fluids, electrolytes, and nutrition - accp

Fluids, Electrolytes, and Nutrition

ACCP Updates in Therapeutics® 2012: The Pharmacotherapy Preparatory Review and Recertification Course

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Judith L. KristELLEr, Pharm.d., BCPsWilkes university

Wilkes-Barre, Pennsylvania



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Learning Objectives:

1. Calculatetheosmolarityofintravenousfluidsandcompare with normal plasma osmolarity.

2. Recommendanappropriateintravenousfluidregi-men and monitoring parameters based on a pa-tient’s clinical characteristics.

3. Discusstheappropriateuseandrisksofhypertonicandhypotonicsaline,andrecommendatreatmentregimenandmonitoringparameterstoensuresafeandeffectiveuseoftheseintravenousfluids.

4. Assess electrolyte abnormalities and recommendanappropriatepharmacologictreatmentplanbasedonindividualpatientsignsandsymptoms.

5. Discussappropriate indicationsfor theuseofen-teralandparenteralnutrition(ENandPN).

6. Recommend a patient-specificEN formula, infu-sionrate,andmonitoringparameters.

7. Recommend a patient-specific PN formula andmonitoringplanbasedonthetypeofintravenousaccess,nutritionalneeds,comorbidities,andclini-calcondition.

8. Discussstrategiesforpreventingcomplicationsas-sociatedwithENandPN.

Self-Assessment Questions:Answers and explanations to these questions may be found at the end of this chapter.

1. A 74-year-oldwoman presents to the emergencydepartment with a 3-day history of cough, tem-peratureto102°F,andlethargy.Shehasthefollow-ingvital signsand laboratoryvalues:bloodpres-sure(BP)72/40mmHg,heartrate(HR)115beats/minute,urineoutput10mL/hour,whitebloodcellcount(WBC)18,000,hemoglobin12.5g/dL,bloodureanitrogen/creatinineratio(BUN/Cr)28/1.7mg/dL(baselineCr1.2mg/dL),bloodglucose82mg/dL,andweight72kg.Aftera500-mLfluidbolusof0.9%sodiumchloride (NaCl),herBPandHRare80/46mmHgand113beats/minute.Herchestradiographisconsistentwithpneumonia.Hermed-ical history includes coronary artery disease andarthritis.Whichoneof the following is themostappropriate treatment?A. Furosemide40mgintravenously.

B. 5%albumin500mLinfusedover4hoursplusnorepinephrinetitratedtomaintainasystolicBPof90mmHgorhigher.

C. 1000-mLfluidboluswith5%dextrose(D5W)and0.9%NaCl.

D. 1000-mLfluidboluswith0.9%NaCl.

2. An order has been received for 3%NaCl. Using0.9%NaCland23.4%NaCl,firstdeterminehowmuch of each is necessary to prepare 1L of 3%NaCl. Second, calculate the osmolarity of 3%NaCl.Finally,determinewhethertheresultantso-lutionshouldbeadministeredthroughacentralorperipheralintravenousinfusion(molecularweight[MW]ofNaClis58.5,osmoticcoefficientis0.93).A. Mix907mLof0.9%NaClplus93mLof

23.4%NaCl;osmolarity=954mOsm/L;central intravenous infusion.

B. Mix907mLof0.9%NaClplus93mLof23.4%NaCl;osmolarity=477mOsm/L;peripheral intravenous infusion.

C. Mix850mLof0.9%NaClplus150mLof23.4%NaCl;osmolarity=954mOsm/L;central intravenous infusion.

D. Mix850mLof0.9%NaClplus150mLof23.4%NaCl;osmolarity=513mOsm/L;peripheral intravenous infusion.

3. A 68-year-oldman is admitted to the hospital forworseningshortnessofbreathduringthepast2weeksattributabletoheartfailure.HisserumNaconcentra-tiononadmissionwas123mEq/L.Otherabnormallaboratory values include brain natriuretic peptide850andCr1.7mg/dL.Chestradiographisconsis-tentwithpulmonaryedema.Thepatientweighs85kgonadmission,whichisup3kgfromhisbaselineweight.Thepatientisnotexperiencingnausea,head-ache,ormentalstatuschanges.Thephysicianorders3%NaCltotreatthehyponatremia.Whichoneofthefollowingrecommendationsisbest?A. 3%NaClisanappropriatechoicebecausethe

hyponatremiaislikelyacute.B. A250-mLbolusof3%NaClisappropriate

ifusedincombinationwithfurosemidetopreventvolumeoverload.

C. 3%NaClisappropriateaslongastheserumNadoesnotincreasemorethan10mEq/Lin24 hours.



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D. Therisksof3%NaCloutweighthepotentialbenefitforthispatient.

4. A55-year-oldmanwithdiabetesandkidneydis-ease presents with hyperkalemia. His laboratoryvaluesincludepotassium(K+)7.2mEq/L,calcium(Ca)9mg/dL,albumin3.5,andbloodglucose302mg/dL.Hiselectrocardiogram(ECG)isabnormalwithpeakedTwaves.Whichoneofthefollowingisthebestrecommendationforinitialtreatmentofhishyperkalemia?A. Regularinsulin10unitsintravenouslyplus50

gofglucoseintravenously.B. 10%Ca++gluconate10mLintravenouslyover

5 minutes.C. Kayexalate15gmixedwith100mLof20%

sorbitolevery4hoursasneeded.D. Na+bicarbonate50mEqintravenouslyover5

minutes.

5. A 68-year-old patient is admitted to the hospitalafteracardioembolicstroke.Hermedicalhistoryis significant for atrial fibrillation, acutemyocar-dialinfarction,anddiabetes.Shehasbeenuncon-sciousfor48hours.Themedical teamdecides tostartfeedingthepatient.Herweightis60kg,andalllaboratoryvaluesincludingglucoseconcentra-tionsarenormal.Althoughshecurrentlyhasnoen-teralaccess,shedoeshaveaperipheralintravenouscatheter. Which one of the following nutritionalregimensisbestforthispatient?A. Initiateparenteralnutrition(PN)containing

60gofaminoacids(AA),500mLof10%lipidemulsion,300gofdextrose,standardelectrolytes,multivitamins,andtraceelementsinavolumeof2000mLadministeredover24hours.

B. InitiatePNcontaining40gofAA,500mLof10%lipidemulsion,200gofdextrose,standardelectrolytes,multivitamins,andtraceelementsinatotalvolumeof2000mLadministeredover24hours.

C. Insertanasogastric(NG)ornasoduodenalfeedingtubeandinfuseIsocal(1kcal/mL)startingat25mL/hourandadvancetoagoalrateof65mL/hour.

D. InsertapercutaneousendoscopicgastrostomyfeedingtubeandinfuseIsocal(1kcal/mL)startingat25mL/hourandadvancetoagoalrateof100mL/hour.

6. A70-year-oldmanisadmittedtothehospitalwithperitonitis caused by severe inflammatory boweldisease.Thepatienthasreceivedadequatefluidre-suscitation,andheisprescribedappropriateantibi-otics.Thephysicianwantsthepatienttohavesev-eraldaysofbowelrest,andheorshehasconsultedthepharmacisttorecommendaPNformulatobeadministeredthroughacentralline.Thepatientishemodynamically stable, with normal electrolyteconcentrations. Weight is 55 kg, prealbumin 20mg/dL,BUN/Cr20/1.1mg/dL,andWBC17,000.Assumingthatappropriateelectrolytes,multivita-mins,andtraceelementsareincluded,whichoneof the followingPNformulaswhenadministeredover 24 hours will provide this patient adequatecalories,AA,andlipid?A. AA10%700mL,dextrose30%325mL,lipid

20%500mL.B. AA10%450mL,dextrose70%400mL,

lipid10%500mL.C. AA10%800mL,dextrose70%350mL,lipid

10%500mL.D. AA15%900mL,dextrose50%500mL,

lipid10%500mL.

7. A59-year-oldmanhasbeenadmittedtothehospi-talafterseveraldaysofvomitinganddiarrhea.Intheemergencydepartment,hehadseveralrunsofnonsustained ventricular tachycardia.His plasmaK+onadmissionwas2.8mEq/L.After receiving200mEqofpotassiumchloride(KCl)infusedover24hours,hisrepeatK+is3.2mEq/L,andhecontin-uestohaverunsofventriculartachycardia.OtherlaboratoryvaluesincludeNa+143mEq/L,magne-sium1.4mg/dL,phosphorus3mg/dL,Ca++9mg/dL,andionizedCa++1.1mmol/L.Whichoneofthefollowingsuggestionsisbesttotreatthispatient’shypokalemia?A. AdministerKCl20mEqintravenouslyover1

houreach×4dosesandrecheckK+.B. Administermagnesiumsulfateasa2-gslow

intravenous infusion.



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C. AdministerK+ phosphate 15 mmol intravenously over 4 hours.

D. AdministerCa++gluconate2gintravenouslyover 5 minutes.

8. Which one of the following nutritional strategiescan prevent gutmucosal atrophy and subsequentbacterialtranslocation?A. PNenrichedwithglutamine.B. PNenrichedwithbranched-chainAA.C. Enteralnutrition(EN).D. Zinc supplementation.



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I. FLuId mAnAgement

A. Distributionoftotalbodyfluid(TBF).

75%ofextracellularfluidisinterstitial(thisfluid“bathesthecells”andis

separatedfromintravascularspacebythesemipermeablecapillarymembrane)

25%ofextracellularfluidisintravascular(about5Lofbloodvolume)

40%ofTBFisextracellular

60%ofTBFis intracellular (enclosedbythecellmembrane)

Figure 1.Distributionoftotalbodyfluid(TBF).

1. Estimatedas60%ofleanbodyweight(LBW)inmenand50%inwomen;anormaladulthasabout42Loffluid

2. Totalbodywaterisfurtherdividedintointracellular(IC)spaceandextracellular(EC)space.a. Around60%ofTBFisIC,and40%isEC;theICandECfluidcompartmentsareseparatedby

thecellmembranes,whicharehighlypermeabletowater.b. TheECcompartmentisfurtherdividedintotheinterstitial(IS)spaceandtheintravascularspace;

theISandintravascularfluidcompartmentsareseparatedbythecapillarymembrane,whichispermeabletoalmostallsolutesexceptproteins.i. Seventy-fivepercentoftheECfluidisintheISspace.ii. Twenty-fivepercentoftheECfluidisintheintravascularspace;theECfluidinthe

intravascularspaceisknownasplasmaandconsistsofabout3L;ifyoualsoconsiderabout2Loffluidfoundinredbloodcells(thus,ICfluid),thetotalbloodvolumeisaround5L.

3. TheapproximatedistributionofTBFintotheICandECcompartmentswithfurtherdistributionoftheECfluidintotheISandintravascularcompartmentsisimportanttorememberfordeterminingthedistributionofintravenousfluid.

B. DistributionofIntravenousFluid1. Crystalloidsareintravenousfluidsthatcancontainwater,dextrose,Na+,Cl-,andotherelectrolytes.

LactatedRinger’s(solution)(LR)isacrystalloidthatcontainsmostlyNa+andCl-,butalsolactate,K+,andCa++.a. SodiumandCl-donotfreelycrossintocells,buttheywilldistributeevenlyintheECspace.b. For0.9%NaClorLR,only25%willremainintheintravascularspace,and75%willdistributein

theISspace;therefore,when1Lof0.9%NaClorLRisadministered,about250mLoffluidwillremain in the intravascular compartment.

2. “Free”waterisequivalenttoD5W.a. D5Wismetabolizedtowaterandcarbondioxide.b. Watercancrossanymembraneinthebody;therefore,itwillbeevenlydistributedinTBF(“free”

becauseitisfreetocrossanymembrane).i. ManyexpertsavoidtheadministrationofD5Wwheneverpossibleinpatientswithelevated

intracranialpressure(ICP)becauseitcancrossintocerebralcells,causingafurtherelevationinICP.

ii. SomepractitionersavoidtheuseofD5Wbecauseoftheriskofhyperglycemia,eventhoughD5Wcontainsonly5gofdextrose/100mL,whichisequivalentto17kcal/100mL.



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c. For D5W,60%willdistributetotheICspaceand40%totheECspace.Ofthe40%distributedtotheECspace,25%willremainintheintravascularspace,and75%willdistributetotheISspace.Therefore,when1LofD5Wisadministeredintravenously,about100mLoffluidwillremaininthe intravascular compartment.

3. Colloidsincludepackedredbloodcells,pooledhumanplasma(5%albumin,25%albumin,5%plasmaproteinfraction),semisyntheticglucosepolymers(dextran),andsemisynthetichydroxyethylstarch(hetastarch),a. Colloidsaretoolargetocrossthecapillarymembrane;therefore,theywillprimarilyremainin

theintravascularspace(althoughasmallportionwill“leak”intotheISspace).b. Exceptfor25%albumin,administering500mLofcolloidwillresultina500-mLintravascular

volumeexpansion.c. Because25%albuminhasanoncoticpressureabout5timesthatofnormalplasma,itwillcausea

fluidshiftfromtheISspaceintotheintravascularspace.Forthisreason,100mLof25%albuminwillresultinabout500mLofintravascularvolumeexpansion.Thishyperoncoticsolutionshouldgenerallybeavoidedinpatientsrequiringfluidresuscitation,becausealthoughtheintravascularspacewillbeexpanded,fluidwillshiftoutoftheISspace,potentiallycausingdehydration.Itmaybeusefulinpatientswhodonotrequirefluidresuscitationbutwhocouldbenefitfromaredistributionoffluid(e.g.,ascites,pleuraleffusions).

d. Hydroxyethylstarchanddextranproductshavebeenassociatedwithacoagulopathyandthereforeshouldbeavoidedinpatientsatincreasedriskofhemorrhage(e.g.,activebleeding,increasedriskofbleeding,kidneydisease).

table 1.DistributionofIntravenousFluid

Intravenous Fluid Infused Volume (mL)equivalent Intravascular Volume expansion (mL)

NS 1000 250LR 1000 250D5W 1000 100Albumin5% 500 500Albumin25% 100 500Hetastarch6% 500 500

D5W=5%dextrose;LS=lactatedRinger’s(solution);NS=normalsaline.

C. FluidResuscitation1. Intravascularfluiddepletioncorrelateswithreducedcardiacfunctionandorganhypoperfusion.2. Signsorsymptomsusuallyoccurwhenaround15%(750mL)ofbloodvolumeislost(e.g.,

hemorrhage)orshiftsoutoftheintravascularspace(e.g.,severesepsis).3. Fluidresuscitationisindicatedforpatientswithsignsorsymptomsofintravascularvolumedepletion.



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table 2.Signs/SymptomsofIntravascularVolumeDepletion

Tachycardia(>100beats/minute)Hypotension(SBP<80mmHg)OrthostaticchangesinHRorBPIncreasedBUN/Crratio>10:1DrymucousmembranesDecreasedskinturgorReducedurineoutputDizzinessImprovementinHRandBPaftera500-to1000-mLfluidbolusBP=bloodpressure;BUN=bloodureanitrogen;Cr=creatinine;HR=heartrate;SBP=systolicbloodpressure.

4. Thegoaloffluidresuscitationistorestoreintravascularvolumeandpreventorganhypoperfusion.5. Becauseintravascularvolumedepletioncancauseorgandysfunctionanddeath,promptresuscitation

is necessary.a. Intravenousfluidsareinfusedrapidly,preferablythroughacentralvenouscatheter.b. Intravenousfluidsareadministeredasa500-to1000-mLbolus,afterwhichthepatientis

reevaluated;thisprocessiscontinuedaslongassignsandsymptomsofintravascularvolumedepletionareimproving.

6. Crystalloids(0.9%NaClorLR)arerecommendedforfluidresuscitation.a. LRishistoricallypreferredinsurgery/traumapatients,butnoevidencesuggestssuperiorityover

NSforfluidresuscitation.b. ThelactateinLRismetabolizedtobicarbonateandcantheoreticallybeusefulformetabolic

acidosis;however,lactatemetabolismisimpairedduringshock.Thus,itmaybeanineffectivesourceofbicarbonate.

7. Colloidshavenotbeenshowntobesuperiortocrystalloidsandareassociatedwithaconsiderablyhighercost.Thefollowingareexamplesofmorecommon,althoughcontroversial,usesofcolloids:a. Semisyntheticcolloidsmaybeconsideredafterfluidresuscitationwithcrystalloid(usually4–6

L)hasfailedtoachievehemodynamicgoalsorwhenclinicallysignificantedemalimitsthefurtheradministrationofcrystalloid.

b. Albuminmaybeconsideredinpatientswithanalbuminconcentrationlessthan2.5g/dLwhohaverequiredalargevolumeofresuscitationfluidsandhavearelativecontraindication(i.e.,increasedriskofhemorrhage)forasemisyntheticcolloid.

c. Albumin(theoretically,25%ispreferred)maybeconsideredinconjunctionwithdiureticsforpatientswithclinicallysignificantedema(e.g.,pulmonaryedemacausingrespiratoryfailure)andanalbuminconcentrationlessthan2.5g/dL,whenappropriatelydoseddiureticsareineffective.

