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Perioperative management of adult diabetic patients.
Review of hyperglycaemia: definitions and
pathophysiology
Gaelle Cheisson, Sophie Jacqueminet, Emmanuel Cosson, Carole Ichai,
Anne-Marie Leguerrier, Bogdan Nicolescu-Catargi, Alexandre Ouattara, Igor
Tauveron, Paul Valensi, Dan Benhamou
To cite this version:
Gaelle Cheisson, Sophie Jacqueminet, Emmanuel Cosson, Carole Ichai, Anne-Marie Leguerrier, et
al.. Perioperative management of adult diabetic patients. Review of hyperglycaemia: definitions and
pathophysiology. Anaesthesia Critical Care & Pain Medicine, Elsevier Masson, 2018, 37 (Supplement
1), pp.S5-S8. �10.1016/j.accpm.2018.02.019�. �hal-02621186�
Guidelines
Perioperative
management
of
adult
diabetic
patients.
Review
of
hyperglycaemia:
definitions
and
pathophysiology
Gae¨lle
Cheisson
a,
Sophie
Jacqueminet
b,
Emmanuel
Cosson
c,d,
Carole
Ichai
e,f,
Anne-Marie
Leguerrier
g,
Bogdan
Nicolescu-Catargi
h,
Alexandre
Ouattara
i,j,
Igor
Tauveron
k,l,m,n,
Paul
Valensi
c,
Dan
Benhamou
a,*
,
working
party
approved
by
the
French
Society
of
Anaesthesia
and
Intensive
Care
Medicine
(SFAR),
the
French
Society
for
the
study
of
Diabetes
(SFD)
aDepartmentofsurgicalanaesthesiaandintensivecare,SouthParisuniversityhospital,hoˆpitaldeBiceˆtre,AP–HP,78,rueduGe´ne´ral-Leclerc,94275Le
Kremlin-Biceˆtre,France
b
Instituteofcardiometabolismandnutrition,Departmentofdiabetesadmetabolicdiseases,hoˆpitaldelaPitie´-Salpeˆtrie`re,AP–HP,75013Paris,France
c
Departmentofendocrinology,diabetologyandnutrition,hoˆpitalJean-Verdier(AP–HP), Paris13university,SorbonneParisCite´,CRNH-IdF,CINFO, 93140Bondy,France
d
UMRU1153Inserm,U1125Inra,CNAM,SorbonneParisCite´,Paris13university,93000Bobigny,France
eDepartmentofversatileintensivecare,hoˆpitalPasteur2,CHUdeNice,30,voieRomaine,06001Nicecedex1,France fInsermU1081,CNRSUMR7284(IRCAN),UniversityHospitalofNice,06001Nice,France
g
Departmentofdiabetologyandendocrinology,CHUdeRennes,hoˆpitalSuduniversityhospital,16,boulevarddeBulgarie,35056Rennes,France
h
Departmentofendocrinologyadmetabolicdiseases,hoˆpitalSaint-Andre´,Bordeauxuniversityhospital,1,rueJean-Burguet,33000Bordeaux,France
i
Bordeauxuniversityhospital,DepartmentofAnaesthesiaandCriticalCareII,MagellanMedico-SurgicalCentre,33000Bordeaux,France
j
Inserm,UMR1034,BiologyofCardiovascularDiseases,universite´ deBordeaux,33600Pessac,France
k
Departmentofendocrinologyanddiabetology,ClermontFerranduniversityhospital,58,rueMontalembert,63000Clermont-Ferrand,France
lUFRme´decine,ClermontAuvergneuniversity,,28,placeHenri-Dunant,63000Clermont-Ferrand,France
mUMRCNRS6293,InsermU1103,GeneticReproductionanddevelopment,Clermont-Auvergneuniversity,63170Aubie`re,France n
Endocrinology-Diabetology,CHUG.-Montpied,BP69,63003Clermont-Ferrand,France
ARTICLE INFO Articlehistory:
Availableonline17March2018 Keywords: Diabetes Perioperative Stresshyperglycaemia HbA1c Ketoacidosis Basal-bolus ABSTRACT
