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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2899_Библиотеки_им_академика_М_И_Перельмана
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Takeafocusedhistorytoidentifypresentingfeaturesofhyperglycaemiaincluding:
Polyuria
Thirst
Urinaryfrequency
Urinaryurgency
Vomiting
Weightloss.
Askaboutinfectivesymptomsthatmayhavecausedhyperglycaemia,e.g.respiratoryand
urinarysymptoms. Establish whether the patientisknownto be diabeticand ask about
alcohol intake and medication (including compliance with antiglycaemic drugs, recent
medicationchanges,andsteroiduse).Askaboutfamilyhistoryofdiabetes(includingage
ofonset),andinfemalesaskabouthyperglycaemiaduringpreviouspregnancies.
Themostcommoncausesofhyperglycaemiaareacuteillness,non-compliancewith diabetic
medication,andalcohol.
Examination
Begin your examination with a general inspection. Signs such as vomiting, abdominal
tenderness,andreducedconsciousnessshouldalertyoutoa possiblediagnosis ofDKA
orHHS.
Performafullphysicalexaminationlookingforsignsofinfection.Thisshouldinclude
listeningtothechest,examiningtheabdomen,andassessingtheskinforsignsofcellulitis
andulcers.
Assess volume status; typically, hyperglycaemia will lead to dehydration and may
presentwithclinicalsignssuchas:
Tachycardia
Hypotensionorposturalhypotension
Drymucousmembranes
Raisedcapillaryrefilltime>2seconds
Reducedskinturgor.
Sweet ‘pear-drop’ breathsuggests underlying ketosis andshould heighten your suspicion of
DKA.
Investigations
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Bedside
CBG
Serum ketones should be measured in people with T1DM with persistent hyperglycaemia (>2
readingsabove12mmol/L,atleast1hourapart),orinanypatientifunwell.InterpretasperTable
17.1
Sendurineforcultureifurinarytractinfectionissuspected
Sputumsampleifthepatientisproducingpurulentsputum
Skinswabsifindicated.
BeawarethatpatientswithT2DMtakingSGLTinhibitors (e.g.dapagliflozin,empagliflozin,
and canagliflozin) can present with euglycaemic DKA. In this situation, the CBG may be
normalbutthepatientmayhaveketoacidosis. Itisimportanttocheckbloodketone levelsin
thesepatients.
Table17.1Interpretationofserumketones
Serumketones(mmol/L) Actiontobetaken
<0.6 Normal
0.6–1.4 Checkin2hours
1.5–2.9 Checkin1hour,considerDKA
>3 PerformVBGtocheckpH,considertreatingasDKA
Note:urinaryketonesarealsoused,areadingof>2+shouldpromptthemeasurementofserumketones
andVBG.
ReproducedunderaCreativeCommonsLicence(CCBY-NC4.0)fromTheuseofvariablerate
intravenousinsulininfusion(VRIII)inmedicalinpatients.October2014.JointBritishDiabetes
Societies,InpatientCareGroup(JBDS09).
Bloods
FBC
CRP
U&E
LFT
Serumglucose
HbA1c
VBG
Bloodculturesifthepatientispyrexial.
Imaging
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• ChestX-rayifchestinfectionissuspected.
Management
A singlereadingof elevatedbloodglucoseinanotherwisewellperson maynotrequire
intervention. If an obvious cause of hyperglycaemia is identified (e.g. infection), this
shouldbetreated.Ifapatientisunwell,considertheneedforaVRII(sometimesreferred
toasa‘slidingscale’)andIVfluids.
Acutemanagement
Persistenthyperglycaemia
IfDKA(seeChapter15)orHHS(seeChapter18)aredetected,theseshouldbetreatedas
pertheirguidelines.
Themanagementofsteroid-inducedhyperglycaemiaiscoveredlaterinthischapter.
AVRIIisindicatedinanunwellpatientwithaCBG>10mmol/L,withoutDKAorHHS,
iftheyarenoteatingordrinking.
If a VRII is not indicated, and the patient is being treated with glucose-lowering
medications,e.g.gliclazide,theseshouldbeoptimized.Ifthepatientisbeingtreatedwith
insulin, consider a ‘correction’ dose of short-acting insulin (2–4 units) if required or
increasetheinsulinregimen.
Be careful to avoid overnight hypoglycaemia due to overtreatment of high blood glucose
beforebedtime.
SettingupVRIIs
Thisisaninfusionoffast-actingorshort-actinginsulin(e.g.Actrapid®).Thestartingrate
dependsonthemostrecentCBG.Initiallypatientsshouldbestartedonthestandard-rate
regimen (Table 17.2). If CBGs remain high despite the VRII (i.e. in insulin-resistant
patients),theratesmaybe changed to an increased rateregimen. If the patientbecomes
hypoglycaemicor is known tobe veryinsulin sensitive, itmaybe appropriate to usea
reduced-rateregimen.