D. MaintenanceIntravenousFluids1. Maintenanceintravenousfluidsareindicatedinpatientswhoareunabletotolerateoralfluids.2. Thegoalofmaintenanceintravenousfluidsistopreventdehydrationandmaintainanormalfluidand

electrolytebalance.3. Maintenanceintravenousfluidsaretypicallyadministeredasacontinuousinfusionthrougha

peripheral or central intravenous catheter.4. Commonmethodsofestimatingthedailyvolumeinchildrenandadults

a. Administer100mL/kgforfirst10kg;then50mL/kgforthenext10–20kg(i.e.,1500mLsofar)plus20mL/kgforeverykilogramgreaterthan20kgor

b. Administer20–40mL/kg/day(foradultsonly).c. Adjustfluidsonthebasisoftheindividualpatient’sinput,output,andestimatedinsensibleloss.



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5. AtypicalmaintenanceintravenousfluidisD5Wwith0.45%NaClplus20–40mEqofKClperliter.TheKClcontentcanbeadjustedfortheindividualpatient.

Patient Cases1. A65-year-oldmanwitha3-dayhistoryoftemperatureto102°F,lethargy,andproductivecoughishospital-

izedforCAP.Hismedicalhistoryincludeshypertensionandcoronaryarterydisease.HisvitalsignsincludeHR104beats/minute,BP112/68mmHg,andtemperature101.4°F.Hisweightis80kg,urineoutput10mL/hour,BUN16,Cr1.7mg/dL,andWBC10.4.Otherlaboratoryvaluesarenormal.Whichoneofthefollow-ingismostappropriateatthistime?A. Furosemide40mgintravenously.B. Albumin25%intravenouslyover60minutes.C. Hetastarch6%500mLintravenouslyover60minutes.D. D5W/0.45%NaClplusKCl20mEq/Ltoinfuseat110mL/hour.

2. After2daysofappropriateantibiotictreatment,thepatientinquestion1hasWBCof9,andheisafebrile.HisBPis135/85mmHg,andhisurineoutputisnow45mL/hour.Hisalbuminis3.2,BUN14,andCr1.4mg/dL.Allotherlaboratoryvaluesarenormal.Hisappetiteisstillpoor,andheisnottakingadequatefluids.Hehasperipheralintravenousaccess.Whichoneofthefollowingismostappropriatetoinitiate?A. PeripheralPNtoinfuseat110mL/hour.B. Albumin5%500mLintravenouslyover60minutes.C. D5W/0.45%NaClplusKCl20mEq/Ltoinfuseat110mL/hour.D. LRsolutiontoinfuseat110mL/hour.

II. OSmOLALItY

A. PlasmaOsmolalityIsNormallyBetween275and290mOsm/kg.1. Terminologyclarification

a. Osmolalityisameasureoftheosmolesofsoluteperkilogramofsolvent(Osm/kg),whereasosmolarityisameasureofosmolesofsoluteperliterofsolution(Osm/L).

b. Plasmaosmolarity(mOsm/L)canbecalculatedbythefollowingequation:osmolarity=osmolality×0.995,illustratingthatthereisnoclinicallysignificantdifferencebetweenthem(i.e.,plasmaosmolarityisabout1%lowerthanplasmaosmolality).

2. Plasmaosmolalityismaintainedwithinanormalrangebythirstandsecretionofargininevasopressin(i.e.,ADH)fromtheposteriorpituitary.

3. SodiumsaltsaretheprimarydeterminantofplasmaosmolalityandthereforeregulatefluidshiftsbetweentheICandECfluidcompartments.

4. Plasmaosmolality(inmilliosmolesperkilogram)canbeestimated:(2×Na+)+(glucose/18)+BUN/2.8.

5. Increasesinplasmaosmolalitycauseanosmoticshiftoffluidintotheplasma,resultingincellulardehydrationandshrinkage.

6. Decreasesinplasmaosmolalitycauseanosmoticshiftoffluidintocells,resultingincellularoverhydrationandswelling.



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B. IntravenousFluidsCanBeClassifiedbyTheirOsmolarityRelativetoPlasma.1. Isotonicfluidwillnotresultinafluidshiftbetweenfluidcompartmentsbecausetheosmolarityis

similar to plasma.2. HypertonicfluidcancausefluidtoshiftfromtheICtotheECcompartmentwithsubsequentcellular

dehydrationandshrinkage.3. Hypotonicfluidwithanosmolaritylessthan150mOsm/LcancausefluidtoshiftfromtheECtothe

ICcompartmentwithsubsequentcellularoverhydrationandswelling.a. Redbloodcellswellingcancausecellrupture(i.e.,hemolysis).b. Braincellscanswell,causingcerebraledemaandherniation;thisismostlikelytooccurwith

acutehyponatremia(occurringinlessthan2days).

C. Definitions1. Equivalentweight=MWdividedbyvalence

a. Amilliequivalent(mEq)=1/1000ofanequivalent.b. Examplesofequivalentweight

table 3.ElectrolyteMW,Valence,andEquivalentWeightelectrolyte mW Valence equivalent Weight (g)Sodium 23 1 23Potassium 39 1 39Chloride 35.5 1 35.5Magnesium 24 2 12

MW=molecularweight.

2. Osmoles=numberofparticlesinsolution(assumingcompletedissociation)a. Amilliosmole=1/1000ofanosmole.b. Examplesofosmoles

table 4. Osmoles

Salt OsmolesNaCl 2KCl 2CaCl2 3

CaCl2=calciumchloride;KCl=potassium chloride;NaCl=sodiumchloride.

3. ConvertingMWtomilliequivalents

table 5. ConvertingMolecularWeighttoMilliequivalents

Convert23.4%NaCl(concentratedNaCl)tomEq/mLMolecularweight(MW)ofNaCl=23+35.5=58.5(addMWofNa+Cl)23.4g × 1equiv × 1000mEq=4mEq/mL100mL58.5g1equiv



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D. CalculatetheOsmolarityofIntravenousFluidsinMilliosmolesperLiter.1. Theosmoticcoefficientcanbeusedtocalculatetheosmolarityofintravenousfluidsbecausesalt

formsdonotcompletelydissociateinsolution.a. WithNaCl,forexample,thereissomeionicattractionbetweenNa+andCl,sotheydonot

completelydissociate,butrather,theyareabout93%dissociatedinsolution(thus,theosmoticcoefficientis0.93).

b. Inclinicalpractice,mostdonotconsidertheosmoticcoefficientwhencalculatingtheosmolarityofNaClorotherelectrolytes,andinreality,theosmoticcoefficientisprobablynotclinicallyrelevant(butisusedinthefollowingexamplesforcompleteness).

2. Normalsaline(NS;0.9%NaCl)

table 6. CalculationforNSmW Osmoles Osmotic Coefficient

58.5g/mol 2 0.930.9g × 1 mol × 2Osm × 1000mOsm × 1000mL×0.93=287mOsm/L100mL58.5g1mol1Osm1L

3. D5W(MW180g/mol)

table 7. Calculation for D5W5g × 1 mol × 1000mOsm × 1000mL=278mOsm/L100mL180g1mol1L

4. OsmolarityofD5W/NS=287mOsm/L+278mOsm/L=565mOsm/L5. OsmolarityofNS+KCl20mEq/L

table 8. CalculationforNSPlusKClStep 1: Convert meq to weight (g)

20mEq×1equiv × 74.5g=1.49gofKCl1000mEq1equiv

Step 2: Calculate mOsm/L

1.49g × 1 mol × 2Osm × 1000mOsm=40mOsm/LL74.5g1mol1Osm

Step 3: Add osmolarity of nS + KCl = 287 mOsm/L + 40 mOsm/L = 327 mOsm/L



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III. HYPeRtOnIC SALIne

A. Concentration:Typicallypreparedas3%(954mOsm/L),7.5%(2393mOsm/L),or23.4%(7462mOsm/L)

B. CommonUsesofHypertonicSaline(HS)1. HSisusedintraumaticbraininjurytoreduceanelevatedICPandtoincreaseBP.

a. TypicallyusedifICPisgreaterthan15mmHgusinganICPmonitorb. IftheserumNaconcentrationisclosetotheupperlimitofnormal(i.e.,145mEq/L),thenitis

preferabletousealowerconcentrationofHS(i.e.,3%).2. HSisusedforsymptomatichyponatremia(symptomsdescribedinhyponatremiasectionbelow).

a. SymptomsgenerallydonotoccurunlessserumNa+is120mEq/Lorless,andtheyincreaseinseverityasNa+decreases.

b. Inanefforttopreventseveresymptomsfromoccurring,somepractitionerstreatasymptomatichyponatremiaiftheserumNa+is120mEq/Lorlessbecauseoftheincreasedriskofsymptomsbelowthislevel.

C. InappropriateUseofHS1. Chronic asymptomatic hyponatremia

a. Asymptomaticsyndromeofinappropriatesecretionofantidiuretichormone(ADH)isusuallytreatedwithfluidrestrictionof1000–1200mLoffluidperday.

b. Hyponatremiaisgenerallyawaterproblem(i.e.,anexcessoffreewater)ratherthanadeficiencyofNa;thus,HSmakeslittlesenseintheabsenceofsymptoms(seeHyponatremiasectionbelow).

2. Hyponatremiaassociatedwithseverehyperglycemia(i.e.,diabeticketoacidosis)a. Typically,serumNawilldecreaseinanon-linearfashioninresponsetohyperglycemia(i.e.,

Na+decreasesbyabout1.6mEq/Lforevery100-mg/dLelevationinglucosebetween100and400mg/dL,butNa+willdecreasebyabout2.4mEq/Lforevery100-mg/dLelevationinglucoseabove400mg/dL).

b. Ashyperglycemiaiscorrectedwithinsulin,theserumNa+willnormalize.3. Hyponatremiaassociatedwithhypervolemia(i.e.,heartfailureleadstotissuehypoperfusion,

whichtriggersthesecretionofADH,causingreabsorptionofwaterfromthekidneysandleadingtohyponatremia)a. Ingeneral,thissituationistreatedwithfluidrestriction.b. Symptomatichyponatremiaisuncommoninpatientswithheartfailure.c. HScouldbeconsideredinsymptomaticpatients;however,theymayneeddiuresistoprevent

worseningvolumeoverload.



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D. PreparationofHS

table 9. CalculationstoPrepareHS

Steps exampleChoosebasesolutions Forthisexample,useconcentratedNaClavailableas23.4%vials

andsterilewatertomake1000mLof7.5%HSSetupalligation 23.4%

7.5%0

Addandsubtract 23.4%7.5parts(from23.4%NaCl) 7.5%0 15.9parts(fromsterilewater) 23.4 parts total

Divide 7.5parts/23.4parts=x/1000mL;x=320.5mLof23.4%NaCl15.9parts/23.4parts=x/1000mL;x=679.5mLofsterilewater

HS=hypertonicsaline;NaCl=sodiumchloride.

E. HSDose1. Doseoptionsfortraumaticbraininjury

a. 3%HS250mLor2–4mL/kgintravenouslyover1–15minutesadministeredforelevatedICPb. 23.4%HS30mLover20–30minutesadministeredforelevatedICP

i. Standingorderssuchas30mLevery4or6hoursareNOTrecommended.ii. IfHSisneededforprolongedreductioninICP,a3%HSconcentrationisgenerally

recommended.2. Dose options for patients with symptomatic hyponatremia

a. TreatmentofpatientswithsymptomatichyponatremiainvolvesasmallbutquickincreaseinserumNa+by0.75–1mEq/L/hourtoaconcentrationof120mEq/L.Then,infusioncanbereducedsothatNa+increasesby0.5mEq/L/hour.

b. Estimateaninfusionrateof3%HSbymultiplyingidealbodyweight(IBW)bydesiredrateofserumNaincreaseperhour.(Note:IBWisusedtoavoidoverdosingobesepatients.)i. Forexample,70kg×1mEq/L/hour=70mL/hourtoincreaseserumNa+by1mEq/Lin1

hour.TheinfusioncanbeadjustedtoachievegoalchangesinserumNa+.ii. Infusionrateof3%HSisgenerally1–2mL/kg/hour.iii. Ingeneral,3%HSisnotrecommendedinasymptomaticpatients;ifusedinanasymptomatic

patient,theadministrationrateshouldgenerallynotexceed0.5–1mL/kg/hour.c. Alternatively,somepractitionersrecommenda250-mLbolusof2%–3%HSover30minutesor

50mLof3%HSadministeredasabolusevery30minutesfortwodoses.

F. AdministrationofHS1. Usecentralintravenousaccessbecausetheosmolarityisgreaterthan900mOsm/L.2. Ifnocentrallineisavailable,canuse2%HS3. Somepractitionersuse3%HSthroughaperipheralintravenousaccesssiteinanemergencybecause

theosmolarityisclosetothecutoffrangeforperipheraladministration.Ifaperipheralsiteisused,monitorforphlebitisandobtaincentralaccessassoonaspossible.

G. ClinicalGoalsandMonitoringforAdministeringHSinPatientswithSymptomaticHyponatremia



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1. Goalsa. Stopsymptoms(describedbelow).b. SafeserumNa+achievedusuallyintherangeof120–125mmol/Ltoavoidadverseneurologic

outcomes.NotethattheimmediategoalforpatientswithsymptomatichyponatremiaisnotanormalserumNa+.

c. ReachedmaximalsafeamountofchangeinserumNa+

i. Maximalsafeamountofchangeisgenerallyregardedas10–12mmol/L(or10–12mEq/L)in24 hours.

ii. Somepractitionerssuggestamaximalchangeof8mmol/Lin24hours.2. MonitorserumNa+every1–4hoursdependingonseverityofsymptoms.

H. ComplicationsofHS1. Centralpontinemyelinolysis(alsoreferredtoasosmoticdemyelinationsyndrome)canoccurwith

rapidcorrectionofhyponatremia.a. Characterizedbypermanentneurologicdamagesuchasparaparesis,quadriparesis,dysarthria,

dysphagia,andcomab. Morelikelytooccurwithrapidcorrectionofchronichyponatremiacomparedwithacute

hyponatremia.ThispartlyexplainswhyitisadvisablenottoadministerHSinpatientswithchronic asymptomatic hyponatremia.

c. PreventbyavoidingchangesinserumNa+ofmorethan10–12mmol/Lin24hoursormorethan18mmol/Lin48hours.

2. HypokalemiacanoccurwithlargevolumesofHS.3. HyperchloremicacidosiscanoccurbecauseoftheadministrationofCl-salts(i.e.,NaCl).Canprevent

byadministeringHSina1:1or2:1ratioofNaClandNa+ acetate4. Hypernatremia5. Phlebitisifadministeredinaperipheralvein6. Heartfailure

a. Fluidoverloadcanoccurbecauseofinitialvolumeexpansion.b. Overtime,HScanhaveadiureticeffect,leadingtointravascularvolumedepletion.

7. Coagulopathycausedbyplateletdysfunction8. HypotensionifHSisadministeredrapidly

I. OtherConsiderationsWhenUsingHS1. Becausehypokalemiacancausehyponatremia,remembertocorrectK+depletionifpresent.AsK+ is

replaced,serumNa+ will increase.2. If150mEqofNa+bicarbonateisaddedto850mLof0.9%NaCl,theresultantsolutionisequivalent

toabout3%HS.Whenaninfusionof150mEqofNa+bicarbonateperliterisindicated,itisrecommendedtoaddNa+bicarbonatetoD5Winsteadof0.9%NaCl.

IV. HYPOtOnIC IntRAVenOuS FLuIdS

A. HypotonicFluidsAdministeredIntravenouslyCanCauseCellHemolysisandPatientDeath.1. Albumin25%dilutedwithsterilewatertomakealbumin5%hasanosmolarityofabout60mOsm/L

andcancausehemolysis.2. “QuarterNS”or0.225%NaClhasanosmolarityof68mOsm/Landcancausehemolysis.

B. AvoidUsingIntravenousFluidwithanOsmolarityLessthan150mOsm/L.



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1. SterilewatershouldNEVERbeadministeredintravenously.2. Someprescribersusehypotonicsalineforapatientwithhypernatremia.

a. Inreality,apatientwithhypernatremiagenerallyneedswater,notNa+.b. Therefore,forpatientswithhypernatremia,enteraladministrationofwaterispreferable.c. Iftheenteralrouteisunavailable,recommendD5Wadministeredintravenously.