Diabetesmellitusisdefinedbychronicelevationofbloodglucoselinkedtoinsulinresistanceand/or insulinopaenia.Itsdiagnosisisbasedonafastingblood-glucoselevelof1.26g/Lor,insomecountries, abloodglycatedhaemoglobin(HbA1c)levelof>6.5%.Oftheseveralformsofdiabetes,type-2diabetes (T2D)isthemostcommonandisfoundinpatientswithotherriskfactors.Incontrast,type-1diabetes (T1D)islinkedtotheautoimmunedestructionofb-pancreaticcells,leadingtoinsulinopaenia.Insulin deficiencyresultsindiabeticketoacidosiswithinafewhours.‘Pancreatic’diabetesdevelopsfromcertain pancreaticdiseasesandmayculminateininsulinopaenia.TreatmentsforT2Dincludenon-insulinbased therapiesandinsulinwhenothertherapiesarenolongerabletocontrolglycaemiclevels.ForT1D, treatmentdependsonlong(slow)-actinginsulin andultra-rapidanaloguesofinsulinadministered accordingtoa‘basal-bolus’schemeorbycontinuoussubcutaneousdeliveryofinsulinusingapump.For patients presenting with previously undiagnosed dysglycaemia, investigations should determine whethertheconditioncorrespondstopre-existingdysglycaemiaortostresshyperglycaemia.Thelatter isdefinedastransienthyperglycaemiainapreviouslynon-diabeticpatientthatpresentswithanacute illness or undergoes an invasive procedure. Its severity depends on the type of surgery, the aggressivenessoftheprocedureanditsduration.Stresshyperglycaemiamayleadtoperipheralinsulin resistanceandisanindependentprognosticfactorformorbidityandmortality.
C 2018TheAuthor.PublishedbyElsevierMassonSASonbehalfofSocie´te´ franc¸aised’anesthe´sieetde
re´animation(Sfar).ThisisanopenaccessarticleundertheCCBYlicense(http://creativecommons.org/ licenses/by/4.0/).
* Correspondingauthor.
E-mailaddress:dan.benhamou@aphp.fr(D.Benhamou).
https://doi.org/10.1016/j.accpm.2018.02.019
2352-5568/ C2018TheAuthor.PublishedbyElsevierMassonSASonbehalfofSocie´te´ franc¸aised’anesthe´sieetdere´animation(Sfar).Thisisanopenaccessarticleunderthe
1. Knowndiabetes
1.1. Definitionofdiabetes
Diabetes mellitus is defined by chronic elevation of
blood-glucoselevelslinkedtoinsulinresistanceand/orinsulinopaenia.A
diagnosisofdiabetescanbemadeinthreesituations:
fastingbloodglucose1.26g/L(7.0mmol/L),ontwooccasions;
plasma-blood glucose2g/L (11.1mmol/L) at 2h after
con-sumingasweetliquidcontainingameasuredamountofglucose
(oralglucosetolerancetest,OGTT);
thepresenceofclinicalsymptoms(polyuria,polydipsia,
unex-plainedweightloss)withplasmaglucose2g/L(11.1mmol/L),
irrespective of the time of blood sampling.Measurement of
fasting blood-glucose level is currently recommended as the
first-linetestfordiabetes[1].
An OGTT (with measurement of fasting blood glucose and
blood-glucoselevelsat2hafteroralconsumptionof75gglucose)
can also be conducted and is more sensitive (Appendix).
Measurementofblood-glycatedhaemoglobin(HbA1c)isproposed
inmanycountriesasadiagnostictestfordiabetesatacut-offvalue
of6.5%[2].
1.2. Maintypesofdiabetes
Practical sheet A summarises the main characteristics of
diabetes.Type-2diabetes(T2D)isthemostcommontypeandis
oftendiscoveredas aninsidious diseasebecause itis
asymp-tomaticatthetimeof screeninghigh-riskpatients.Thus,T2D
may be discovered when in the hospital for surgery, with
chronic complications already present. The main risk is a
hyperosmolarhyperglycaemic statewhenpolyuria/glycosuria
andhyperglycaemia(>1.80g/L[10mmol/L])arenot
compen-satedforby polydipsiaor parenteral hydration inan
uncon-sciouspatient.
Type-1diabetes(T1D)islinkedtotheautoimmunedestruction
of
b
-pancreaticcells,which synthesiseinsulin.Thetwocompo-nentsforthephysiologicalsecretionofinsulinarethennolonger
active,namely:
‘basal’secretion(or‘liveinsulin’,whichiscontinuousoverthe
nycthemeralperiod),andrepresentsapproximately50%ofdaily
requirements;
prandialsecretion(or‘insulinproducedwheneating’).