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Table17.2Starting(standard)rateofVRII
Capillarybloodsugar(mmol/L) Startingrate(mL/hour)
<4 0
4.1–8.0 1
8.1–12.0 2
12.1–16.0 4
16.0–20.0 5
20.1–24.0 6
>24.0 8
AdaptedunderaCreativeCommonsLicence(CCBY-NC4.0)fromTheuseofvariablerateintravenous
insulininfusion(VRIII)inmedicalinpatients.October2014.JointBritishDiabetesSocieties,Inpatient
CareGroup(JBDS09).
Regularlong-actingsubcutaneousinsulinshouldalwaysbecontinuedalongsideaVRII.
Fluidresuscitation
IfreceivingaVRII,patientswillrequireIVfluidsasperlocalguidelines.Elderlypatients
atrisk offluidoverloadshouldreceive25–30mL/kgin 24hours (usuallyapproximately
2L).Patientswhoaredehydrated,e.g.vomiting,willrequireadditionalIVfluidtoreplace
losses.
If a patient is at risk of fluid overload, e.g. heart failure, consider using smaller
volumesof10%glucoseratherthangreatervolumesofalowerpercentageglucose.
Insulin drives potassium (K+) into cells, therefore consider concurrent potassium
chloride(KCL)replacementdependingonK+level:
K+>5.5:noreplacementrequired
K+3.5–5.5:supplementwith0.15%KCL(20mmol)
K+<3.5:supplementwith0.3%KCL(40mmol).
Ifusing0.9%sodiumchloride(NaCl)forIVfluid,whenglucoselevelsare<14mmol/L,
considerswitchingfromNaClto5%dextrosetoavoidhypoglycaemia.
Remember:whileonaVRIIitisimportanttoregularlymeasurepH,glucose,K+,andketones
tomonitorclinicalimprovement.
Treatmentafterstabilization
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DiscontinuingVRIIs
When a patientiseatingand drinkingwithstablebloodsugar levels,considerstopping
the VRII. Ensure they have eaten a meal at least 30 minutes before restarting oral
hyperglycaemicmedication.MeasureCBG1hourafterstoppingtheVRII,andfourtimes
overthenext24hourstoensurethatthereisnoreboundhyperglycaemia.
Consider a referral to the diabetes team of anyone who has required IV insulin
treatment.
Specialconsiderations
Steroid-inducedhyperglycaemia
Steroids causehyperglycaemia andglucoselevelsshould be expected to rise4–8 hours
afteranoralsteroiddose,orsoonerfollowingaparenteraldose.
Often,butnotalways,glucoselevelsimproveasthesteroiddoseisreducedorstopped;
therefore,anytreatmentthathasbeeninitiatedwillneedtobetitrateddownagain.
Ifapatienthassteroid-inducedhyperglycaemia,theyshouldbetestedfordiabetes(see
Chapter26)atleast6weeksaftertheirsteroidcoursehascompleted.
Glucosemonitoringfrequencyforpatientsonsteroidtherapy
Patientswithoutadiabetesdiagnosis:OD.If>12mmol/L,escalatetestingfrequencytoQDS
Patientswithadiabetesdiagnosis:QDStesting.
Treatingsteroid-inducedhyperglycaemia
IfCBGis>12mmol/Lmorethantwicein24hours,commencetreatment.
Insulin treatment may be more appropriate than oral treatment if hyperglycaemia
persiststhroughouttheday.
If the patient is acutely unwell, they should be started on a VRII pending specialist
diabetesteamreview.
Optionsfortreatment
Non-diabetic
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Sulfonylurea,e.g.gliclazide,startingdose40mgOD
10unitsofbasalinsulintobegiveninthemorning,e.g.Humulin®I,Insuman®Basal
Amultipledailyinjectionregimenmayberequiredforsteroidtreatmentsinvolvingmultipledaily
dosages.
T1DM
Increaseinsulindosagesby2unitsevery24–48hoursandseekspecialistdiabetesteamreview.
T2DMnotreceivinginsulintherapy
Commencegliclazide40mgODorescalatecurrentdoseby40mgifthepatientisalreadytakingit
(maximumdose240mginthemorning,maximumdailydose320mg)
Metformin,escalatedosetoamaximumof1gBD.
T2DMalreadyoninsulintherapy
Iftakingbasalinsulinintheevening,considerswitchingthedosetomorning.
Patientswithdiabeteswhoareundergoingsurgery
ThisguidanceiscoveredinChapters92and93.
Furtherreading
1.RaineT,CollinsG,HallC,etal.(2018).Hyperglycaemia.In:OxfordHandbookfortheFoundation
Programme,5thed(p.330).Oxford:OxfordUniversityPress.
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Chapter18
Hyperglycaemichyperosmolarsyndrome
Guideline: Joint British Diabetes Societies Inpatient Care Group (The
managementofthehyperosmolarhyperglycaemicstate(HHS)inadultswith
diabetes):
https://abcd.care/sites/abcd.care/files/site_uploads/JBDS_Guidelines_Current/JBDS_06_The_Management_of_Hyperosmolar_Hyperglycaemic_State_HHS_%20in_Adults_FINAL_0.pdf
OUPdisclaimer:OxfordUniversity Press makesno representation, express
or implied, that the drugdosagesarecorrectand thatthe recommendations
are an exclusive or mandatory course of care. All health professionals
readingthistexthavearesponsibilitytoevaluateitsappropriatenessandtake
theindividualneedsofthepatientintoaccount.