C. PreventaPotentiallyFatalErrorbyRecommendingOneoftheFollowingAlternativesinPlaceof0.225%NaCl:1. Recommendchanging0.225%NaCltoD5WaloneoracombinationofD5Wand0.225%NaCl.2. Alternatively,ifthereareconcernsrelatedtohyperglycemiawithusingD5W(50gofdextroseor170

kcal/L),recommendusing2.5%dextroseand0.225%NaCl.3. Alternatively,couldrecommendaddingKCltoincreaseosmolarity4. Recommendadministeringwaterenterally(bymouthorfeedingtube)

V. HYPOnAtRemIA And HYPO-OSmOLAL StAteS

A. SodiumSaltsArethePrimaryDeterminantsofPlasmaOsmolality(andsubsequentfluidshiftsbetweentheICandECcompartments).1. AreductioninserumNa+lessthan136mEq/Lusuallycorrelateswithareductioninplasma

osmolality.2. Hyponatremiawithsubsequenthypo-osmolalitycausesfluidtoshiftintocells(cellular

overhydration).Hypotonichyponatremiacanbedividedintothreetypesonthebasisofvolumestatus:

table 10.ClassificationofHyponatremiaHypervolemic Hyponatremia normovolemic Hyponatremia Hypovolemic Hyponatremia

Description CausedbyexcessNa+andfluidbutfluidexcesspredominates

NormaltotalbodyNa+withexcessfluidvolume(i.e.,dilutional)

DeficitofbothNa+andfluid,buttotalNa+isdecreasedmorethantotalbodywater

Example Heartfailure,cirrhosis, nephroticsyndrome

SIADH Fluidloss(e.g.,emesis,diarrhea,fever),third-spacing,renalloss(diuretics)

Diagnosis UrineNa+<25mEq/Lindicatesedematousdisorders(i.e.,heartfailure,cirrhosis,nephriticsyndrome);UrineNa+>25mEq/Lindicatesacute or chronic renal failure

Urineosmolality>100mOsm/Kg(indicatesimpairedwaterexcretion);urineNa>40mEq/L

UrineNa+<25mEq/LindicatesanonrenallossofNa+(e.g.,emesis,diarrhea);urineNa+>40mEq/LindicatesarenallossofNa+

Treatment Sodiumandwaterrestriction; treatunderlyingcause;vasopressinreceptorantagonists (e.g.,conivaptan,tolvaptan)

Ifdrug-inducedSIADH,removeoffendingagent;fluidrestriction;demeclocycline;vasopressinreceptorantagonists(e.g.,conivaptan,tolvaptan)

Fluidresuscitation(seeabove)

SIADH=syndromeofinappropriatesecretionofantidiuretichormone.



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3. Inselectcases,hyponatremiawillbeassociatedwitheitheranormalorelevatedplasmaosmolality.a. ThisisknownaspseudohyponatremiabecauseNa+contentinthebodyisnotactuallyreduced,

butrather,shiftsfromtheECcompartmentintothecellstomaintainplasmaosmolalityinanormalrange(thus,serumNa+willbelow).i. Severehyperlipidemiacanbeassociatedwithanormalorelevatedplasmaosmolality.ii. Severehyperglycemia(i.e.,duringdiabeticketoacidosis)isassociatedwithanelevated

plasma osmolality.b. Oncetheunderlyingconditioniscorrected,Na+willshiftoutofthecells,andhyponatremiawill

resolve.

B. CausesofHyponatremia1. Replacement of lost solute with water

a. Lossofsolute(e.g.,vomiting,diarrhea)usuallyinvolvesthelossofisotonicfluid;therefore,alone,it will not cause hyponatremia.

b. Afterthelossofisotonicfluid,hyponatremiacandevelopwhenthelostfluidisreplacedwithwater.c. Oneofthemostcommoncausesofhyponatremiainhospitalsisthepostoperativeadministration

ofhypotonicfluid.2. VolumedepletionandorganhypoperfusionstimulateADHsecretiontoincreasewaterreabsorptionin

thecollectingtubules,potentiallycausinghyponatremia.3. SyndromeofinappropriateADHsecretionandcortisoldeficiencyarebothrelatedtoexcessiverelease

ofADH.4. Medications,includingthiazidediureticsandantidepressants(especiallyselectiveserotoninreuptake

inhibitors,butalsotricyclicantidepressants),cancausehyponatremia.Drug-inducedhyponatremiaismorelikelyinelderlypatientsandinthosewhodrinklargevolumesofwater.

5. Renalfailureimpairstheabilitytoexcretediluteurine,predisposingtohyponatremia.

C. SymptomsofHyponatremia

table 11. SymptomsofHyponatremia

Serum Sodium (meq/L) Clinical manifestations120–125 Nausea,malaise115–120 Headache,lethargy,obtundation,unsteadiness,confusion110–115 Delirium,seizure,coma,respiratoryarrest,death

1. Symptomsaregenerallyattributabletohypo-osmolality,withsubsequentwatermovementintobraincellscausingcerebraloverhydration.

2. Ifhyponatremiaoccurschronically,cerebralcellswellingispreventedbyosmoticadaptation.a. Solutesmoveoutofbraincellstopreventtheosmoticshiftofwaterintobraincells.b. Forthisreason,patientswithchronichyponatremiamayshowlesssevereornosymptoms.

3. NeurologicsymptomsarerelatedtotherateofchangeintheserumNa+andtothedegreeofchangeinserumNa+.

4. Acutehyponatremiaoccursover1–3days.

D. TreatmentofHyponatremia1. Treatunderlyingcause.2. RaiseserumNa+atasaferate,definedasachangenogreaterthan10–12mEq/Lin24hours.



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3. Treatmentdependsonvolumestatus,thepresenceandseverityofsymptoms,andtheonsetofhyponatremia(thelattertwohavebeendiscussedpreviously).a. Ifthepatientisnormovolemicoredematous,therearetwotreatmentoptions:

i. Fluidrestrictionisthetypicalfirst-linerecommendation.NotethatNaadministrationisnotrecommendedandthatitcanworsenedema.

ii. Vasopressinantagonists(e.g.,intravenousconivaptan,oraltolvaptan)canbeusedinnormovolemic(i.e.,SIADH[syndromeofinappropriatesecretionofantidiuretichormone])orhypervolemic(i.e.,heartfailure)patientstopromoteaquaresis,increaseserumNa+,alleviatesymptoms,andreduceweight;however,thisapproachiscostlyandhasnotbeenshowntoimproveclinicaloutcomes(i.e.,fallprevention,hospitalization,hospitallengthofstay,mortality)inprospectiverandomizedcontrolledtrials.VasopressinantagonistsaresubstratesandinhibitorsofcytochromeP4503A4isoenzymes;monitorfordruginteractionswithother3A4inhibitorsthatcouldincreaseeffectandleadtoarapidincreaseinserumNa+. Fluidrestrictionincombinationwithavasopressinantagonistduringthefirst24hourscanalsoincreasetheriskofoverlyrapidcorrectionofserumNa+.Ifneeded,fluidrestrictioncanbeusedafter24hours.

b. Ifpatienthasintravascularvolumedepletion,needtoreplacevolumefirstwithintravenouscrystalloids(e.g.,0.9%NaCl)i. Untilintravascularvolumeisrestored,patientwillcontinuetosecreteADH,causingwater

reabsorptionandsubsequenthyponatremia.ii. Onceintravascularvolumeisrestored,ADHsecretionwilldecrease,causingwatertobe

excreted.ThiscanleadtoarapidcorrectionofserumNa+;carefulmonitoringisrequiredtopreventoverlyrapidcorrection.

iii. Volumestatuscanbeassessedbyskinturgor,jugularvenouspressure,andurineNa+.c. Onceintravascularvolumeisrestored,maystillneedtoadministerNa+ to patients who

experiencedvolumedepletion,diuretic-inducedhyponatremia,oradrenalinsufficiencyi. TheamountofNa+(inmilliequivalents)neededtoraisetheserumNa+ to a safe concentration

ofabout120mEq/LisestimatedusingLBWasfollows:0.5(LBW)×(120−Na+)forwomen(multiplyLBWby0.6formen).LBWhasbeenestimatedusingweightinkilogramsandheightincentimetersformalesasLBW=[(0.3)(kg)+(0.3)(cm)−29]orforfemalesasLWB=[(0.3)(kg)+(0.4)(cm)−43];formulapublishedin1966(JClinPathol1966;19:389)

ii. Alternatively,theequationabovecanbemodifiedtoestimatetheNa+deficitinthefollowingmanner:0.5(LBW)×(140−Na+)forwomen(multiplyLBWby0.6formen).IfcalculatingtheNa+deficit,itisrecommendedtoadminister25%–50%ofthedeficitduringthefirst24hourstopreventtheoverlyrapidcorrectionofserumNa+.

iii. RegardlessofthemethodusedtoestimateNa+replacement,theamountofNa+administeredshouldbeguidedbyserialserumNa+ concentrations.

d. PatientswithsymptomatichyponatremiashouldbetreatedwithHS(seesectiononHS).4. Correcthypokalemiaifpresentwithhyponatremia.

a. HypokalemiawillcauseareductioninserumNa+becauseNa+ enters cells to account for the reductioninICK+ to maintain cellular electroneutrality.

b. AdministrationofK+ will correct hyponatremia.c. UsecautionwhengivingK+topreventoverlyrapidcorrectionofserumNa+.



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Patient Cases3. A72-year-oldwomanwithahistoryofhypertensionhasdevelopedhyponatremiaafterstartinghydrochlo-

rothiazide3weeksearlier.Sheexperiencesdizziness,fatigue,andnausea.HerserumNa+is116mEq/L.Herweightis60kg,BPis86/50mmHg,andHRis122beats/minute.Whichoneofthefollowinginitialtreatmentregimensismostrecommended?A. 0.9%NaClinfusedat100mL/hour.B. 0.9%NaCl500-mLbolus.C. 3%NaClinfusedat60mL/hour.D. 23.4%NaCl30-mLbolusasneeded.

4. Forthepatientdescribedabove,whichoneofthefollowingisthebesttreatmentgoalforthefirst24hoursincorrectingherserumNa+fromherinitialvalueof116mEq/L?A. IncreaseNa+concentrationto140mEq/L.B. IncreaseNa+concentrationto132mEq/L.C. IncreaseNa+concentrationto126mEq/L.D. MaintainserumNa+between116mEq/Land120mEq/L.

5. Onedaylater,thepatientfromthequestionabovehasimprovedsomewhat.HerBPisnow122/80mmHg,andherHRis80beats/minute.HerserumNa+is120mEq/L,andK+is3.2mEq/L;shestillfeelstired.Sheiseatingaregulardiet.HerECGisnormal.Whichoneofthefollowingisthebestrecommendation?A. D5W/0.9%NaClplusKCl40mEq/Ltoinfuseat100mL/hour.B. 0.9%NaClinfusedat100mL/hour.C. 3%NaClinfusedat60mL/hour.D. Micro-K20mEqbymouthevery6hours×4doses.

VI. HYPeRnAtRemIA And HYPeROSmOLAL StAteS

A. SerumNa+Greaterthan145mEq/LGenerallyCausesHyperosmolality.1. Theosmoticgradientassociatedwithhypernatremiacauseswatermovementoutofcellsandintothe

ECspace.2. Symptomsareprimarilyrelatedtothedehydrationofbraincells.

B. CausesofHypernatremia1. Lossofwaterbecauseoffever,burns,infection,renalloss,gastrointestinal(GI)loss2. RetentionofNa+becauseoftheadministrationofHSoranyformofNa+

C. PreventionofHypernatremiaThroughOsmoregulation1. Plasmaosmolalityismaintainedbetween275and290mOsm/kgdespitechangesinwaterandNa+intake.2. HypernatremiaispreventedfirstbythereleaseofADH,causingwaterreabsorption.3. Hypernatremiaisalsopreventedbythirst.

a. Hypernatremiaprimarilyoccursinadultswithalteredmentalstatuswhohaveanimpairedthirstresponseordonothaveaccesstoortheabilitytoaskforwater.

b. Hypernatremiacanalsooccurininfants.



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D. CerebralOsmoticAdaptation1. Similartopatientswithhyponatremia,patientswithchronichypernatremiacanhavecerebralosmotic

adaptation.a. Braincellstakeupsolutes,Na+,andK+,thuslimitingtheosmoticgradientbetweentheICandEC

fluidcompartments.b. Thispreventscellulardehydration,anditwillincreasethebrainvolumetowardanormalvalue

despitehypernatremia.2. Becauseofosmoticadaptation,patientswithchronichypernatremiamayberelativelyasymptomatic.

E. SymptomsofHypernatremiaArePrimarilyNeurologic.1. Similartohyponatremia,thesymptomsofhypernatremiaarerelatedtotherateofincreaseinplasma

osmolalityandthedegreeofincreaseinplasmaosmolality.2. Earliersymptomsincludelethargy,weakness,andirritability.3. Symptomscanprogresstotwitching,seizures,coma,anddeathiftheserumNa+isgreaterthan158

mEq/L.4. Cerebraldehydrationcancausecerebralveinrupturewithsubsequentintracerebralorsubarachnoid

hemorrhage.

F. TreatmentofHypernatremia1. Rapidcorrectionofchronichypernatremiacanresultincerebraledema,seizure,permanent

neurologicdamage,anddeath.a. Withosmoticadaptation,thebrainvolumeisraisedtowardnormaldespiteanelevatedserum

osmolarity.b. Osmoticadaptationcombinedwitharapidreductioninplasmaosmolalitycancauseanosmotic

gradient,causingwatertomoveintobraincellswithsubsequentcerebraledema.2. Inpatientswithsymptomatichypernatremia,serumNa+shouldbereducedslowlybynomorethan

0.5mEq/L/houror12mEq/L/day.3. Treathypernatremiabyreplacingwaterdeficitslowlyoverseveraldaystopreventoverlyrapid

correctionofserumNa+.a. UsingLBW,theestimatedwaterdeficit(inliters)=(0.4×LBW)×[(serumNa+/140)−1]in

women(multiplyLBWby0.5inmen).b. Notethatinwomenandmen,thetotalbodywateristypicallyabout50%and60%ofLBW.Thus,

somesourcesrecommendavariationontheaboveequationasfollows:waterdeficit=(0.5×LBW)×[(serumNa+/140)−1]inwomen(multiplyLBWby0.6inmen).However,hypernatremicpatientsaregenerallywaterdepleted;thus,theequationusingthelowervaluesabove(i.e.,40%or0.4and50%or0.5)isreasonable.

4. AdministerfreewaterorallyorintravenouslyasD5W.5. IfconcurrentNa+andwaterdepletion(e.g.,vomiting,diarrhea,diuretic-induceddepletion),canusea

combinationofD5Wand0.25%NaCl6. Ifpatientishypotensivebecauseofvolumedepletion,firstrestoreintravascularvolumewith0.9%

NaCltorestoretissueperfusion.NSisthepreferredcrystalloidforfluidresuscitation,andinthehypernatremicpatient,itisstillrelativelyhypotonic.



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Patient Case6. A74-year-oldwomanhasbeenreceivingJevitytubefeedingsat60mL/hourforthepast8daysthrough

hergastrostomyfeedingtube.Sherecentlysufferedanischemicstroke;sheisresponsive,butshedoesnotcommunicate.HerserumNa+was142mg/dLonthedaytheJevitywasstarted,andithasrisensteadilyto149,156,and163mg/dLondays3,4,and8,respectively,afterthestartofthetubefeedings.Herweightis50kg.Whichoneofthefollowingisthebesttreatmentforherhypernatremia?A. Administersterilewaterintravenouslyat80mL/hour.B. AdministerD5Wintravenouslyat80mL/hour.C. AdministerD5W/0.2%NaClintravenouslyat80mL/hour.D. Administerwaterbyenteralfeedingtube200mLevery6hours.

VII. dISORdeRS OF K+

A. NormalPlasmaK+ConcentrationsAre3.5–5mEq/L.

B. PotassiumIsthePrimaryICCation(maintainselectroneutralitywithNa,theprimaryECcation).

C. PotassiumBalanceIsMaintainedBetweentheICandECCompartmentsbySeveralFactors,Including:1. β2-adrenergicstimulation(causedbyepinephrine)promotescellularuptakeofK

+.2. InsulinpromotescellularuptakeofK+.3. PlasmaK+concentrationdirectlycorrelateswithmovementofK+inandoutofcellsowingtopassive

shiftsbasedontheconcentrationgradientacrossthecellmembrane.(Anormalresponsetodiarrhea-inducedhypokalemiaisforK+toshiftoutofthecellspassively,minimizingthereductioninplasmaK+concentration.)