Substitutionofbasalinsulinshouldneverbestopped,evenina
subject withnormoglycaemia, due to the majorrisk of
hyper-glycaemia followed by ketosis and diabetic ketoacidosis. In
general,patientswithT1Darefamiliarwiththisruleofsurvival.
‘Pancreatic’diabetes,secondarytopancreaticdiseases,isless
common.Itfeaturessevereinsulinopaenia,withanincreasedrisk
ofhypoglycaemiabecauseofasimultaneousdecreaseinglucagon
secretion.
Diabetesthat developsduringpregnancy isdiscussed in the
textnamed‘Specificsituations’.
1.3. Treatmentofdiabetes
1.3.1. Type-2diabetes
Practical sheets E‘Treatment ofdiabetes: non-insulin drugs’
and F ‘Treatment of diabetes: insulin’ summarise the main
characteristicsoftreatmentsavailableforT2D.T2Dmayrequire
treatmentwithinsulin:this is known asinsulin-requiring T2D.
Insulin and oral glucose-lowering drugs may be combined
[1]. Injectable non-insulin treatments also exist, namely
gluca-gon-likepeptide1(GLP1)receptoragonists,includingsomethat
canbeinjectedweekly.Thedrugsinthisclassreducethespeedat
which the stomach empties after a meal, which may lead to
gastroparesis.Preoperativeadministrationofthesetreatmentsis
indicatedinthetextnamed‘Preoperativeperiod’.
1.3.2. Type-1diabetes
PatientswithT1Darealwaystreatedwithinsulin.Themost
widely used method is by basal-bolus, depicted in Practical
sheetFtitled‘Treatmentofdiabetes:insulin’.Basalsecretionof
insulin is substituted by one or two injections of slow- or
intermediate-acting insulin. Basalinsulin should be supplied
constantly,althoughthedosemayhavetobedecreasedifthere
ishypoglycaemia. Substitution of prandial insulinisdone by
injecting an ultra-rapid analogue of insulin, with a larger
amountinjectedaftera mealrichincarbohydrates.Insulinis
generally injected before the meal, although it may be
sometimes administered just after a meal if the amount of
carbohydratesconsumedispreciselyknown.Rapid(ornormal)
insulinisnolongerusedbecauseithasadelayedaction(20min
vs.5minforultra-rapidanalogues)andthedurationofactionis
less adapted to meals (6h compared to the post-prandial
requirementsof3h).
An insulin pump is often used for subcutaneous (SC)
administration of insulin in T1D and sometimes in T2D.
Programmable electronic pumps (the size of a mobile phone)
containaninsulinreservoiranddeliverinsulinsubcutaneouslyand
continuously24-ha day.Thepatientrefillsthereservoir
(ultra-rapidanalogueofinsulin),whichisconnectedtoaninfusionline
andacannula(6or9mm),whichisinsertedsubcutaneously.The
catheter shouldbechanged by thepatienteverythree days to
prevent alterations to the equipmentand because diffusion of
insulinthenbecomeslesseffective.Thereservoir,thetubeandthe
needleshouldbechangedatthesametime.
Thissystemreproducesthebasal-bolusschemeby
discontinu-ous SC injections of slow-acting and ultra-rapid analogues of
insulin: continuous infusion of a small amount of ultra-rapid
insulin reproduces basal insulin and is the basal output. The
amountis determinedand programmedbya diabetologist and
maybemodifieddependingon thetimeofday(day,night).To
reproduceabolus,theoutputisacceleratedusingeitheraremote
controlordirectlyonthepumpbythepatient(1IUbolus=1IUof
ultra-rapidinsulinanalogue).
The system is reliablebut the major risk is ketoacidosis if
delivery of insulin is interrupted (catheter obstruction, line
kinkingbutnottriggeringthepumpalarm,needlewithdrawal),
empty reservoir; pump stopping...). Ifthe dose of ultra-rapid
insulininfusedperhourisverylow,theeffectoftheinsulinwill
stopafterapproximately2hours.Suddenandtotallackofinsulin
inapatientwithT1Dleadstoketoacidosiswithinafewhours.If
the pump is removed, basal insulin should be replaced
immediately eitherbya SC injection of slow-acting insulin or
intravenous(IV)administrationofultra-rapid-actinginsulinand
an infusion pump. These aspects are developed further in
PracticalsheetsPtitled‘Administrationofinsulinintravenously
with an infusionpump/SC insulin’and Q ‘General basal-bolus
scheme’.
