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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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Insulin treatment causes movement of potassium ions into cells which causes
hypokalaemia. Potassium should therefore be checked prior to commencing each
infusionofIVfluid.Theresultisthenusedtodeterminehowmuchpotassiumchloride
(KCl)shouldbeaddedtothesubsequentinfusion.
Potassiumlevel>5.5mmol/L:noKClinnextinfusion
Potassiumlevel3.5–5mmol/L:40mmol/LKCl
Potassiumlevel<3.5mmol/L:40mmol/LKClandrequestseniorreview.
Fixedrateinsulininfusion
Prescribeaninsulininfusionof50unitsofshort-actinginsulin,e.g.Actrapid®,mixedwith50mL
0.9%saline
Theinfusionrateshouldstartat0.1 units/kg/hourandshould commenceafterthefirstbagofIV
fluidshasbegun
Continueanylong-actinginsulinthatthepatientisusuallyprescribed.
IV fluids and insulin may be given through the same cannula, butonly ifit is a large-bore
cannulaanditisattachedtoasplitconnectorwithone-wayvalves.
Monitoring
General
RegularroutineobservationsandmonitoringofGCSscore
ContinuouscardiacmonitoringifthepatienthassevereDKA(Box4.2).
Bloods
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CheckABGandketonelevelshourly:
Aimforbloodketonestofallbyatleast0.5mmol/L/hour(ifketonemonitoringisunavailable,
aim for bicarbonate level to rise by 3.0mmol/L/hour or blood glucose levels to fall by
3.0mmol/L/hour).Ifthisisnotachieved,callforseniorhelpandconsiderincreasingtheFRII
by1mmol/hour.
If the CBG machine is unable to calculate a precise measurement (because glucose is
>27mmol/L),thenusetheglucosevaluefroma serumsampleprocessedinthelaboratory or
bloodgasmachine.
If the glucose level is <14mmol/L, add a 10% glucose infusion at a rate of 125ml/hour.
ContinuethesalineinfusionandFRII;however,considerreducingtherateoftheFRIIto0.05
units/kg/hourtoreducetheriskofhypokalaemiaandhypoglycaemia.
VBGafter1hour,after2hours,andthen2-hourly(recordpH,potassium,andbicarbonatelevels)
duringthefirst6hours,andthenagainat12hours.
Examination
Reassessfluidstatusafter12hoursofIVfluids,orsoonerifanyclinicalconcern.Aimforaurine
outputofatleast0.5mL/kg/hour.
Ifthepatientisincontinentoranuric,considercatheterizationtoensureaccuratefluidbalance
assessment.
Treatmentafterstabilization
EnsurepatientsreceiveprophylacticLMWH(seeChapter99)unlesscontraindicated.
Resolution
DKAhasresolvedwhen:
Bloodketonesare<0.6mmol/LAND
VenouspHis>7.3ORbicarbonateis>18mmol/L.
Ifthepatientisnoteatingordrinking,continueIVfluidsandswitchtoavariablerateinsulin
infusion(VRII)
If theyareeatinganddrinking regular meals,restartthepatient’sinsulin regimen(orstarta
new regimen under the guidance of an inpatient diabetes team if newly diagnosed). Give
short-actinginsulinjustbeforeameal,andstoptheFRII1hourafterthemeal.
All patients with DKA should be reviewed by the local diabetes team within 24 hours of
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admission.Considerationshouldbegiventochanginginsulindosagesfollowingresolutionof
DKA. Allpatientsshould bedischargedwithacareplanwhichshouldbecopied tothe GP.
This should includespecificadvice abouthowtomanagediabetesduring illness,follow-up
arrangements,andcontactdetailsforthediabetesteamtohelpavoidfurtheradmissions.
Specialconsiderations
Complications
Potassiumimbalances
HypokalaemiaandhyperkalaemiaarepotentialcausesofmortalityinpatientswithDKA.
Hypoglycaemia
There is a smallrisk of hypoglycaemia(<4mmol/L) during the treatmentof DKA. This
canbeassociatedwithcardiacarrhythmias,braininjury,anddeath.
Cerebraloedema
This is a rare complication in children and young adults and is associated with rapid
administrationoflargevolumesofIVfluids.
Pulmonaryoedema
Thismayoccurinpatientsatriskoffluidoverloadandreflectstheneedforcautionwith
fluidreplacement.