D. NormalPlasmaConcentrationsofK+AreMaintainedbyRenalExcretion.

E. Hypokalemia(K+concentrationlessthan3.5mEq/L)1. Causesofhypokalemia

a. Reducedintakeseldomcauseshypokalemiabecauserenalexcretionisminimizedbecauseofincreasedrenaltubularabsorption.

b. IncreasedshiftofK+intocellscanoccurwiththefollowing:i. IncreasedpHii. Insulinoracarbohydrateloadiii. β2-receptorstimulationcausedbystress-inducedepinephrinereleaseoradministrationofa

β-agonist(e.g.,albuterol,dobutamine)iv. Hypothermia

c. IncreasedGIlossesofK+canoccurwithvomiting,diarrhea,intestinalfistulaorenteraltubedrainage,andchroniclaxativeabuse.

d. Increasedurinarylossescanoccurwithmineralocorticoidexcess(e.g.,aldosterone)anddiureticuse(e.g.,loopandthiazidetype).

e. HypomagnesemiaiscommonlyassociatedwithhypokalemiacausedbyincreasedrenallossofK+;correctionofplasmaK+requiressimultaneouscorrectionofserummagnesium.



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2. SymptomsofhypokalemiagenerallyoccurwhenplasmaK+isbelow3mEq/Landcanincludethefollowing.a. Muscleweaknessoccursmostcommonlyinthelowerextremitiesbutcanprogresstothetrunk,

upperextremities,andrespiratorymuscles.MuscleweaknessintheGItractcanmanifestasparalyticileus,abdominaldistention,nausea,vomiting,andconstipation.

b. ECGchanges(flattenedTwavesorelevatedUwave)c. Cardiacarrhythmias(bradycardia,heartblock,ventriculartachycardia,ventricularfibrillation)d. Digoxintoxicitycanoccurdespitenormalserumdigoxinconcentrationsinthepresenceof

hypokalemia.e. Rhabdomyolysiscanoccurbecausehypokalemiacancausereducedbloodflowtoskeletalmuscle.

3. Treatmentofhypokalemiaa. Potassiumdeficitcanbeestimatedas200–400mEqofK+forevery1-mEq/Lreductioninplasma

K+(assumingnormaldistributionofK+betweenECandICcompartments).b. AlthoughtheK+deficitcanbeestimated,K+replacementisguidedbyK+concentrations;recheck

every2–4hoursifK+islessthan3mEq/L.c. PotassiumCl-isthepreferredsaltinpatientswithconcurrentmetabolicalkalosisbecausethese

patients typically lose Cl-throughdiureticsorGIloss.Thisisthemostcommonpresentationofhypokalemia.

d. Potassiumacetatecanbeadministeredintravenously,orK+bicarbonatecanbeadministeredorallyforpatientswithametabolicacidosisthatrequiresfrequentK+ supplementation.

e. GuidelinesforadministeringK+

i. PatientswithoutECGchangesorsymptomsofhypokalemiacanbetreatedwithoralsupplementation.

ii. AvoidmixingK+indextrose,whichcancauseinsulinreleasewithasubsequentICshiftofK+.iii. Toavoidirritation,nomorethanabout60mEq/Lshouldbeadministeredthrougha

peripheral vein.iv. Recommendedinfusionrateis10–20mEq/hourtoamaximumof40mEq/hour(thefaster

rateshouldbeinfusedthroughacentralvenouscatheter).v. PatientswhoreceiveK+atratesfasterthan10–20mEq/hourshouldbemonitoredusinga

continuousECG.

table 12.K+ Replacement

Plasma K+ (meq/L)

treatmenta Comments

3–3.5 OralKCl60–80mEq/dayifnosignsorsymptoms (dosesgreaterthan60mEqshouldbedividedto avoidGIadverseeffects)

RecheckK+daily

2.5–3 OralKCl120mEq/dayorIV60–80mEqadministeredat10–20mEq/hourifsignsorsymptoms

MonitorK+ closely (i.e.,2hoursafterinfusion)

2–2.5 IVKCl10–20mEq/hour ConsidercontinuousECGmonitoringLessthan2 IVKCl20–40mEq/hour RequirescontinuousECGmonitoring

aTreatmentdosesareforpatientswithnormalkidneyfunctionandshouldbereducedforpatientswithkidneydysfunctionorelderlypatients.ECG=electrocardiogram;GI=gastrointestinal;IV=intravenous;KCl=potassiumchloride;K+=potassium.



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F. Hyperkalemia1. Causesofhyperkalemia

a. Increasedintakeb. ShiftofK+fromtheICtotheECcompartmentcauseshyperkalemiaandcanoccurwiththe

following:i. Acidosisii. Insulindeficiencyiii. β-Adrenergicblockadeiv. Digoxinoverdosev. Rewarmingafterhypothermia(e.g.,aftercardiacsurgery)vi. Succinylcholine

c. Reducedurinaryexcretioncanoccurwithi. Kidneydysfunctionii. Intravascularvolumedepletioniii. Hypoaldosteronismiv. Potassium-sparingdiureticsv. Angiotensin-convertingenzymeinhibitorsandangiotensinreceptorblockers

2. Symptomsofhyperkalemiaa. Muscleweaknessorparalysisiscausedbychangesinneuromuscularconductionandtypically

occurswhenplasmaK+exceeds8mEq/L.b. Abnormalcardiacconductioncanfirstmanifestaspeaked,narrowedTwaves(typically,when

plasmaK+exceeds6mEq/L),wideningoftheQRS,andcanprogresstoventricularfibrillationandasystole.

c. NotallpatientswillexperienceECGchanges,andtheinitialmanifestationofhyperkalemiacanbeventricularfibrillation;thus,consideremergencytreatmenteveninpatientswithnoECGchangesifplasmaK+exceeds6.5mEq/L.

d. Conductiondisturbancesareenhancedbyhypocalcemia,hyponatremia,acidosis,andrapidelevationintheplasmaK+ concentration.

3. Pseudohyperkalemiashouldbesuspectedifthereisnoapparentcauseorsymptomsofhyperkalemia.a. CanoccurifK+isreleasedfromcellswhile–orafter–obtainingthebloodspecimen;usually

becauseoftraumaduringvenipunctureb. CanoccurfrommeasurementoftheserumratherthantheplasmaK+concentration;causedbyK+

releaseduringcoagulation4. Treatmentofhyperkalemia

a. PatientswithanasymptomaticelevationintheplasmaK+whodonothavesignsorsymptomscanbetreatedwithacationexchangeresin(e.g.,Napolystyrenesulfonate)alone.

b. Urgentandimmediatetreatmentisrequiredforpatientswiththefollowingsignsorsymptoms:i. PlasmaK+above6.5mEq/Lii. Severemuscleweaknessiii. ECGchanges

c. Calciumshouldbeadministeredintravenouslytopatientswithsymptomatichyperkalemiatopreventhyperkalemia-inducedarrhythmiasevenifpatientsarenormocalcemic.i. Calciumgluconatecanbeadministeredperipherallyandispreferredovercalciumchloride

(CaCl)becauseofareducedriskoftissuenecrosis;doseis10mL(equivalentto1g,90mgelemental,or4.65mEq)of10%Ca++gluconateadministeredover2–10minutes;mayrepeatin5minutesifnoimprovementinECG.Calciumchloridecanbeusedifcentralintravenousaccessisavailable;however,thedoseshouldbeadjustedbecause10mL(1g,270mgelemental,or13.6mEq)provides3timestheamountofelementalCaascalciumgluconate.



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ii. Onsetiswithinminutes,butdurationisshort(30–60minutes).iii. WillnotreduceplasmaK+,butwillantagonizetheeffectofK+incardiacconductioncellsiv. Useinurgentcircumstanceswhilewaitingforothermeasures(e.g.,insulinandglucose)to

lowerplasmaK+.v. Avoiduseinpatientsreceivingdigoxinbecausehypercalcemiacanprecipitatedigoxin

toxicity,andtherearereportsofsuddendeath.d. Thefollowingtreatmentoptionsaretransient,causingatemporaryshiftofK+fromtheECfluid

intothecells,andshouldbeusedforsymptomatichyperkalemia.i. Insulinandglucose

(a) Doseisregularinsulin10unitsintravenouslyplus25–50gofglucoseadministeredasa50%dextroseintravenouspushtopreventhypoglycemia.

(b) TypicallylowersplasmaK+by0.5–1.5mEq/Lwithin1hourandmaylastforseveralhours(c) Ifpatientsarehyperglycemic,insulinalonecanbeadministered.(d) Morepredictableinpatientswithkidneyfailurethansodiumbicarbonateorβ2-adrenergic

agonists(e) Cautionwithincreasedriskofinsulinerrorswhenusedinemergencysituations(e.g.,

nursespreparinginsulininfusions).Errorsinvolvingcalculations(100units/mL)anduseof4-or10-mLsyringesinsteadofaninsulinsyringearecommon.

ii. Sodiumbicarbonate(a) Doseis50mEqofsodiumbicarbonateinfusedslowlyover5minutes;mayrepeatin30

minutesifneeded(b) MaylowerplasmaK+within30–60minutesandpersistforseveralhours(c) Theefficacyofbicarbonateisdisputed,anditseemsleasteffectiveinpatientswith

advancedkidneydisease;maybeeffectiveinpatientswithunderlyingmetabolicacidosisiii. β2-adrenergicagonists(e.g.,albuterol)

(a) Doseisalbuterol10–20mgnebulizedover10minutesor0.5mgintravenously(notavailableintheUnitedStates).

(b) WilllowerplasmaK+by0.5–1.5mEq/L(c) Onsetiswithin90minuteswithinhalation.(d) Avoiduseinpatientswithcoronaryischemiabecauseofriskoftachycardia.(e) Upto40%ofpatientswillnotrespondtoinhaledalbuterol;therefore,itisnot

recommendedasasingleagentforurgenttreatmentofhyperkalemia;consideruseincombinationwithinsulin.

e. ThetreatmentoptionsaboveshouldbefollowedbyoneofthefollowingagentstoremoveexcessK+fromthebody.i. Diuretics

(a) Looporthiazide-typediureticsincreaseK+renalexcretion.(b) Ineffectiveinpatientswithadvancedkidneydisease

ii. Cation-exchangeresin(a) ExchangesNa++forK+,resultinginGIexcretionofK+

(b) Becauseofaslowonset(2hours)andunpredictableefficacy,Na++ polystyrene sulfonate (Kayexalate)isnotindicatedforemergencytreatmentofhyperkalemia.

(c) Oraldoseofsodiumpolystyrenesulfonateis15grepeatedevery6hoursasneeded.Thiscanbemixedin20–100mLofwaterorsyrup,butitisnolongerrecommendedtomixin70%sorbitolbecauseoftheriskofintestinalnecrosis(therearereportsaswellwiththepremixed33%sorbitolsuspension,but70%sorbitolappearstohaveastrongercorrelationwithintestinalnecrosis).Oralsorbitolcanpreventconstipationassociatedwiththeresin;however,thehighestriskofintestinalnecrosisoccurswhenadministeredtopatientswithin1weekofsurgery(occursinabout1.8%ofpatients).



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(d) Althoughtheoralrouteismoreeffective,canalsogive30–50gasaretentionenemamixedin100–200mLofanaqueousvehicle(e.g.,water,10%dextrose)thathasbeenwarmedtobodytemperatureandkeptincolonfor30–60minutesorupto3hours.Irrigatecolonafterenema.(1) Sorbitolisnotrecommendedasavehicleforrectalusebecauseoftheriskof

intestinalnecrosisandotherseriousGIadverseevents.PatientswithkidneydiseaseareatincreasedriskoftheseGIadverseeffects.

(2) CautioninpatientswithkidneyfailureorheartfailurecausedbyNaretentioniii. Dialysis

(a) Usedwhenothermeasuresareineffectiveorwhenseverehyperkalemiaispresent(b) PlasmaK+fallsbymorethan1mmol/Linthefirsthourofdialysisandbyabout2

mmol/Lafter3hoursofdialysis.(c) HemodialysisremovesK+fasterthanperitonealdialysis.(d) MonitorforreboundincreaseinK+afterdialysis.(e) Usedinpatientswithadvancedkidneydisease

Patient Case7. A61-year-oldman isbrought to theemergencydepartmentwithshortnessofbreathandbilateral lower

legedema.PertinentvitalsignsandlaboratoryvaluesincludeHR30beats/minute,BP102/57mmHg,K+ 7.9mEq/L,Na+139mEq/L,glucose228mg/dL,Ca++8.8mg/dL,digoxin2.0ng/mL,BUN49,andCr2.4mg/dL.HisECGshowswideQRSandpeakedTwaves.Hismedicalhistoryincludesheartfailure,atrialfibrillation,coronaryarterydisease,peripheralarterialdisease,anddiabetes.Thepatienthasperipheralintravenousaccessandanexternalpacemaker.Whichoneofthefollowingismostappropriate?A. Calciumgluconate10mLintravenouslyover2minutes.B. Insulin10unitsintravenously.C. Sodiumbicarbonate50mEqintravenouslyover10minutes.D. Albuterol10mgnebulizedover10minutes.

VIII. dISORdeRS OF mAgneSIum HOmeOStASIS

A. NormalSerumMagnesiumConcentrationIs1.7–2.3mg/dL(1.4–1.8mEq/Lor0.85–1.15mmol/L).

B. Hypomagnesemia(serummagnesiumconcentrationlessthan1.7mg/dL)1. Usuallyassociatedwithimpairedintestinalabsorption(e.g.,ulcerativecolitis,diarrhea,pancreatitis,

chroniclaxativeabuse),inadequateintake,hypokalemia,orincreasedrenalexcretion(e.g.,diureticuse)a. Commoninhospitalizedpatientsb. Usuallyassociatedwithalcoholismanddeliriumtremens

2. Oftenoccursconcurrentlywithhypokalemiaandhypocalcemia3. Signsandsymptoms

a. Neuromuscularsymptomsincludetetany,twitching,andseizures.b. Cardiovascularsymptomsincludearrhythmias,suddencardiacdeath,andhypertension.

4. Treatmenta. Oralsupplements(e.g.,magnesiumoxide,magnesium-containingantacidsorlaxatives)canbe

usedforasymptomaticpatients;however,treatmentislimitedbythehighfrequencyofdiarrhea.



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b. Symptomaticpatientsshouldinitiallybetreatedwith1–4g(8–32mEq)ofmagnesiumsulfatebyslowintravenousinfusion(about1g/hourtoavoidhypotensionand/orincreasedrenalexcretionbecauseofrapidadministration),followedbyabout0.5mEq/kg/dayaddedtointravenousfluidandadministeredasacontinuousinfusion.Foremergencytreatment(e.g.,torsades),magnesiumcanbeadministeredbyintravenouspush.

c. Reducedosebyhalfinpatientswithkidneyinsufficiency.d. Aroundhalfofadministeredmagnesiumisexcretedintheurine;therefore,magnesium

replacementshouldoccurover3–5days.

C. Hypermagnesemia(serummagnesiumgreaterthan2.3mg/dL)1. Rarelyoccursandisgenerallyassociatedwithchronickidneydisease2. Signsandsymptomsincludenausea,vomiting,bradycardia,hypotension,heartblock,asystole,

respiratoryfailure,anddeath;signsandsymptomsrarelyoccurunlessmagnesiumconcentrationisgreaterthan4–5mg/dL.

3. Treatmenta. Discontinueallmagnesium-containingmedications.b. Asymptomaticpatientswithnormalkidneyfunctioncanbetreatedwith0.9%NaClandloop

diuretics.c. Symptomaticpatientsshouldbetreatedwith100–200mgofelementalCaadministered

intravenouslyover5–10minutesforcardiacstability.d. Hemodialysismaybeneededforpatientswithkidneydisease.

IX. dISORdeRS OF PHOSPHORuS HOmeOStASIS

A. NormalSerumPhosphorusConcentrationIs2.5–4.5mg/dL.

B. Hypophosphatemia(serumphosphorusconcentrationlessthan2.5mg/dL)1. Causes of hypophosphatemia

a. Increasedrenalelimination(e.g.,diuretics,glucocorticoids,sodiumbicarbonate)b. Rapidlyrefeedingpatientswithchronicmalnutrition(seerefeedingsyndromeinNutritionsection)c. Respiratoryalkalosisd. Treatmentofdiabeticketoacidosis;phosphorusshiftsintotheICcompartmentasdiabetic

ketoacidosisiscorrected2. Signsandsymptoms

a. Tissuehypoxiacanoccurbecauseofadecreaseinoxygenreleasetoperipheraltissues.b. Neurologicmanifestationsincludeconfusion,delirium,seizures,andcoma.c. Pulmonaryandcardiacsymptomscanincluderespiratoryfailure,difficultyweaningfrom

mechanicalventilation,heartfailure,andarrhythmias.d. Otherorgansystemsaffectedincludemuscle,hematologic,bone,andkidney.

