1

Autonomic nervous system in neonate compared with child and adult

i _-•--' ^ r ^ ^ ^ ^ ^ ^ ^ ^

Williams (2005) are shown in Table 2.Babies with abnormal clinical signs, or

at risk of disordered metabolic adaptation,will require blood glucose monitoringand close observation. Table 3 lists theabnormal clinical signs suggested inmost general neonatal textbooks. Thesymptoms of hypoglycaemia reflect twomajor physiological pathways. The firstis caused by activation of the sympatheticnervous system, which causes symptoms oisweating, hypothermia, bounding pulses andtachycardia for example. The second groupof symptoms is due to neuroglycopeniawhich causes symptoms such as irritability,lethargy, and muscle weakness.

These symptoms vary with the gestationalage of the newborn baby. It must beremembered that the neonatal response tostress is predominantly vagal through theparasympathetic nervous system as opposedto sympathetic in the child and adult (seeFigure 4).

TABLE 3 ^ ^ ^ ^ ^ ^ ^ ^ ^ ^ HClinical signs associatedhypoglycaemia

Change in level ofconsciousness

Changes in behaviour

Changes in vital signs

With

• lethargy• drowsiness• coma

• irritability• jitteriness• poor feeding• hypotonia

yapnoea• bradycardia• hypothermia• sweating• bounding pulses

Now do Time out 2Now do Time out 3

Glucose is an essential nutrient for the brain.Abnormally low levels have the potentialto produce long term neurological injury(Mchta 1994, Kalhan and Riley 1996).The term 'hypoglycaemia' refers to a lowblood glucose concentration {Hawdon et ul1994). A 'normal range' for blood glucosevalues in the neonate has not been properlydefined. However, it is known that valuesare influenced by birthweight, gestationalage, feeding method and postnatal age(Deshpande and Ward Platt 2005). There ismuch controversy over the definition of theminimum 'safe' blood glucose value, thatis, the value below which there is a risk oflong-term neurodevelopmental impairment(Cornblath <f/a/2000).

Early neonatal studies conducted byCornblath and Reisner (1965) determinedarbitrary theoretical definitions ofhypoglycaemia as; <1.1 mmol/l in preterminfants irrespective of post natal age.However, tbe validity and reliability ofsuch a rigid definition of hypoglycaemiaapplicable to all neonates is questionable.Blood glucose concentrations represent acontinuum, and a single value, like anysingle data item is unreliable and unlikely torepresent a threshold of abnormality withor without clinical signs of hypoglycaemia.A single value only represents a point intime representative of glycaemic status.In response to this challenge, manyNeonatologists have adopted a policy basedon pragmatic operational thresholds. Forexample, blood glucose concentrations

Apart from thephysiological causesof hypoglycaemia inthe preterm baby there arepathological conditions outsidethe remit of this article whichcause either;• Disorders of excessive glucose

utilisation• Disorders of glucose under-

productionAccess the World HealthOrganization documentHypoglycaemia atid the Newborn:Review ofthe literature section2.4 to identify and be able todescribe the most common causeswww.who.int/reproductive-health/docs/hypoglycamia_newborn.htm

An area of medico-legal concern is theinfant/child who hashypoglycaemia due to thepossibility of illicit exogenousinsulin administration. Accessthe Clothier report (1994)Independent inquiry relatingto deaths and injuries on thechildren's ward at Granthamand Kestevan General Hospital.London, HMSO www.dh.gov.uk(Clothier ef 0/1994).You will note that this report wasa key influence in the promotion ofclinical supervision

42 paediatric nursing July vol 18 no 6

continuing professionai development

Answer tbe followingmultiple choicequestions. All questionsand answers are developed fromthe information within this articleI Most glycogen storage takesplace at what gestational age?a. 24 weeksb. 30 weeksc. 34 weeks2. After birth there is a decreasein the blood level of which of thefollowing?a. glucagonb. epinephrinec. insulin3. Which of the following is a signof hypoglycaemia?a. diuresisb. hypothermiac. respiratory acidosis4. Which of the following infantsare at risk for hypoglycaemia?(more than one answer)a. Infant of diabetic motherb. A jittery infantc. SGA infantd. 37 week gestation infant born toa GBS positive mother5. The level of hypoglycemiaresulting in serious sequelae iswell defined by scientific studies.True/False

at which clinical interventions such asadniinistrarion ot a dextrose bolus shouldbe given. Such policy often also employs a'safety margin' based on 'risk". For example,1̂ policy may advise rh;it in the nutritionalmanagement of normoglycacmia bloodyiucose 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 fuelssuch as the small for gcstational age infant(Hawdon and W.ird Phitt 1994).

Such protocols reflect contemporary legalLidvice to move awiiy from precise universalrmmerical definitions of continuous variablestowards a more flexible approach whichtakes into account not only the plasmaglucose concentration but also the clinicalstate ofthe neonate (Williams 2005).Indeed Williams argues that as there is noempirical basis to show that the preterm isat any greater risk than their term healthycounterparts to cerebral Injury secondaryto hypoglycaemia. This suggests that thecriteria for intervention should be based onthe presence of clinical symptoms. Thus.,rhe 'symptomatic' baby with a serum bloodglucose <2.5mmol/l should receive 3m!/kg/hour 10 per cent dextrose to increase theblood glucose to >3.0mmol/l.

Most neonates, however, are free ofsymptoms (Cornblatb et al 2000). Also,the signs linked with hypoglycaemia arenonspecific and may occur m conjunction

with other clinical conditions. This makesthem unreliable markers for hypoglycaemia.Additionally, when present, these clinicalsigns have been found to present at varyingblood glucose concentrations in differentbabies., or may not be evident at all eventbough the baby is experiencing severehypoglycaemia (Cornblath and Icbord 2000}.Therefore, the nurse needs to determinenot only whicb biibies are at particular riskand require routine testing of serum glucoselevels in order to provide a trend, hut alsobe acutely mindful that changes in tone,vital signs and level of consciousness mayor may not be present or reliable. This ischallenging. For example Parker ct al (1990)researched the prevalence of 'jitteriness' andits correlates in a study of term newborns.They found that in 40 per cent of the 'jittery'newborns, "jitteriness' was not attributableto low serum glucose levels. Furthermore,a liberal assessment is critically importantas the level of hypoglycaemia resulting inserious sequelae is not defined by scientificstudies. This is further compounded by alack of accurate and precise methods oftesting at the cot-side.Now do Time out 4

• In the September Issue of PaediatricNursing the remaining elements of thetriangle, hypoxia and hypothermia, trillhe addressed.

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