Localtrustguidelines:pleaserefertoyourlocalguidelinesasnecessary.
Overview
Hyperglycaemichyperosmolarstate(HHS)isamedicalemergencywithamortalityof10–
20%.1Ittypicallyaffectsolderpatients,sometimesasafirstpresentationofT2DMandit
developsoverdays,ascomparedwithDKA(seeChapter14)whichdevelopsoverhours.
HHSischaracterizedbyseveredehydrationalongwithhyperglycaemiawhichresultsina
hyperosmolar state. Treatment involves rehydration and restoration of electrolyte
disturbancesinacautiousmannerthatavoidsrapidanddangerouscellularfluidshifts.
Diagnosis
History/diagnosticcriteria
Diagnosisshouldbeconsideredwhenthefollowingfeaturesarepresent:
Severedehydration—indicatedbyhypovolaemiaandhypernatraemia
Marked hyperglycaemia (≥30mmol/L) without significant hyperketonaemia (<3mmol/L) or
acidosis(pH>7.3,bicarbonate>15mmol/L)
Osmolality≥320mOsm/kg.
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PatientscanpresentwithamixtureofHHSandDKA.Considerinthepresenceofsignificant
hyperketonaemia.
Examination
Systematically examine the patient using an ABCDE approach (Table 18.1).
Hyperglycaemiaresultsinanosmoticdiuresiswhichcausesdehydration.
Table18.1HHSexaminationfindings
A
Checkforevidenceofairwaycompromiseduetoreducedconsciouslevel
B
Hypoxia
C
Tachycardia
Hypotension
JVPnotvisible
Coolperipheries
Prolongedcapillaryrefilltime
D
↓GCSscoreiscommonwhenosmolality>330mOsm/kg
Limbweaknessmaybeasignofraisedurea
E
Sunkeneyesandlongitudinalfurrowsonthetonguesuggestdehydration
Examinefeetforulceration
CallforhelpearlyinHHSpatients
The patient usually has some impairment of conscious level due to significant
metabolic derangement and they may be more dehydrated than they appear—water
moves from cells into the extracellular space, temporarily preserving intravascular
volume.
Investigations
Use biochemicalparametersinconjunctionwithclinicalfindings. Look forprecipitating
factors,e.g.infectionoravascularevent.
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Bedside
Point-of-carecapillaryglucoseandketones
UrinalysisandMC&S
ECG—cardiaceventscanbeaprecipitantorcomplicationofHHS.
Bloods
FBC
U&E:
Tocalculateosmolality(Box18.1)
If patientshaveacuteorchronickidneyinjury,thismaybecontributingtotheiracidosisand
willneedstrictfluidbalancemanagement
CRP
VBG(includingHCO
3
–
/lactate)
Serumglucoseandketones
HbA1c
Bloodcultures.
Box18.1Osmolalitycalculation
2Na++glucose+urea
Imaging
ChestX-ray.
Escalation
Considerescalationtohigherdependencycareifanyofthefollowingarepresent:
SerumpH<7.1(DKAmaycoexist)
Potassiumderangementonadmission
GCSscore<12
Oxygensaturation<92%onair
Signs of shock: systolic blood pressure <90mmHg, heart rate >100bpm or <60bpm, or
hypothermia
Signs of severe dehydration: osmolality >350mOsm/kg, sodium >160mmol/L, or creatinine
>200µmol/L
Macrovascularevent,e.g.myocardialinfarctionorotherseriouscomorbidity.
Management
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Acutemanagement
Correct biochemical abnormalities slowly to prevent vascular complications and avoid
pathology caused by rapid cellular fluid shifts (e.g. sudden drop in blood pressure,
cerebraloedema,centralpontinemyelinolysis).
Afterinitialassessment,usethetreatmentalgorithm(Fig.18.1)to:
Normalizeosmolality(Box18.1)
Replacefluid/electrolytelosses(Box18.2andTable18.2)
Reduceglucose(aimtoreduceto10–15mmol/L).
Box18.2Expectaninitialriseinsodium
Serum osmolality reduces when blood glucose is lowered. Water shifts into the intracellular
space,andserumsodiumconcentrationrises
A fallin glucoseof5.5mmol/L willcausea2.4mmol/Lrise insodium.Arisegreaterthanthis
indicatesinadequatefluidresuscitation
Risingsodiumisonlyaconcernifosmolalityisnotfallingconcurrently.
Source:Themanagementofthehyperosmolarhyperglycaemicstate(HHS)inadults.February2022.
JointBritishDiabetesSocieties,InpatientCareGroup(JBDS06).
Table18.2Potassiumreplacement—aimtomaintainwithinnormalrange
Potassiumlevelinfirst24hours(mmol/L) Potassiumreplacementininfusionsolution
>5.5 Nil
3.5–5.5 40mmol/L
<3.5 Seniorreview—additionalpotassiumrequired
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