3. Preventionandtreatmenta. Preventhypophosphatemiabysupplementingintravenousfluidwith10–30mmol/Lintravenous

phosphorusinpatientsatriskofhypophosphatemia(e.g.,malnourished,alcoholism,diabeticketoacidosis).

b. Oralphosphorusproducts(e.g.,K-PhosNeutral;alsocontainK+andNa)canbeusedforasymptomaticpatients,buttheyarepoorlyabsorbed.

c. Symptomaticpatientsshouldreceive15–30mmol(or0.5–0.75mmol/kgofIBW)ofphosphorus(Na+phosphateorK+phosphate)administeredintravenouslyover3–6hours(maximalrateis7.5mmol/hour).Note:Na+content(4mEqper3mmolphosphate)andK+content(4.4mEqper3mmolphosphate)



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C. Hyperphosphatemia1. Typicallyoccursinpatientswithchronickidneydiseaseorhypoparathyroidism2. Ingeneral,patientsareasymptomatic,buttheycanhavesignsandsymptomsincludinghypocalcemia,

ECGchanges,paresthesias,andvascularcalcifications.3. Treatment(seetreatmentofhyperphosphatemiaintheNephrologychapter)

X. dISORdeRS OF CALCIum HOmeOStASIS

A. NormalSerumCa++ConcentrationIs8.5–10.5mg/dL(totalCa++includesboundandunboundCa++),andNormalIonizedCa++Is1.1–1.3mmol/L.

B. DistributionofCa1. ECfluidcontainslessthan1%ofthetotalbodystoresofCa++;99%oftotalbodystoresofCa++

isinskeletalbone.a. AbouthalfofCa++intheECcompartmentisboundtoplasmaproteins(primarilyalbumin).b. TheactiveformofCa++istheunboundorionizedCa++.

2. IonizedCa++isregulatedbyparathyroidhormone,phosphorus,vitaminD,andcalcitonin.

C. Hypocalcemia1. Occursinpatientswithchronickidneydisease,hypoparathyroidism,vitaminDdeficiency,

alcoholism,andhyperphosphatemia,aswellasinpatientsreceivinglargeamountsofbloodproductsorpatientsundergoingcontinuousrenalreplacementtherapy(CRRT[i.e.,Ca++ chelates with citrate in bloodproductsorCRRT])

2. FactorsthatcauseanincreaseinECCa++bindingtoalbumin(e.g.,metabolicalkalosis)cancauseareductioninplasma-ionizedCa++concentration,leadingtosymptomatichypocalcemia.

3. AlowserumalbuminwillcauseafalselylowtotalserumCa,soanadjustmentisnecessary.Forevery1-g/dLdecreaseinserumalbuminlessthan4g/dL,add0.8mg/dLtototalserumCaconcentration to correct the value.

4. Signsandsymptomsincludetetany,musclespasms,hypoactivereflexes,anxiety,hallucinations,lethargy,hypotension,andseizures.

5. Treatmenta. Asymptomatichypocalcemiaassociatedwithhypoalbuminemiaistypicallyassociatedwith

normalionizedCa++concentrationsandthereforedoesnotrequiretreatment.b. AsymptomatichypocalcemiacanbetreatedwithoralCa++supplementsatadoseof2–4g/dayof

elemental Ca++;patientsmayalsorequirevitaminDsupplementation.c. Symptomatichypocalcemiaistreatedwith200–300mgofelementalCa++administered

intravenouslyover5–10minutes,followedbyacontinuousinfusion.i. Equivalentto1gofCaCl2(273mgofelementalCa

++)administeredthroughacentralintravenouscatheter;peripheraladministrationofCaCl2canresultinseverelimbischemia

ii. Equivalentto2–3gofCa++gluconate(180–270mgofelementalCa++);preferredforperipheralintravenousadministration

iii. Do not infuse Ca++ataratefasterthan60mgofelementalCa++perminute;rapidadministration,whichisnotrecommended,isassociatedwithhypotension,bradycardia,orasystole.

iv. ThedurationofabolusdoseofCa++isideally1–2hours,followedbyacontinuousinfusionrateof0.5–2mg/kg/hourofelementalCa++.

D. Hypercalcemia(serumCa++concentrationgreaterthan10.5mg/dL)isusuallyrelatedtomalignancyorhyperparathyroidism;seeOncologySupportiveCarechapter.



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XI. enteRAL nutRItIOn

A. Indication:Enteralnutritionisusedinhemodynamicallystablepatientsatriskofmalnutritioninwhomitisanticipatedthatoralfeedingswillbeinadequateforatleast1–2weeks.Malnutritionisassociatedwithpoorwoundhealingandincreasedriskofinfection.AccordingtotheAmericanSocietyforParenteralandEnteralNutrition(ASPEN)guidelines,well-nourishedadultswithoutexcessivemetabolicstresscanusuallytoleratelittletononutritionforupto7days.

B. ENContraindications1. Completeintestinalobstruction2. GIfistula(ifafeedingtubecannotbeplacedawayfromthefistulaorifhigh-outputfistula,whichis

definedasgreaterthan500mL/dayofoutput)3. Extremeshortbowel4. Severediarrheaorvomiting5. Hemodynamicinstabilityorintestinalischemia6. Paralyticileus(however,manypatientscanbefedthroughthesmallbowel,despiteanileus)7. Note:TheabsenceofbowelsoundsisNOTacontraindicationfortheprovisionofEN

(i.e.,positivebowelsoundsarenotrequiredforENinitiation).ENpromotesgutmotility.

C. ENAdministrationRoutes1. Orogastrictubesarepreferredinpatientswithnasal/facialtraumaorsinusitis,buttheyare

uncomfortableforalertpatients.2. NGtubesarethemostcommontubesforshort-termenteralaccess,andtheycanbeusedforstomach

decompressioninadditiontofeeding.a. Prolongedusecancausesinusitisornasalmucosalulceration.b. PatientswithagastricileuswillnottolerateNGfeedingsandwillhaveanincreasedriskof

aspiration.3. NasoduodenaltubesaresmallerandmoreflexiblethanNGtubes.

a. Ideally,thetipisplacedpastthepyloricsphinctertoimprovetubefeedingtoleranceandpreventaspiration.

b. Thesetubes,whicharesmallerthanNGtubes,willclogifnotflushedappropriately.c. Patientswithagastricileusmaytoleratethistypeoffeedingtube.

4. NasojejunaltubesareadvancedintothefourthportionoftheduodenumorpasttheligamentofTreitz.5. Gastrostomytubes(alsoknownasPEGtubesforpercutaneousendoscopicgastrostomy)areplaced

throughtheabdominalwallintothestomachforpatientsrequiringlong-termfeeding.6. Jejunostomytubesareplacedthroughtheabdominalwallintothejejunumusuallytofacilitate

immediatepostoperativeorpostinjuryfeeding.

D. ENDelivery1. Gravitycontrolreferstodeliverywithtubingthatisfittedwitharollerclamptoallowinfusioninto

thestomachasdesired.2. Continuousinfusionusinganenteralfeedingpumpismostcommonlyusedinhospitalsbecauseof

thereducedriskofaspirationcomparedwithbolusfeedings;mustbeusedforduodenalorjejunalfeedings

3. Cyclicfeedingsareadministeredcontinuouslyfor10–12hours(overnight)tofacilitatepatientmobilityduringthedaytime.

4. Intermittentbolusfeedingof100–300mLfor30–60minutesevery4–6hourscanonlybeusedforfeedingtubesendinginthestomach.



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E. BenefitofEN1. ENispreferredinpatientswithafunctionalGItractbecauseitisassociatedwithalowerriskofinfection

thanPN.EarlyadministrationofENisassociatedwithdecreasedinfectionandshorterlengthofstay.2. GImucosalatrophyoccurswithanabsenceofEN.Thiscanleadtoanincreasedriskofbacterial

translocationbecausegutbacteriacancrosstheweakenedintestinalbarrier.

F. ENFormulations1. Typicallycontaincarbohydrate,fat,protein,electrolytes,water,vitamins,andtraceelementsinvarying

amounts2. Intactorpolymericformulasareusedinpatientswithnormaldigestiveprocesses,andtheytypically

contain1–1.2kcal/mL.ExamplesincludeOsmoliteandIsocal.a. Thesearegenerallyinexpensiveandanappropriatefirstchoiceformanypatients.b. Somepolymericformulasareconcentratedforpatientsrequiringfluidrestrictionandcontain2

kcal/mL.ExamplesincludeMagnacal,TwoCalHN,andDeliver2.0.c. Somepolymericformulasaredesignedfororaladministrationandareusedtosupplementthe

patient’sdiet.ExamplesincludeBoostandEnsure.3. Elementalformulasareeasilydigestedforpatientswithimpaireddigestivecapacityormalabsorption

(e.g.,shortbowel,pancreaticinsufficiency);theyaretypicallymoreexpensivethanpolymericEN.ExamplesincludeOptimental,Peptamen,VitalHN,andVivonexTEN.

4. SomeENcontainsfiberforpatientswithconstipation.ExamplesincludeUltracalandJevity.5. Disease-specificEN

a. ENforpatientswithrenalfailureistypicallyconcentrated(i.e.,2kcal/mLtoadheretofluidrestrictions)andcancontainreducedamountsofproteinandelectrolytes(fornondialysispatients)ormoreproteinandmoderateelectrolytes(fordialysispatients).ExamplesincludeMagnacalRenalandNepro.

b. SomeENproductsdesignedforpatientswithrespiratoryfailurehavemorecaloriesfromfat(40%–55%oftotalcalories)andfewerfromdextrosetoreducetheproductionofCO2(dextroseismetabolizedtowaterandCO2)andfacilitateventilatorweaning.However,excessiveCO2

productionisprimarilycausedbyoverfeedingwithtotalcaloriesratherthanthetotalamountofdextrose;therefore,thesemoreexpensiveformulationsmaynotbenecessaryaslongasthepatientisnotbeingoverfed;examplesincludePulmocare,Respalor,andNutriVent.

c. ENforpatientswithdiabeteshasmorecaloriesfromfat,fewercaloriesfromcarbohydrates,andaddedfibertoimproveglycemiccontrol.ExamplesincludeChoiceDMandGlucerna.

d. ENforpatientswithhepaticfailureandhepaticencephalopathycontainsmorebranched-chainAAandlessaromaticAA,whichmayimproveencephalopathy(controversial).NutriHepisanexample.

e. ENforhighlystressedpatients(e.g.,trauma,burninjury,acuterespiratorydistresssyndrome,sepsis)isenhancedwithprotein,arginine,glutamine,omega-3fattyacids,nucleotides,orbetacarotene.Theseenteralformulationsaredesignedtoenhanceimmunefunctionandclinicaloutcomes.ExamplesincludeImpactGlutamineandOxepa.

G. ENComplications1. Impropertubeplacementordisplacement2. Cloggedfeedingtubes

a. Preventbyflushingfeedingtubebefore,between,andaftertheadministrationofeachdrug.b. Unclogfeedingtubeswithwarmwater,cola,pancreaticenzymes,orNabicarbonate.

3. Aspiration pneumoniaa. Preventbykeepingtheheadofbedelevatedat30–45degrees.b. Preventbymonitoringgastricresidualsanddiscontinuinginfusionifgastricresidualvolumeis

greaterthan250–500mL.



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i. PreventdelaysingastricemptyingusinganENformulawithlessfat.ii. Gastricmotilitycanbeincreasedwithmetoclopramide(5–20mgintravenouslyevery6hours)

and/orerythromycin(250mgintravenouslyevery6–8hoursadministereduntiltoleratingENforatleast24hours);cancombinemetoclopramideanderythromycin,butmonitorfordiarrheaandtachyphylaxis

c. AdministeringENpastthepyloricvalveusingaduodenalfeedingtubecanpreventaspirationpneumonia.

d. PreventalsobyinitiatingENataslowrate(e.g.,20mL/hour)andadvanceevery4–6hoursastoleratedtogoalrate.

4. Diarrheaa. Morecommonwithelementalproductsbecauseofahigherosmolarityb. Considerothercausesofdiarrheasuchasantibioticuse,infection,lactoseintolerance,magnesium,

andsorbitolinliquidpreparations.5. Constipationcanbepreventedbyaddingfiberormetoclopramide.6. Dehydration7. HypernatremiaoccurswhenpatientsaregiveninsufficientwaterwhilereceivingEN.

a. Patientsrequireabout1mLofwaterforeachcalorie.b. Hypernatremiatypicallyoccursinpatientswithalteredmentalstatus.c. Calorie-dense(i.e.,1.5or2kcal/mL)ENformulashavelesswaterthanproductscontaining1

kcal/mLandthereforerequireadditionalwatertopreventhypernatremia.8. Nasopharyngealerosions,epistaxis,tracheoesophagealfistula9. Sinusitis10. Electrolyteabnormalitiesaremostlikelytooccurinpatientswhodeveloprefeedingsyndrome

(discussedlater).

Patient Case8. A72-year-oldfemalepatientweighing65kgisreceivingMagnacalRenal,acalorie-richtubefeedingde-

signedforpatientswithkidneydisease.Thepatient’sbaselineandcurrentCris1.5mg/dL,andherurineoutputisabout50mL/hour.Thetubefeedingisinfusingatagoalrateof35mL/hourthroughanNGfeed-ingtubeproviding2kcal/mL,35mEq/LofNa+,and710mL/Lofwater.Thepatient’sserumNa+ was 140 mEq/Lwhenthetubefeedingwasinitiatedafewdaysago,andnow,herNa+is145mEq/L.Whichoneofthefollowingrecommendationsisthebestapproachforpreventinghypernatremiainthispatient?A. ChangetoanENformulawithalowerconcentrationofNa+.B. AdministerintravenousD5Wat45mL/hour.C. Administer200mLofwaterthroughafeedingtubeevery4hours.D. Reducethetubefeedingto30mL/hour.

H. ENMonitoring1. Bloodglucoseconcentration2. Headofbedelevationto30–45degrees3. Gastricresidualsarechecked,andinfusionrateisgenerallyheldorreducediftheresidualamount

exceeds250–500mL(appliestogastrictubefeedingsonly,notsmallbowel).AccordingtotheSocietyofCriticalCareMedicineandASPENguidelines,holdingENforgastricresidualvolumeslessthan500mLintheabsenceofothersignsofintoleranceshouldbeavoided.

4. GItolerance



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a. Abdominalpainand/ordistensionb. Stoolfrequencyandvolumec. Gastricresidualsd. Nausea/vomiting/diarrhea

5. Prealbuminweekly.(Exception:Notrecommendedincriticallyillpatientsbecauseitreflectsacute-phaseresponseratherthannutritionalstatus)

6. SerumNaandotherelectrolytes7. Woundhealingisasignofadequatenutritionaltherapy.

I. DevelopinganENRegimen

table 13. DevelopinganENRegimen

Steps Calculation guide exampleDeterminecaloricrequirements 25–30kcal/kg/dayORestimate

energyrequirementsusinganequationsuchastheHarris- Benedictequation(seemoredetailsinParenteralNutritionsectionandCriticalCarechapter)

A60-kgpatientwouldrequireabout25kcal/kg/day×60kg=1500kcal

Chooseaformulaandassessthecalories per milliliter

Usually1,1.2,1.5,or2kcal/mL Ultracalprovides1kcal/mL

Determine infusion rate (VolumeofEN)/24hours 1500mL/24hours=62.5mL/hourMakesurepatientwillreceive enoughprotein

Seeproductinformationtofindproteincontent(seeproteinrequirementsinParenteral Nutritionsection)

Ultracalprovides45g/Lofprotein;therefore,1500mLwillprovide67.5gofproteinor1.1g/kgforapatientweighing60kg

Makesurepatientwillreceiveabout 1mLofwaterforeachcalorie

Seeproductinformationtofind water content

Ultracalprovides830mL/Lofwater.Apatientreceiving1500mL/daywouldneedabout250mLofadditionalwater.Thiscanbeadministeredaswaterflushesthroughthefeedingtube(i.e.,60–70mLevery6hours)

EN=enteralnutrition.

J. DrugAdministrationUsingEnteralAccess1. Liquidsarepreferable,andtheyshouldbedilutedwith2–3timesthemedicationvolume,withsterile

waterforirrigation.2. Diarrheacanoccurwithmedicationshavingahighosmolality(e.g.,medicationsmixedinsorbitol).3. Flushwith20mLofwaterbeforeandafterdrugadministration.4. Donotcrushsustained-releaseorenteric-coatedpills.5. Mixcrushedtabletsorcapsulecontentswith10–15mLofsterilewaterforinjection,andadminister

eachdrugseparately.6. Mayneedtodiscontinuetubefeedingsbeforeandafterdrugadministrationtemporarilytoprevent

reducedbioavailability(e.g.,fluoroquinolones,phenytoin,warfarin,bisphosphonates)7. Considerfeedingtubelocationandsubsequentdrugabsorption(e.g.,forefficacy;antacidsneedtobe

administeredintothestomach,nottheduodenum).



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XII. PARenteRAL nutRItIOn

A. PNistheadministrationofintravenousnutritioninpatientswithanonfunctioningorinaccessibleGItractinwhichthedurationofPNisanticipatedtobeatleast7days(i.e.,itisanticipatedthatthepatientwillbeunabletobefedorallyorenterallyforatleast7days).