If the patient develops hypoglycaemia, it is necessary to
immediately administer 15g of carbohydrate orally (see text
entitled‘Postoperativeperiod’).Thepumpshouldnotberemoved
as the staff may forget to reconnect it, which would lead to
ketoacidosis.Ifseverehypoglycaemiaoccurs,itispossibletostop
thepumptemporarilyfor1 2hmaximum,butitisessentialto
restartitrapidly.
G.Cheissonetal./AnaesthCritCarePainMed37(2018)S5–S8 S6
2. Unexpecteddyglycaemia
2.1. Stresshyperglycaemia
2.1.1. Definition
The surgical procedure and its inherent metabolic effects
induceastressedstatethatcausesperioperativehyperglycaemia,
known as ‘stress hyperglycaemia’. According to the American
DiabetesAssociation,stresshyperglycaemiaisdefinedastransient
hyperglycaemiainapreviouslynon-diabeticpatientsubmittedto
anacuteillnessorthathasundergoneaninvasiveprocedure[2].It
is characterisedby blood-glucose levels1.80g/L (10mmol/L),
with levels returning to normal (<1.26g/L or 7mmol/L) after
removal of the stressor and withdrawal of glucose-lowering
treatment,ifitwasstartedpreviouslyinapatientwhoseHbA1c
was<6.5%.
2.1.2. Aggravatingfactors
Theseverityofstresshyperglycaemiadependsonthetype
of surgery, the aggressiveness of the procedure and its
duration [3–5]. Its prevalence varies between 30 and 80%
dependingonthetypeofsurgery,withthehighestprevalence
observedduringcardiacsurgery.Itisthereforenotsurprising
thatmoststudiesconductedtoassessperioperativeglycaemic
controlhavebeencarriedoutinthesettingofcardiacsurgery
with extracorporeal circulation [5–12]. Other risk factors
include catecholamine infusion, corticosteroid use, obesity,
age,hypothermia, hypoxia,cirrhosis,trauma,extensiveburns
and sepsis.
2.1.3. Mechanismsofstresshyperglycaemia
The main mechanism responsible for perioperative stress
hyperglycaemiaisperipheralinsulinresistance[13],whichisan
independent risk factor for morbidity and mortality [12]. In
addition,stimulationofendogenousglucoseproductioncanalso
occur[14]andthereisanincreaseinrenalreabsorptionofglucose
[6] or a decrease in glucose clearance [15]. Stress hormones
(glucagon,cortisol,catecholamines)andmediatorsof
inflamma-tion(interleukin1and6)releasedduringsurgicalstressmaylead
toperioperativeinsulinresistance[16].Insulinresistanceaffects
lipidmetabolismwiththeincreasedreleaseoffreefattyacids[17],
thusfurtheraggravatinginsulinresistance.
Perioperativeinsulinresistancemaylastforseveraldaysafter
theinvasive procedure and initially involves insulin-dependent
peripheral tissues [18,19]. Perioperative blood loss, as well as
prolonged immobilisation, both affect glucose metabolism by
skeletalmusclesandaccentuateperioperativeinsulinresistance.
Finally, prolonged perioperative fasting induces a decrease in
hepaticglycogensupplyandanincreaseinneoglucogenesis,lipid
andproteinmetabolism,which,inturnaggravatesperioperative
insulinresistance[20].
2.1.4. Pathophysiologicalconsequencesofstresshyperglycaemia
Hyperglycaemiaabolishedischaemicpreconditioning[21]and
resulted in endothelial dysfunction [22], decreased phagocytic
activityofpolymorphonuclearneutrophils[23]andincreasedthe
formation oflesions in theblood / brain barrierin a model of
murine cerebral ischemia [24]. These deleterious effects of
hyperglycaemia are caused by mitochondrial abnormalities in
non-insulin-dependentcellswhereglucosetransporters(GLUT4)
areover-expressedduringstress[25].