Furtherreading
1. Wass J, Owen K (eds) (2014). Diabetic hyperglycaemic emergencies. In: Oxford Handbook of
Endocrinology and Diabetes, 3rd ed (pp. 683–4). Oxford: Oxford University Press. Available at:
https://doi.org/10.1093/med/9780199644438.003.0013
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Chapter16
Hypercalcaemia
Guideline: Society for Endocrinology Endocrine Emergency Guidance
(Emergency management of acute hypercalcaemia in adult patients):
https://ec.bioscientifica.com/view/journals/ec/5/5/G9.xml
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
Hypercalcaemia is defined as a serum concentration of calcium >2.60mmol/L.
Approximately50% of extracellular calcium is bound to albumin, therefore totalserum
calciumlevelsrequirecorrectingforserumalbuminconcentration.
Calcium homeostasis is regulated through intestinalabsorption, bone resorption, and
renaltubularreabsorption.Theseareprimarilycontrolledbyparathyroidhormone(PTH)
and vitamin D. Hypercalcaemia results from an abnormality of one or more of these
processes.
Hypercalcaemiacanbeclassifiedaccordingtoseverity(Table16.1).
Table16.1Severityofhypercalcaemia
Severity Adjustedserumcalcium(mmol/L)
Mild 2.6–3.0
Moderate 3.0–3.5
Severe >3.5
CausesofhypercalcaemiaarelistedinTable16.2.
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Table16.2Causesofhypercalcaemia
Primary
hyperparathyroidism
a
Adenoma(80–85%)
Hyperplasia
Carcinoma—rare
Multipleendocrineneoplasia
Malignancy
a
PTH-relatedpeptidesecretedbysolidtumours(80%)
Osteoclastactivatingfactors
Metastaticbonedestruction
Granulomatousdisorders
Sarcoidosis
Granulomatosiswithpolyangiitis
TB
Histoplasmosis
Drugs
Thiazidediuretics
Lithium
VitaminAtoxicity
VitaminDtoxicity
Theophyllinetoxicity
Highboneturnover
Paget’sdiseasewithimmobilization
Thyrotoxicosis
Immobilization
Renalfailureassociated
Tertiaryhyperparathyroidism
Aluminiumtoxicity
Rhabdomyolysis (biphasic with initial hypocalcaemia and then hypercalcaemia
candevelop)
Familial
Familialhypocalciurichypercalcaemia
Miscellaneous
Adrenalinsufficiency
Milk-alkalisyndrome
Phaeochromocytoma
a
Mostcommoncausesofhypercalcaemia,accountingfor90%ofcases.
Diagnosis
History
Obtainathoroughhistory,includingfamilyhistoryandsignsof underlyingmalignancy.
Patientswithacutehypercalcaemiamaypresentwiththefollowing:
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Polyuriaandpolydipsia
Mooddisturbances:depression,memoryloss,confusion,coma
Abdominalpainduetonephrolithiasis,nephrocalcinosisorconstipation
Muscleweaknessandbonepain
Proximalmyopathy
Nausea
Symptomsduetoarrhythmias,e.g.palpitations.
A wayto remember thetypical symptomsofhypercalcaemiais ‘painful bones,renal stones,
abdominalgroans,andpsychicmoans’.
Patients may have symptoms from the underlying cause of their hypercalcaemia, e.g.
nightsweats,weightloss,oranorexiasecondarytoanunderlyingmalignancy.
They may also have symptoms from conditions that may develop as a result of
hypercalcaemia(Box16.1).
Box16.1Conditionsthatmaydevelopasaresultofhypercalcaemia
Pancreatitis
Pepticulceration
Cardiomyopathy
Kidneydisease.
Examination
UsetheABCDEapproachtoexaminepatients(Table16.3).
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Table16.3FindingssuggestiveofacutehypercalcaemiainanABCDEexamination
C
Hypertension
Dehydration
D
Confusion
Hyporeflexia
Hypotonia
Paresis
Coma
E
Itching
Conjunctivitis
Renalangletenderness(stones)
Cornealcalcification
Fragility/pathologicalfractures
Investigations
Bedside
ECG:shortenedQTinterval,prolongedPRinterval,andarrhythmias.
Bloods
Calcium(Box16.2),phosphate,PTH,vitaminD,U&E,andLFT(includingalbumin).