B. IndicationsforPN1. Severepancreatitis2. Peritonitis3. Severeinflammatoryboweldisease(e.g.,Crohndisease,ulcerativecolitis)4. Extensivebowelresection(e.g.,shortbowelsyndrome)causingmalabsorptionormaldigestion5. Completebowelobstruction6. Severeintractablevomitingordiarrhea7. Inabilitytomeetfullnutritionalneedsbyenteralroutealone(canusePNassupplementtoEN)

C. IntravenousInfusionofPN1. PNisusuallyadministeredthroughacentralline.Thisincludesanyintravenouscatheter(e.g.,

peripherallyinsertedcentralcatheterorPICC,Hickman,Port-a-Cath)wherethetipofthecatheterisinthesuperiorvenacavaoradjacenttotherightatrium(femoralcathetersshouldbeavoidedbecauseofhigherriskofvenousthrombosisandcatheter-relatedinfection).

2. Peripheralaccessisdefinedasthecathetertippositionoutsidethecentralvesselsorinferiororsuperiorvenacava;ifaperipheralveinisusedforPNadministration,theosmolaritymustnotexceed900mOsm/L.PeripheraladministrationcanbeusedinpatientswithanappropriateindicationforPN(seeabove)inwhomcentralintravenousaccessisunavailableandtheneedforPNisexpectedtobelessthan2weeks.a. Finaldextroseconcentrationshouldbe10%orless.b. FinalAAconcentrationshouldbe2.5%–4%.c. Caconcentrationshouldbe5mEq/Lorless.d. Potassiumconcentrationshouldbe40mEq/Lorless.

3. Inhospitalizedpatients,PNistypicallyadministeredasacontinuousinfusion,whichshouldbecompletedwithin24hours.

4. AmbulatorypatientsmaypreferacyclicPNinwhichthePNisusuallyinfusedfor12hoursovernight.

5. Infusionsaregenerallybettertoleratedbypatientsiftheyareremovedfromtherefrigerator30–60minutesbeforeinfusion.

table 14. EstimatingtheOsmolarityofPN

nutrient estimated OsmolarityAminoacids 10mOsm/LDextrose 5mOsm/LLipidemulsion20% 1.3–1.5mOsm/LSodium 2mOsm/mEqPotassium 2mOsm/mEqCalciumgluconate 1.4mOsm/mEqMagnesiumsulfate 1mOsm/mEq

PN=parenteralnutrition.



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D. TypesofPNAdmixtures1. 2-in-1referstoPNinwhichallnutrientsaremixedinthesameintravenousbag,exceptforlipids.

a. Lipidsareinfusedseparatelyatnofasterthan0.1g/kg/hour.b. Rapidadministrationoflipidsisassociatedwithheadache,fever,nausea,hypertriglyceridemia,

dyspnea,cyanosis,flushing,sweating,andbackorchestpain.c. Lipidinfusiontimeshouldbelessthan12hoursbecauseofthepotentialformicrobialgrowth

afterthistime(growthisreducedwhenlipidsaremixedwithdextroseandAA,asinthe3-in-1below,becauseofreducedpHandincreasedosmolarity).

d. Administrationtubingfora2-in-1shouldbechangedevery72hours;lipidtubingshouldbediscardedafteruse(nolongerthan12hours).

2. 3-in-1referstoPNinwhichallnutrientsaremixedinthesameintravenousbagtoformalipidemulsion.a. Stabilityofa3-in-1dependsonthepH,whichisprimarilydeterminedbythefinalconcentration

ofAA(maintainbetween2.5%and4%).b. Donotaddconcentrateddextrosedirectlytoalipidemulsionwhenmixing(seeorderofmixing

below).c. AvoidexcessiveamountsofCaandmagnesium(seerecommendeddosesbelow).d. Administrationtubingfora3-in-1shouldbechangedevery24hours.

table 15.2-in-1PNComparedwith3-in-1PN

Advantages disadvantages

2-in-1 Longerstability(1–2months)VisualinspectioneasierFilterusing0.22-micronfilter(bacteria-eliminating)

IncreasednursingtimeRequirestwosetsoftubingIncreasedbacterialgrowthinlipidsMaximum12-hourhangtimeofseparatelipids

3-in-1 Time-efficientfornursesSinglebagwithsingletubingDecreasedveinirritationInhibitedbacterialgrowth

Shorterstability(1–2days)Complexcompounding(withoutautomatedcompounder)VisualinspectiondifficultEmulsioninstabilityMustfilterusing1.2-micronfilter,not0.22-micronLimitedcompatibilitywithmedicationsCatheter occlusion more common

E. NutritionalComponentsofPNFormulation1. DextroseusedforcompoundingPNisusually70%andcontains3.4kcal/g.Glycerol(orglycerin)is

anothercarbohydratesourcethatprovides4.3kcal/gandisusedinpremixedparenteralproducts(e.g.,ProcalAmine)

2. Fatemulsionisavailableas10%or20%andcontainsabout10kcal/g;alsoavailableasa30%formulationforcompoundingin3-in-1only

3. AAavailableas3%–20%andprovide4kcal/g4. Electrolytesareaddedtomaintainphysiologicserumconcentrations.5. Multivitaminsandtraceelementsareaddedonthebasisoftherecommendeddailyamount.

F. DevelopingaPNRegimenforAdministrationThroughaCentralIntravenousLine1. Determinecaloricrequirements.

a. Forpatientswithabodymassindex(BMI)lessthan30kg/m2,administer25–35kcal/kg/daybasedonactualbodyweight(BMI=(wtinkg)/(htinmeters)2)



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b. IfBMIexceeds30kg/m2,canadminister11–14kcal/kgbasedonactualbodyweightor22–25kcal/kgbasedonIBWi. Alternatively,somepractitionersadvocateusingadjustedbodyweight(ABW)rather

thanIBW.ii. ABW=[(actualweight–IBW)×0.25]+IBW.

c. Permissiveunderfeedinginvolvestheadministrationofabout80%ofcaloricrequirements,anditcanbeconsideredinitially(exceptinpatientswithkidneyfailurerequiringhemodialysis;thesepatientshaveincreasedproteinandcaloricrequirementstomaintainapositivenitrogenbalance).

d. Acommonlyusedmethodistoestimatebasalenergyexpenditure(BEE)usingtheHarris-Benedictequation:i. Men: BEE=66+13.7(wtinkg)+5(htincm)–6.8(ageinyears).ii. Women: BEE=655+9.6(wtinkg)+1.8(htincm)–4.7(ageinyears).

e. Energyexpendituremayalsobeestimatedthroughindirectcalorimetryincriticallyillpatients(seeCriticalCarechapter).

2. Determinefluidrequirements.a. Usually30–35mL/kg/dayor2500–3500mL/day(forpatientswithoutfluidrestrictions)to

maintainurineoutputintherangeof0.5–2mL/kg/hourb. Fluidrequirementsforpatientswithfluidrestrictions(e.g.,kidneyand/orcardiacdysfunction)

shouldbeindividualized.c. DonotusePNforfluidreplacement,butformaintenancefluidonly.

3. Determineprotein(AA)requirements.a. ForpatientswithaBMIlessthan30kg/m2,proteinisusuallyintherangeof0.8–2g/kg/dayon

thebasisofactualbodyweight(maybehigherinburnortraumapatients).i. Maintenance0.8–1g/kg/dayii. Moderatestress1.3–1.5g/kg/dayiii. Severestress1.5–2g/kg/day

b. ForpatientswithaBMI30–40kg/m2,cangive2g/kg/dayproteinbasedonIBW.ForpatientswithaBMIgreaterthan40kg/m2,cangive2.5g/kg/daybasedonIBW

c. Patientswithkidneydysfunctionmayneedaproteinrestrictiontopreventuremia.i. Kidneydysfunctionwithoutdialysis0.5–1g/kg/dayii. Kidneyfailurewithintermittenthemodialysis1.2–1.5g/kg/day(1.5–2.5g/kg/dayif

continuousrenalreplacement)d. Caloriesfromprotein(4kcal/g)shouldbeincludedinthetotalcaloricprovisionstoprevent

overfeeding.e. For3-in-1formulations,thefinalAAconcentrationshouldbe2.5%–4%toprovideadequate

bufferingcapacityandpreventlipidemulsiondestabilization.f. Completeproteinrequirementscanbeprovidedonday1ofPN(i.e.,thereisnoneedtoslowly

titrateuptorecommendedamount).4. Calculateremainingcalories,andadministerabout20%–30%oftotalcaloriesaslipidandthe

remainderasdextrose.a. Makesuredextroserateofadministrationdoesnotexceedthemaximalrateofhepaticoxidation

of4–6mg/kg/minute(maybelowerincriticallyillpatients,somonitorforhyperglycemiaandadjustamountofdextroseprovidedifneeded).i. Initialdextroseamountscanbeintherangeof150–200g/day.ii. Mayneedtoreduceto100–150g/dayinitiallyinpatientswithdiabetesorstress-induced

hyperglycemia;increasegraduallyduringfirst3–4daystogoalsifbloodglucosevaluesarelessthan150mg/dL



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b. Ahigherpercentageofcaloriesfromlipid(upto50%–60%or2.5g/kg/day)canbeprovidedforashorttimeincertaincases(e.g.,hyperglycemia,hypercapnia).

c. Essentialfattyaciddeficiencycanbepreventedbysupplying2%–4%oftotalcaloriesaslipid(canadministerlipidemulsiononceevery1–2weeks).

5. Estimateadailymaintenanceamountofelectrolytes,vitamins,andtraceelements(seebelow).a. ElectrolyteabnormalitiesshouldbeaddressedandcorrectedbeforePNisinitiated.Avoid

replacingelectrolytedeficienciesusingPNinacutelyillpatients.b. Maintenanceelectrolytes(amountswillvaryandshouldbeindividualized)

i. Sodium60–150mEq/day(1–2mEq/kg/day)ii. Potassium40–80mEq/day(1/mEq/kg/day)iii. Phosphate10–40mmol/day(or15mmol/1000kcal)iv. Calcium10–15mEq/day(gluconateispreferredtopreventincompatibilities)v. Magnesium8–20mEq/day(sulfateformispreferredoverchloridetoprevent

incompatibilities)vi. Chlorideandacetatesaltformsshouldbeusedinaratioof1:1or1.5:1(thesesaltformsdo

nothavespecificrecommendedamounts).vii. Electrolyteadjustment

(a) Typicallywillneedincreasedamountsofmagnesium,phosphorus,andK+duringthefirstfewdaysofPNbecauseofICshifts

(b) Chlorideandacetatesaltformscanbeadjustedasneededtomaintainacid-basebalance(seebelowunder“Monitoring”)

c. Standardtraceelementscontainselenium,chromium,copper,manganese,andzinc (e.g.,MTE-5).i. Patientswithhigh-outputfistulas,diarrhea,burns,orlargeopenwoundsmayrequire

additionalzincsupplementation.ii. Patientswithchronicdiarrhea,malabsorption,andshort-gutsyndromemayrequire

additionalseleniumsupplementation.iii. Patientswithseverecholestasisshouldhavecopperandmanganeserestrictedtoprevent

accumulationandtoxicitybecausebothundergobiliaryelimination.d. Parenteralmultivitaminshouldbeaddeddaily(generallycontains150mcgofvitaminK).

i. Additionalthiamine(25–100mg)canbesupplementedinpatientswithahistoryofalcoholabuse.

ii. Duringshortagesofparenteralvitamins,canreducefrequencyofadministrationto3times/weekorcanadministerindividualvitaminsdaily(i.e.,thiamine,ascorbicacid,niacin,pyridoxine,folicacid)ormonthly(i.e.,vitaminB12)



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table 16. CentralPNCalculations

Exampleofacentral3-in-1PNformulafora70-kgpatienthospitalizedwithischemicbowel:(fora2-in-1PNformula,thelipidsarehungseparately)

1.Totalcaloriesestimatedas30kcal/kg×70kg=2100kcal

2.Fluidrequirementsestimatedas1500mL+(20mL/kg×50kg)=2500mL/day

3.Estimatedproteinneedsare1.5g/kg×70kg=105gofprotein.Considerprotein-basedcaloriesaspartoftotalcalories:4kcal/g×105g=420kcalfromprotein.Using10%AA-basedsolution,willneed1050mLtoequal105gofprotein(canroundto1000mLifthismakescompoundingeasier)

4.Determinecaloriesfromfatanddextrose.Totalcaloriesneededis2100kcal−420kcalfromAA=1680remainingcaloriesneeded.Administer25%–30%oftotalkilocaloriesaslipid,orabout500kcalfromlipid.Using10%lipidemulsion,willneed500mLtoequal500kcal(around1kcal/mL)

Totalcaloriesneededis2100kcal−420kcal(AA)−500kcal(lipid)=1180kcalneededfromdextrose.Assuming3.4kcal/g,thenneedaround350gofdextrose.Usinga70%basedextrosesolution,willneed500mLtoequal350gor1190kcal

Calculatetherateofdextroseadministrationinmilligramsperkilogramperminute: [(350g/24hours)×(1000mg/g)×(1hour/60minutes)]/70kg=3.5mg/kg/minute Thisisanappropriaterateofdextroseadministration

5.Finalformulawillcontainthefollowing: AA10%1050mL Lipid10%500mL Dextrose70%500mL Electrolytes,multivitamins,andtraceelements(about100mL) Finalvolumeof2150mLtoinfuseat2150mL/24hour=90mL/hour (Finalvolumeassumespatientisreceivingabout350mLoffluidfromothermedications)

6.FinalconcentrationofmacronutrientsinPNis: AA105g/2150mLfinalvolume=4.9% Lipid50g/2150mL=2.3% Dextrose350g/2150mL=16%

7.FinalcaloricvalueofPNis: AA105g×4kcal/g=420kcal Lipid50g×10kcal/g=500kcal Dextrose350g×3.4kcal/g=1190kcal Totalcalories=420+500+1190=2110kcal/70kg=30kcal/kg 24%oftotalcaloriesareprovidedaslipid

AA=aminoacids;PN=parenteralnutrition.

G. DevelopingaPNRegimenforAdministrationThroughaPeripheralIntravenousLine1. Willlikelynotmeetnutritionalneedsbasedonmacronutrientandmicronutrientconcentration

restrictions(seeabove)2. Foradditionalcalories,increasepercentageofcaloriesadministeredaslipid.



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table 17. PeripheralPNCalculations

Exampleofaperipheral3-in-1PNformulafora70-kgpatient:1.Totalcaloriesestimatedas30kcal/kg×70kg=2100kcal2.Fluidrequirementsestimatedas1500mL+(20mL/kg×50kg)=2500mL/day;prescriberwantsPNto

containnomorethan2000mL3.Calculateamountofdextroseas2000mL×10%=200gofmaximaldextroserecommended4.CalculateamountofAAas2000mL×3%=60gofmaximalAArecommended5.Addabout500kcalaslipid(canaddmoreifpatienttolerates).Canuse10%or20%lipidemulsion6.Calculatevolumesofar.Using70%dextrose,need286mLtoequal200gofdextrose.Using10%AA,

willneed600mLtoequal60g.Using10%lipid,willneed500mL.Willaddelectrolytes,traceelements,multivitamins,andenoughsterilewaterforatotalvolumeof2000mL

7.Finalformulawillcontainthefollowing: AA10%600mL Lipid10%500mL Dextrose70%286mL Electrolytes,multivitamins,andtraceelements Sterilewateraddedfor2000mLfinalvolumetoinfuseat2000mL/24hours=83mL/hour8.FinalconcentrationofmacronutrientsinPNis: AA60g/2000mLfinalvolume=3% Lipid50g/2000mL=2.5% Dextrose200g/2000mL=10%9.FinalcaloricvalueofperipheralPNis: AA60g×4kcal/g=240kcal Lipid50g×10kcal/g=500kcal Dextrose200g×3.4kcal/g=680kcal Totalcalories=240+500+680=1420kcal/70kg=20kcal/kg 35%oftotalcaloriesareprovidedaslipid

H. OrderofMixing(formanualcompounding)1. Adddextrose,AA,sterilewater2. Addphosphate.3. Addotherelectrolytes(exceptCa)andtraceminerals.4. MixwelltoensurephosphateisevenlydistributedandtopreventprecipitationwithCa.5. AddCa.6. Observeforprecipitatesorcontaminants.7. Addlipidif3-in-1formulation.(Note:DonotmixdextroseandlipidsdirectlybecausethelowpHof

dextrosecandestabilizethelipidemulsion.)8. Addvitaminslast,asclosetothetimeofPNadministrationaspossibleinacutecaresettings,orjust

beforeinfusioninpatientsreceivinghomePN.

I. FactorsAssociatedwithCaandPhosphatePrecipitationinPN1. IncreasingpH(morebasic)increasestheriskofCaandphosphateprecipitation.2. IncreasingCaorphosphateconcentrationincreasestheriskofprecipitation.

a. IfCaconcentrationis6mEq/Lorlessandphosphateconcentrationis30mmol/Lorless,theriskof precipitation is low.