Perioperativeinsulinresistanceleadstotheincreasedreleaseof
free fatty acids [17], which are potentially harmful to the
myocardium, and modify protein metabolism, thus leading to
increased protein catabolism and delayed healing [26]. Insulin
therapymitigatestheconsequencesofinsulinresistance,suchas
thepostoperativeneuro-hormonalresponsetostress[8]andthe
perioperativerelease of free fattyacids fromperipheral tissues
during surgery, withextracorporeal circulation in non-diabetic
patients[27].
2.2. Stresshyperglycaemiaorundiagnosedpre-existing
dysglycaemia?
Itisestimatedthatmorethan500,000patientshave
undiag-nosedT2DinFrance.Theprevalenceishighamonghospitalised
patientsduetotheirageandcomorbidities.Inastudyof40,836
inpatients, of whom 19% had known diabetes, 47% underwent
perioperativescreeningofblood-glucoselevels.Screeningshowed
that18% hadblood-glucoselevels>1.8g/L(10mmol/L).
Hyper-glycaemiawasobservedin40%ofdiabeticand6%ofnon-diabetic
patients[28].
Hyperglycaemiarevealedpostoperativelydoesnotdistinguish
patientswithunknowndiabetesbeforesurgeryfromthosewith
stresshyperglycaemia. However,measurement ofHbA1clevels,
whichreflectglycaemiccontrolovertheprevious8–12weeks,can
distinguishbetweenthesetwosituations[29].HbA1c6.5%has
beenusedasadiagnosticcriterionforthispurposesince2009in
some countries [2] and identifies one-third more undiagnosed
diabetic patients compared to using fasting
blood-glucose1.26g/L (7mmol/L). However, routine measurement
ofHbA1cisnotrecommendedfortheFrenchgeneralpopulation
duetoitscost[1].
Thesimplestmethodistodetectundiagnoseddysglycaemiain
thepreoperativeperiod(PracticalSheetC).Indeed:
pre-diabetesfoundduringpreoperativeevaluationsignalsarisk
forstresshyperglycaemiaanditscomplications;
complicationsof undiagnoseddiabetes mayoccur duringthe
perioperativeperiodduetoacuteglycaemicinstabilityand/or
unrecognisedchronicdiabeticcomplications(seetext
‘Preoper-ativeperiod’).
Thus, theserisksshouldbeidentifiedand avoided wherever
possible.
Weproposethatscreeningshouldbecarriedoutinsubjects
with signsofdiabetes (primarysyndrome)or thatare atvery
high-risk: i.e.metabolicsyndrome,familial historyofdiabetes,
previousacutecoronarysyndromeorcerebrovascularaccident,
previous treatment with diabetogenic drugs, history of
gesta-tional diabetes, previous transient hyperglycaemia [30]. We
recommendscreening bymeasuringfastingbloodglucoseand
HbA1c levels.This positionconcerning theuse of HbA1c as a
diagnosticcriterionfordysglycaemiahasalreadybeendescribed
in therecommendationsfor the managementof patients with
acute coronary syndrome [31]. The diagnostic criteria are
summarisedinAppendix1.
Disclosureofinterest
Theauthorsdeclarethattheyhavenocompetinginterest.
Themembers of the working partyhave received support
from the French Society of Anaesthesia and Intensive Care
Medicine (SFAR) and the French Society for the Study of
Diabetes(SFD)fortransportandaccommodationwhen
neces-sary.Thetwonationalbodieshavealsoprovidedhonorariafor
Appendix1. Diagnosticcriteriafordysglycaemia.
Interpretationoffastingblood-plasmaglucoselevelsand
oral-glucosetolerancetest(OGTT)results(2hafteringestionof75g
glucose)[1].
Glycaemia OGTT(2hafteroralingestionof
75gglucose)g/L(mmol/L) Fastingglucose (g/L[mmol/L]) <1.40(7.8) 1.40-1.99 (7.8-11.0) 2.00 (11.1) <1.10(6.1) Normal Glucose intolerance Diabetes 1.10-1.25 (6.1-6.9) Fasting hyperglycaemia Fasting hyperglycaemia andglucose intolerance Diabetes
1.26(7.0) Diabetes Diabetes Diabetes
InterpretationofHbA1clevels[2]
HbA1c <5.7% 5.7-6.4% 6.5%
Normal Riskofdevelopingdiabetes Diabetes
MeasurementofHbA1clevelstodiagnosedysglycaemiaisnot
recommendedinFrance[1].
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