Box16.2Interpretationofbloods
Avoidprolongedtourniquetapplicationandrepeatserumcalciumtoconfirmdiagnosis
HighcalciumandhighPTH = primaryortertiaryhyperparathyroidism
HighcalciumandlowPTH = malignancyorotherlesscommoncauses.
Imaging
ChestX-raymayrevealunderlyingmalignancyorgranulomatousdisease
Ifevidenceofprimaryhyperparathyroidismispresent,furtherneckimaging(suchasultrasoundor
sestamibiscanning)isindicated.
Management
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Severe, symptomatichypercalcaemiaislife-threatening.Theinitialacutemanagementof
hypercalcaemiafocusesonrehydrationandstoppinganycausativemedication.Diagnosis
of the underlyingdiseaseis essentialinordertoreverse themechanismof the impaired
calciumbalance.
Acutemanagement
Vigorousrehydration
Sincemostpatientswithhypercalcaemiaare dehydrated,4–6Lof0.9%salineshouldbe
infused in 24 hours if there are no contraindications, e.g. congestive cardiac failure.
Volume expansion with saline enhances urinary calcium excretion because calcium is
coupled to sodium in the kidneys. After 24hours of fluid resuscitation, recheck serum
calciumlevelbeforeconsideringadministeringbisphosphonates.
Monitorfluidbalanceintheelderlyandpatientswithrenalimpairmentandconsideringgiving
furosemideifappropriateforoverloadonly.
Intravenousbisphosphonates
These agents inhibit osteoclast activity; however, they may take 72 hours to reach full
therapeuticeffect.Commenceoncevolumerepleteifcalciumisstillelevatedandmonitor
serum calcium response. Occasionally a second dose is needed. Rarely, hypocalcaemia
maydevelopifthepatientisvitaminDdeficient.
Zoledronicacid4mgover15minutesOR
Pamidronate30–90mgat20mg/hourOR
Ibandronicacid2–4mg.
Second-linetreatments
Glucocorticoids
Inhibit 1,25OHD production and are useful in hypercalcaemia caused by vitamin D
intoxication, granulomatous disorders, and lymphoma. Prednisolone given at a dose of
40mgdailyisusuallyeffectivewithin72hours.
Denosumab
Understrictspecialistsupervision.
Calcitonin
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Works predominantly by inhibiting osteoclast bone resorption, while it also enhances
calciumandphosphateurinaryexcretion.
Renaldialysis
May be indicated in severe renal failure and is a very effective method of treating
hypercalcaemiashouldtheabove-mentionedmeasuresnotbesuccessful.
Parathyroidectomy
Occasionally considered in the acute presentation of primary hyperparathyroidism, if
resistanttopharmacologicalmeasures.
Furtherreading
1. NICE Clinical Knowledge Summaries (2019). Hypercalcaemia. Available at:
https://cks.nice.org.uk/topics/hypercalcaemia/
2. Levi R, Silver J (2011).Hypercalcaemia.In: Wass JAH,StewartPM, AmielSA,Davies MJ (eds)
OxfordTextbook of Endocrinology and Diabetes, 2nd ed (pp. 642–52). Oxford: Oxford University
Press.Availableat:https://doi.org/10.1093/med/9780199235292.003.0411
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Chapter17
Hyperglycaemia
Guidelines:JointBritishDiabetesSocietiesforInpatientCare(Management
of hyperglycaemia and steroid (glucocorticoid) therapy, 2021):
https://abcd.care/sites/abcd.care/files/site_uploads/JBDS_08_Steroids_DM_Guideline_FINAL_28052021.pdf
Joint British Diabetes Societies for Inpatient Care (The use of variable rate
intravenous insulin infusion (VRIII) in medical inpatients, 2014):
https://abcd.care/sites/abcd.care/files/resources/JBDS_IP_VRIII.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
Hyperglycaemiaisdefinedaseitherfastingserumglucose>7mmol/L,orrandomglucose
>11.1mmol/L. It is a common occurrence in diabetic and non-diabetic patients (stress
hyperglycaemia), and is associated with prolonged hospital stays, worse outcomes, and
increased mortality. In diabetic patients, hyperglycaemia can develop into the lifethreateningemergenciesofDKA(seeChapter15)andHHS(seeChapter18).
Diagnosis
CBGmeasurementispartofroutinenursingcare.Historyandexaminationareimportant
inidentifyingthecauseandcontextofthehyperglycaemia,andestablishinghow unwell
thepatientis.
History
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