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b. CaClismorelikelytoprecipitatewithphosphatethanCagluconate;CaClshouldneverbeusedincompoundingPNformulations.

3. ThefinalconcentrationofAAshouldbeatleast2.5%orhighertopreventCaandphosphateprecipitation.a. AAformsolublecomplexeswithCaandphosphate.b. AAprovideabuffersystemtomaintainalowerpHofthePNinanacceptablerangetoprevent

Ca or phosphate precipitation.4. Asthetemperatureincreases,theriskofprecipitationincreases.

a. PNshouldberefrigeratedifnotadministeredwithin24hoursofcompounding.b. Ifrefrigerated,PNshouldbeadministeredwithin24hoursofrewarming.

5. A1.2-micronfilter(usedfora3-in-1PN)maynotpreventembolismofaCaphosphateprecipitatebutshouldbeusedanywaytoreducetherisk.

6. Orderofmixingadditives(seeabove)7. ThePNshouldbeagitatedoftenduringcompoundingtoensureadequatemixtureintosolution.

J. MedicationAdditivesinPN1. Ingeneral,medicationsshouldnotbeaddedtoPNifitcanbeavoided.2. DonotaddthefollowingtoPN:Ceftriaxone(precipitateswithCa),phenytoin(canchangethepH

ofPN),medicationscontainingpropyleneglycolorethanolasdiluents(e.g.,furosemide,diazepam,lorazepam,digoxin,phenytoin,etoposide),irondextran(trivalentcationsdestabilizethelipidemulsionin3-in-1PNformulations)

3. Incompatibledrugsshouldbeadministeredthroughaseparateintravenouscatheteroraseparatelumenofacentralvenouscatheterifpossible.

4. IfanincompatibleintravenousdrugneedstobeadministeredthroughthesameintravenouscatheterasthePN,thePNshouldbestopped,followedbyacompatibleflushbeforeandafterdrugadministration.ThevolumeofflushshouldbesufficienttocleartheentirecatheterofPNandofdrug(typicallyaround10mLifflushingtheportclosesttothepatient);fordrugsrequiringlongerinfusiontimes,seebelowforprecautionstopreventreboundhyperglycemiawithprolongedinterruptionsofPN.

5. OnlyregularinsuliniscompatiblewithPN.

K. PNComplications1. Catheter-relatedinfectionsareprimarilycausedbyStaphylococcus aureus andCandida albicans.2. Catheterinsertioncomplications(e.g.,pneumothorax,incorrectplacement)3. Peripheralvenousthrombophlebitiscanoccurwithperipheralcatheterplacement;riskisincreasedby

day4ofcatheterization;therefore,siteshouldberotatedevery3days.4. Fluidimbalance5. Acid-baseimbalancesareusuallyrelatedtothepatient’sunderlyingcondition;however,excessiveCl

saltsinthePNcancauseametabolicacidosis,whereasexcessiveacetatesaltsinthePNcancauseametabolicalkalosis.

6. Hyperglycemiacanleadtonosocomialandwoundinfections.7. Gutatrophy8. Overfeedingcancausehepaticsteatosis,hypercapnia(elevatedCO2),hyperglycemia,andazotemia.9. Essentialfattyaciddeficiency

a. Symptomsincludeskindesquamation,hairloss,impairedwoundhealing,hepatomegaly,thrombocytopenia,fattyliver,andanemia.

b. Canoccurwithin1–3weeksofalipid-freePN



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10. Refeedingsyndromecanoccurinacutely(canincludecriticallyillpatients)orchronicallymalnourishedpatientsbyinitiatingENorPN.a. Characterizedbyhypophosphatemia,hypokalemia,hypomagnesemiab. Cancausecardiacdysfunction,respiratorydysfunction,anddeathc. Preventionofrefeedingsyndrome:

i. Identifypatientsatrisk(e.g.,anorexia,alcoholism,cancer,chronicallyill,poornutritionalintakefor1–2weeks,recentunintentionalweightloss,malabsorption)

ii. Initially,providelessthan50%ofcaloricrequirements;thenadvanceoverseveraldaystodesiredgoal.

iii. SupplementvitaminsbeforeinitiatingPNaswellasK+,phosphate,andmagnesium(ifneeded);monitordailyforatleast1week;andreplaceelectrolytesasneeded(manypatientswillneedaggressiveelectrolytereplacementduringthefirstweekofPN).

11. Aluminumtoxicitya. Morelikelytooccurinpatientsonlong-termPNorinthosewithrenaldysfunction(aluminumis

renallyeliminated)b. AccumulatesinboneandinterfereswithboneCauptake,causingosteopeniac. Neurotoxicityd. Aluminumcontaminatesmanyintravenouselectrolytesandintravenousfluids.e. Seedruglabelsforamountofaluminumcontent(mandatedbytheFDA[U.S.FoodandDrug

Administration]).12. Hepatobiliarydisorders(includessteatosis,cholestasis,andgallbladdersludgeorstones)canoccur

withlong-termadministrationofPN.a. Steatosis(orfattyliver)isassociatedwithoverfeedingandatransientelevationin

aminotransferaseconcentration.Althoughitisusuallybenign,itcanprogresstofibrosisorcirrhosisinpatientsreceivinglong-termPN.

b. Cholestasisusuallyoccursinchildren,butitcanalsooccurinadultsreceivinglong-termPNandcanprogresstocirrhosisandliverfailure;aconjugatedbilirubinconcentrationgreaterthan2mg/dListheprimarysign.

c. Gallbladderstasisisassociatedwiththedevelopmentofgallstones,sludge,andcholecystitisandismoreattributabletoalackofENthantoPNadministration.

13. Osteoporosisandosteomalaciacanoccurinpatientsreceivinglong-termPN,andtheyareassociatedwithhigherproteindoses(causesincreasedCaexcretion)andchronicmetabolicacidosis(becauseofinsufficientacetate).

Patient Case9. A43-year-oldmaletraumapatient(wt100kg,ht6′3′′),wasrecentlyextubatedandisreceivingPN.HisPN

formulacontains35kcal/kg,1.2g/kgofprotein,dextroseinfusingat4.4mg/kg/minute,and25%oftotalcaloriesas lipid.Hehasgraduallydevelopedsymptomsofhypercapniaandhasdevelopedarespiratoryacidosis.Themedicalteamisconsideringstrategiestocorrectthistoavoidreintubation.WhichoneofthefollowingchangestothePNformulacouldbestcorrectthissituation?A.ChangePNtoENandmaintaincurrentcaloricgoals.B.ReducedextroseamountinPNto3mg/kg/minuteandincreaselipidtomaintaincurrentcaloricgoal.C.ChangeelectrolytestotheacetatesaltinthePNtocorrecttheacid-baseimbalance.D.Reducethecaloriesto25kcal/kgtopreventoverfeeding.



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L. MonitoringPatientsWhoAreReceivingPN1. Monitorforinfection(temperature,WBC,intravenousaccesssite).2. Monitorforperipheralveinthrombophlebitisand/orinfiltration(ifperipheralaccess);symptoms

includepain,erythema,andtendernessorapalpablecordatthesiteoftheperipheralvein;treatbyremovingcatheter.

3. Monitorfluidstatus(weight,edema,vitalsigns,inputandoutput,temperature).4. Monitor nutritional status.

a. Prealbuminisveryusefulinmonitoringtheeffectsoflong-termnutritionsupportinpatientswhoarenotcriticallyill(seeMonitoringENabove).i. Values

(a) Normalrange16–40mg/dL(b) Moderatemalnutrition11–16mg/dL(c) Severemalnutritionislessthan11mg/dL.

ii. Goalformalnourishedpatientsisanincreaseofatleast3–5mg/dL/weekuntilwithinnormalrange.

b. Serumalbumin(normal3.5–5g/dL)isapoorpredictorofnutritionalstatusbecauseithasalonghalf-lifeandconcentrationsfluctuateduringillness.

5. Monitorforhyperglycemiaandhypoglycemia.a. Acommongoalbloodglucoseis150mg/dLorless,althoughthereisnoconsensusforacutelyill

hospitalizedpatients.b. Regularinsulin(initially0.05–0.2unitofdextrosepergram)canbeaddedtothePNforpatients

usingaconsistentdosage.c. Forpatientswithhyperglycemiaorfluctuatinginsulindosages,insulincanbesupplemented

separatelyfromthePN,althoughthispracticevariesbypractitioner.d. AbruptdiscontinuationofPNisusuallytoleratedinnondiabeticpatients,butrebound

hypoglycemiamayoccurinotherpatients;avoidbygraduallytaperingoffPNover1–2hours;checkbloodglucose30minutesto1hourafterdiscontinuationofPN.IfPNisdiscontinuedabruptly,canavoidreboundhypoglycemiabyadministrationof5%or10%dextrose(unnecessaryifPNisadministeredthroughaperipheralcatheter)

6. Monitorforelectrolyteandacid-baseimbalances.TheClandacetatesaltscanbeadjustedonthebasisoftheacid-basestatusofthepatient.a. Formetabolicalkalosis,NaandK+canbeadministeredastheClsalts.b. Formetabolicacidosis,NaandK+canbeadministeredastheacetatesalts(acetateisconvertedto

bicarbonate).c. Forrespiratoryacid-basedisorders,correcttheunderlyingcauseoradjusttheventilatorsettings

asneeded.7. Monitortriglycerideconcentrationsandwithholdlipidsinpatientswithaconcentrationgreaterthan

400mg/dL.Whencalculatinglipidrequirements,accountforanydrugsmixedinalipidemulsion(e.g.,propofol,clevidipine).

8. Monitor hepatic function.9. MonitorforpatientreadinessfororalorENsupport.

a. Well-nourished,relativelyhealthypatientscanchangeimmediatelyfromPNtooral/EN.b. Elderly,debilitated,and/ormalnourishedpatientsmayneedatransitionperiodinwhichoralor

ENfeedingsaregraduallyincreased,coincidingwithareductioninPN.



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Patient Cases10. Apatientweighing70kgreceivespropofolat45mcg/kg/minute.Propofolisavailableataconcentration

of10mg/mLandismixedina10%lipidemulsion.Assumingthepatientisreceivingthisinfusionratefor24hours,whichofthefollowingbestapproximatesthetotalcaloriesprovidedbythepropofolinfusionina24-hourperiod?A. 200kcal.B. 250kcal.C. 300kcal.D. 500kcal.

11. Apatientwhoweighs65kgisreceivingPNafterabdominalsurgery.ThePNcontainsabout1600kcalin-cluding100gofprotein,500kcalaslipid,and200gofdextrose.Thefollowingadditivesarealsoincludedina24-hourinfusionofPN:NaCl50mEq,Na+acetate100mEq,K+acetate60mEq,Na+ phosphate 30 mmol,magnesiumsulfate12mEq,Ca++gluconate10mEq/day,multivitamins10mL,andseveral traceelements3mL.ThepatienthasanNGtubeinplaceandissuctioningabout400–500mL/day,whichisbe-ingreplacedwithaninfusionof0.9%NaCl.After48hoursofPN,thepatienthasthefollowinglaboratoryvalues:Na+140mEq/L,K+3.8mEq/L,Cl- 93mEq/L,bicarbonate35mEq/L,pH7.5,Pco247mmHg,andbicarbonate36mEq/L.WhichoneofthefollowingadjustmentstothePNformulaisbestatthistime?A. Increaselipidstoprovide750kcalandreducedextroseto130g.B. IncreaseNaacetateto150mEq/dayanddiscontinueNaCl.C. IncreaseNaClto150mEq/dayanddiscontinueNa+ acetate.D. Addsodiumbicarbonate50mEqtoPN.

12. A75-year-old,50-kgwomanisreceivingPNafteranextensivebowelresection.Sheisexpectedtorequireabout1weekofPN.Sheisreceivingthefollowingmacronutrientsinherformula:70%dextrose300mL,10%lipid300mL,and10%AA750mL.Ifthesemacronutrientsareinfusedover24hours,whichofthefollowingmostcloselyapproximatesthetotalcaloriesthatthispatientisreceiving?A. 20kcal/kg.B. 26kcal/kg.C. 30kcal/kg.D. 35kcal/kg.

13. Thepatientinquestion12hasreceivedthePNformulaabovefor3days.Herbloodglucoseconcentrationshaverangedfrom200to280mg/dL.Shehasordersforthefollowingslidingscaleofregularinsulin:bloodglucose200–250give2units,bloodglucose251–300give4units,andbloodglucose301–350give6units.Shehasbeenreceivingabout14–16unitsofinsulindailythroughthesliding-scaleorders.Hermedicalhis-toryissignificantforhypertension,diabetes,chronicobstructivepulmonarydisease,andcoloncancer.Shewasrecentlyinitiatedonmethylprednisolone60mgintravenouslyevery6hoursforachronicobstructivepulmonarydiseaseexacerbation.Today,thedosewillbereducedto40mgintravenouslyevery8hours.Whichoneofthefollowingisthebestrecommendationtobettercontrolthispatient’sbloodglucose?A. Addinsulinglargine10–20units/daytoPN.B. Change70%dextroseinPNtoD5W.C. Increasethesliding-scaleinsulinto4unitsforbloodglucose200–250,8unitsforbloodglucose

251–300,and12unitsforbloodglucose301–350.D. AddNPH(neutralprotamineHagedorn)insulin5–10unitssubcutaneouslyevery12hours.



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ReFeRenCeS

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guidelines for potassium replacement in clinicalpractice.Acontemporary reviewby theNationalCouncil on Potassium in Clinical Practice. ArchInternMed2000;160:2429–36.

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3. Kellum JA,Cerda J,KaplanLJ, et al. Fluids forprevention and management of acute kidney in-jury.IntJArtifOrgans2008;31:96–110.

4. Kraft MD, Btaiche IF, Sacks GSS, et al. Treat-ment of electrolyte disorders in adult patients inthe intensive care unit.Am JHealth Syst Pharm2005;62:1663–82.

5. Perel P, Roberts I. Colloids versus crystalloidsforfluidresuscitationincriticallyillpatients.Co-chraneDatabaseSystRev2007:CD000567.

6. PoldermanKH,SchreuderWO,StrackvanSchijn-delRJ,etal.Hypernatremiaintheintensivecareunit:anindicatorofqualityofcare?CritCareMed1999;27:1105–8.

7. RoseBD,PostTW.Clinical Physiology ofAcid-BaseandElectrolyteDisorders,5thed.NewYork:McGraw-Hill,2001.

8. Sterns RH. Hypernatremia in the intensive careunit: instant quality—just add water. Crit CareMed1999;27:1041–2.

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10. Vincent JL,WeilMH. Fluid challenge revisited.CritCareMed2006;34:1333–7.

nutrition1. A.S.P.E.N.BoardofDirectors.Guidelinesfor the

use of parenteral and enteral nutrition in adultand pediatric patients. J Parenter Enter Nutr2002;26(Suppl):1SA–138SA.

2. Bankhead R, Boullata J, Brantley S, et al.A.S.P.E.N.EnteralNutritionPracticeRecommen-dations.JParenterEnterNutr2009;33:122.

3. BtaicheIF,KhalidiN.Metaboliccomplicationsofparenteralnutritioninadults,part1.AmJHealthSystPharm2004;61:1938–49.

4. BtaicheIF,KhalidiN.Metaboliccomplicationsofparenteralnutritioninadults,part2.AmJHealthSystPharm2004;61:2050–7.

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AnSWeRS And eXPLAnAtIOnS tO PAtIent CASeS

1. Answer CAlthoughthispatient’sBPisnotnecessarilylow,it islikelylowcomparedwithhisbaseline,consideringhishistory of hypertension. In addition to his relativelylowBP,hisothersignsandsymptomsofintravascularvolume depletion include an increased BUN/Cr ratioandareducedurineoutput.Crystalloidsorcolloidsareappropriatefluidsforresuscitation,makinghetastarch(Answer C) the best option. Furosemide (Answer A)may increase his urine output, but at the cost of fur-therdepletingtheintravascularvolume.Albumin25%(Answer B) should be avoided for fluid resuscitationbecauseitcausesashiftoffluidfromtheISspaceintotheintravascularspace,whichcanpotentiatehisdehy-dration.AnswerDwouldbeappropriateforamainte-nanceinfusion;however,D5W/0.45%NaClplusKCl20mEq/Lwouldnotprovideoptimal replacementof theintravascularspacegiventhedistributioninTBF.

2. Answer CThispatienthasnocurrentsignsorsymptomsofintra-vascularvolumedepletion,sohedoesnotrequirefluidresuscitation.Becauseheisnottakingadequatefluidsbymouth,heshouldbeadministeredmaintenancein-travenousfluid topreventdehydrationandelectrolyteimbalances.Thisis typicallyaccomplishedbyacom-binationoffreewater(asD5W)and0.45%NaClwithK+.The infusion rate is calculated as 1500mL+ (60kg×20mL/kg)=2700mL/24hoursorabout110mL/hour.Parenteralnutrition(AnswerA)is inappropriatebecausethereisnoevidencethatthepatient’sGItractisnonfunctional.Albumin5%(AnswerB)orLRsolu-tion(AnswerD)shouldbereservedforfluidresuscita-tioninpatientswithsignsorsymptomsofintravascularvolumedepletion.

3. Answer BAlthoughthispatientisexperiencingsymptomatichy-ponatremia,she isalsoshowingsignsof intravascularvolumedepletion.ThisintravascularvolumedepletionisapotentstimulusforADHsecretion,whichwillpo-tentiate hyponatremia. In patients with hyponatremia and intravascular volume depletion, it is important torestore intravascularvolumefirst topreventorganhy-poperfusionaswellastoinhibitthesecretionofADH.Fluid resuscitationshouldbeaccomplishedwith0.9%

NaClasafluidbolus,followedbyareevaluationoffluidstatus.Aslowerinfusionof0.9%NaCl(AnswerA)willnotquicklyrestore intravascularvolume.Once the in-travascular volume is restored, secretionofADHwillcease.ThiscanbefollowedbyawaterdiuresiswithasubsequentriseintheserumNa+concentration.Ofim-portance,thepatientshouldbemonitoredcloselytopre-ventariseinserumNa+greaterthan10–12mEq/L/day.IfserumNa+risestoofast,0.45%NaClcanbeinfusedtoslowtherateofriseofserumNa+concentration.Hy-pertonicsaline(AnswerCandAnswerD)wouldnotbeadvisableunlessthepatientcontinuedtohavesymptomsofhyponatremiaafterappropriatefluidresuscitation.

4. Answer CTopreventcentralpontinemyelinolysisinpatientswithhyponatremia, it is recommended that the serumNa+ concentrationberaisedbynomorethan10–12mEq/Lin24hours.Ofemphasis, thegoalisnottoachieveanormal serum Na+ concentration in 24 hours. Rapidcorrection of chronic hyponatremia can cause perma-nentneurologicdamage.

5. Answer dThis patient has hyponatremia and hypokalemia. Inpatientswith hypokalemia, there is a reduction in ICK+.Tomaintaincellularelectroneutrality,Na+ will shift intocells.AsK+isreplaced,Na+willshiftoutofcells,and theserumNa+ concentrationwill rise.Therefore,inthiscase,thehypokalemiashouldbecorrectedfirst,whichwillcauseasubsequentimprovementinthehy-ponatremia.BecausethispatienthasnoECGchangesrelatedtothehypokalemia,oralsupplementationwithK+isrecommendedoverintravenousreplacement(An-swerA).Adoseof60–80mEq/dayshouldcauseanin-creaseintheK+concentrationofabout1.5mEq/L.Be-causethepatientiseatingaregulardiet,sheshouldnolonger require intravenous fluids (AnswerB).Hyper-tonicsaline(AnswerC)isincorrectbecausethispatientisnotexperiencingserioussymptomsofhyponatremia.

6. Answer dThispatienthasnotbeengivenenoughwater,andsheis unable to communicate (or feel) thirst. Thismedi-cal error can be prevented by administering about 1mLofwater foreverycalorieadministered. It should



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alsobepreventedbymonitoringserumNaconcentra-tionsandadjustingwaterintakeasneeded.Tocorrectthehypernatremia,watershouldbeadministeredpref-erably through the enteral feeding tube. If this is notpossible,thenitcanbereadministeredintravenouslyasD5W(AnswerBorC)butneverassterilewater(An-swerA).Sterilewateradministeredintravenouslycancausehemolysisanddeath.Thepatient’swaterdeficit(inliters)canbeestimatedbytheequation0.4×LBW×[(Na+/140)−1].Watershouldbereplacedoverseveraldays,takingcaretoavoidchangesinserumNa+greaterthan10–12mEq/Lin24hours.

7. Answer BThis patient hasECGchanges consistentwith hyper-kalemia.Insulin(AnswerB)willhavethefastestonsetandmostpredictableactionof loweringserumpotas-sium.Calciumgluconate(AnswerA)shouldbeavoidedinthispatientbecauseitcanpotentiatedigoxintoxicityand bradycardia. The efficacy of sodium bicarbonate(AnswerC)isnotwellestablished.Albuterol(AnswerD)canbeefficaciouswhenaddedtoinsulin,butitmaynotbeeffectiveinabout40%ofpatientsandisthere-fore not recommended as initial therapy or asmono-therapyforhyperkalemia.

8. Answer CThis patient is receiving a calorie-dense EN formulathattypicallyhaslesswaterthanotherenteralproducts.Therefore,althoughsheisnotcurrentlyhypernatremic,thepatient isat riskofdevelopinghypernatremiabe-causeofinsufficientwaterintake.Thiscanbeprevent-ed by administering additional water. The preferredrouteisenteralifpossible.Theadditionalwaterneededonadailybasiscanbeestimatedas1mL/kcal.There-fore, if this patient is receiving the enteral feeding at35mL/hour×2kcal/mL, she is receiving1680kcal/day.Sheisonlyreceiving710mL/Lofwaterofenteralformula,whichamountsto596mL/dayforthe840mLofenteralfeedingdaily(35mL/hour×24hours=840mL/day).Becausesheisreceiving1680kcal,sheneedsabout1680mL/dayofwater.Subtractingthewaterfromthefeedingsfromthetotalneeded,1680−596=1084mL is needed.This can be divided and administeredthroughthegastricfeedingtubeasaround180mL/doseevery4hours.Ofnote,thepatientshouldbemonitoredforfluidoverload,especiallygivenherchronickidneydisease.Giventhispatient’sstablekidneydiseaseand

heradequateurineoutput,sheshouldbeabletotoler-atethisamountoffreewater.Theamountoffreewa-terneededonadailybasisisanestimationandshouldbeadjustedonthebasisofspecificpatientparameters(e.g., serumNa+, input, output, dailyweight, edema).Freewatershouldnotbeadministeredas intravenousdextrose (Answer B) unless enteral administration isnot feasible.AnswerA is incorrect because reducingNawillnotpreventhypernatremia;theproblemisre-latedtotoolittlewaterratherthantoomuchNa+. An-swerDisincorrectbecausethecaloricgoalsshouldnotbesacrificed,andtheywouldnoteliminatetheproblemofinsufficientwateradministered.

9. Answer dThis patient is developing a respiratory acidosis pos-siblybecauseofoverfeeding.Althoughdextroseisme-tabolizedtowaterandCO2,itgenerallywillnotcausearespiratoryacidosisunlessthepatientisbeingoverfed.Therefore,byreducingthetotalcaloriesto25kcal/kg,theriskofoverfeedingisdiminished,andreintubationcanbeavoided.AnswerAisincorrectbecausepatientscanbeoverfedwitheitherPNorEN.AnswerBisin-correctbecauseevenwithreducingthedextroseinthePN, the patient can still develop symptoms of over-feeding.AnswerCisincorrectbecausetheunderlying(overfeeding)causeshouldbecorrected,ratherthanad-justingtheacetatetotreatarespiratoryacidosis.

10. Answer dTodeterminetheamountofcaloriesprovidedbypro-pofol,itmustfirstbedeterminedhowmanymillilitersa day are infused. For this patient receiving 45mcg/kg/minuteofpropofolandweighing70kg,454mLisinfuseddaily(assumingaconstantinfusionrate).Next,assumingthata10%lipidemulsionprovidesabout1.1kcal/mL,itcanbecalculatedthat454mL/dayofpropo-folprovidesaround500kcal/day.

11. Answer CThispatienthasdevelopedametabolicalkalosislikelysecondarytothelossofgastricfluidthroughNGsuc-tioning.The low serumCl- andelevated serumbicar-bonateconcentrationssupportthistheory.Inaddition,the acid base is consistentwith ametabolic alkalosiswith a compensatory respiratory acidosis. The treat-ment in this circumstance is to replace the lost fluidwith0.9%NaCl,whichisbeingdone.Inaddition,Na+



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andK+canbeadministeredas theCl-salt, rather thantheacetatesalt.Forthiscase,onlyNa+isconvertedtoCl-salt,andK+isleftastheacetatesaltinitially.Withdailymonitoring,theratioofCl-toacetatecanbead-justedfurtherifneeded.AnswerBisincorrectbecauseitwould likelyworsen themetabolic alkalosis asNa+ acetateisconvertedtobicarbonate.AnswerAisincor-rectbecausehypercapniaisacompensatoryresponse,nottheprimaryacid-basedisturbance.AnswerDisin-correctforseveralreasons.First,itisneveradvisabletoaddNa+bicarbonatetoPNbecauseofincompatibilityandincreasingtheriskofCa++-phosphate precipitation. Second,Na+bicarbonateistheincorrecttreatmentforametabolicalkalosisbecauseitcanworsenalkalosis.

12. Answer BThetotalcaloriesarecalculatedbyaddingthecaloriesprovidedbydextrose,lipid,andAA.Dextroseprovides714kcal(210g×3.4kcal/g);lipidprovidesabout300kcal(30g×10kcal/g);andAAprovides300kcal(75g×4kcal/g).Addingthesetogetherprovidescaloriesof1314kcal/50kg=26.3kcal/kg.

13. Answer dThis patient’s hyperglycemia could be attributable toeitherstressorcorticosteroids.Becausethecorticoste-roiddoseisbeingtapereddownward,thebloodglucoseconcentrationswillalsolikelydecreasewithtime.Forpatientswithafluctuatingbloodglucoseconcentration,itcanbedifficulttoaddinsulintoPNbecauseitcan-notbeadjustedinatimelymanner.Regardless,AnswerA is incorrect because long-acting insulin should notbeaddedtoPN.IfinsulinisaddedtoPN,itshouldberegularinsulin.Althoughsomeexpertspromote“per-missiveunderfeeding,”AnswerBisincorrectbecauseit would provide insufficient calories for this patient.Sliding scales of insulin can be usefulwhen used inconjunctionwithabaselineofinsulininpatientswithafluctuatingbloodglucoseconcentration.However,aslidingscale(AnswerC)shouldnotbeusedasthepri-maryinterventionforbloodglucosecontrolbecauseitis reactive and fails toprevent hyperglycemia. In ad-dition,theslidingscaledescribedrecommendsinsulinonlywhenthebloodglucosereaches200,whichistoohigh.AnswerDiscorrectbecauseitprovidesabaselineofinsulinthatcanbeadjustedinatimelymannerasthebloodglucoseconcentrationsfluctuateon thebasisofthe patient’s status.



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AnSWeRS And eXPLAnAtIOnS tO SeLF-ASSeSSment QueStIOnS

1. Answer: dThispatientcontinuestohavehypotensionandtachy-cardia, both signs of intravascular volume depletion.TheimprovementinBPandtachycardiaafterafluidbo-lusalsoindicatesintravascularvolumedepletion.Fluidadministrationshouldcontinueuntilthereisnofurtherimprovementinvitalsigns.Patientswithintravascularvolume depletion require a rapid bolus of crystalloid(either0.9%NaClorLR) in theamountof500–1000mL(orabout20mL/kg),followedbyareassessment.Arapidbolusisessentialtopreventorgandysfunctioncausedbyhypoperfusion.Althoughthepatienthaspoorurineoutput,administrationoffurosemide(AnswerA)willworsenvolumedepletion.Asvolumeisreplaced,urineoutputwilllikelyincrease.Administrationof5%albumin in combination with a vasopressor (AnswerB) shouldnotbe the initial treatment as longasvitalsignsareimprovingwiththeadministrationoffluidbo-luseswith 0.9%NaCl. In addition, colloids aremoreexpensive,andthereisnoevidenceshowingimprovedoutcomesforfluidresuscitationcomparedwithcrystal-loids. Furthermore,infusionofalbuminover4hoursis incorrectbecause itwouldnotrestore intravascularvolume rapidly enough to prevent organ dysfunction.IntravenousfluidcontainingD5W(AnswerC)isnotap-propriateforfluidresuscitationregardlessofthebloodglucoseconcentration.

2. Answer AToanswerthisquestion,analligationmustfirstbesetupusing0.9%and23.4%NaCl.If0.9%NaClcontains154mEq/L,then3%shouldcontainaround513mEq/L.Aftercompletingthealligation,thecorrectamountscanbedouble-checkedbyverifyingtheamountofNaClinthepreparedproduct:907mLof0.9%NaClcontains140mEqofNaCl;93mLof23.4%NaClcontains372mEq ofNaCl; therefore, 140mEq + 372mEq = 512mEq/LofNaClinthefinalproduct.Theosmolarityiscalculatedas(3g/100mL)×(1mol/58.5g)×(2Osm/mol)×(1000mOsm/Osm)×(1000mL/L)×0.93=954mOsm/L.Becauseoftheosmoticcoefficient(0.93),theNaCl does not completely dissociate in solution. Al-thoughuseoftheosmoticcoefficientprovidesamoreaccurateosmolarity,itislikelynotclinicallyrelevantincalculatingtheosmolarityofintravenousNaCl.There-fore,itissafetoestimatetheosmolarityofNaClasei-

ther954or1026mOsm/Lbecausethereisnoapparentclinicaldifferencebetweentheseosmolarities.Becausetheosmolarityisgreater than900mOsm/L, theinfu-sionshouldbeadministered throughacentral line, ifpossible,topreventpainandirritation.

3. Answer dInthiscase,hyponatremiaislikelybecauseofconges-tiveheartfailureandhaslikelydevelopedoverapro-longedperiod (not acuteonset).Patientswith chronichyponatremia because of heart failure are typicallyasymptomatic.Rapidcorrectionofchronichyponatre-mia is associatedwith permanent neurologic damagecaused by central pontinemyelinolysis. Furthermore,HScanworsenvolumeoverloadinpatientswithheartfailure.Althoughhyponatremiaisasignofworseningheart failure, correction of hyponatremia in patientswithheartfailuredoesnotimproveoutcomes.Forthesereasons,therisksofcorrectingtheserumsodiumwithHS(AnswerA,AnswerB,andAnswerC)outweighthepotentialbenefits.

4. Answer BPatientswith hyperkalemia andECG changes shouldbetreatedfirstwithCa+forcardiacstability.AfterCa++ administration, other measures can be taken to shiftK+ fromtheECcompartment to theICcompartment.Insulin (AnswerA) can accomplish this; however, inthis hyperglycemic patient, insulin should be admin-isteredwithoutglucose.Sodiumpolystyrenesulfonate(Kayexalate;AnswerC)canbeadministered,butitisnoteffectiveimmediatelyandisthereforenotappropri-ate forfirst-line treatment of symptomatichyperkale-mia.Sodiumbicarbonate (AnswerD) is incorrectbe-causeitdoesnottreatcardiacinstability.

5. Answer CThispatientisnottakingadequatenutritionalintakebe-causeofhermentalstatus.BecauseherGItractisfunc-tional,itshouldbeusedforfeedingtopreventgutmu-cosalatrophy.AnNGornasoduodenalfeedingtubeisappropriate for enteral access for short-term nutritional support.Apercutaneousgastrostomytube(AnswerD)requiresasurgicalprocedureandisusedforlong-termnutritionalsupport.Thepatientshouldreceivebetween25and35kcal/kg/day.ThePNformulas(AnswerAand



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AnswerB)shouldnotbeusedinapatientwithafunc-tionalGItract.AlthoughAnswerBwouldbeanappro-priatePNformulaforperipheraladministration,PNisassociatedwithmorecomplicationsthanEN.

6. Answer CThiscorrectformulaprovidesabout30kcal/kgofcalo-ries, 1.5 g of protein per kilogram (AA), and30%oftotalcaloriesaslipid.AnswerAisincorrectbecauseitprovides1000caloriesaslipid,whichisabout62%ofthe totalcaloriesprovided.AnswerB is incorrectbe-cause itcontainsonly0.8g/kgofAA,an insufficientamountconsideringthepatient’sstressandtheappar-entabsenceofkidneyinjury.AnswerDisincorrectbe-cause it contains too much AA.

7. Answer BThis patient has hypomagnesemia and hypokalemia.Correction of hypokalemia requires correction of hy-pomagnesemiatopreventrenallossofK+.Magnesiumshould be administered slowly to avoid hypotensionand increasedrenalexcretioncausedbyrapidadmin-istration.

8. Answer CEnteralnutritionpreventsgutmucosalatrophyandsub-sequentbacterialtranslocation.BacterialtranslocationisthecrossingofbacteriafromtheGItractintothesystemiccirculation.Enteralnutritionisassociatedwithfewerin-fectiouscomplicationsthanisPN,whichmaybepartlybecauseofareductioninbacterialtranslocation.



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fluids, electrolytes, and nutrition - accp

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