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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2804_Библиотеки_им_академика_М_И_Перельмана
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whichthetotalamountofdailyformulaisdividedintofourtosixequalportions.
Bolusfeedingsaregivenbysyringeasrapidlyastolerated.
Gravityfeedingsareinfusedover30–60minutes.
Thepatient’supperbodyshouldbeelevatedby30–45degreesduringfeedingandforatleast2hours
afterward.Tubesshouldbe flushedwithwateraftereachfeeding.Intermittentfeedingsare useful for
patientswhocannotbe positionedwith continuoushead-of-the-bedelevationor whorequire greater
freedom from feeding. Patientswhoexperiencenausea andearly satietywithbolusgravityfeedings
mayrequirecontinuousinfusionataslowerrate.
Continuousfeedingcanoftenbestartedat20–30mL/handadvancedby10mL/hevery6hoursuntil
thefeedinggoalisreached.Patientswhohavegastroparesisoftentolerategastrictubefeedingswhen
theyarestartedataslowrate(e.g.,10mL/h)andadvancedbysmallincrements(e.g.,10mL/hevery
8–12 hours). Patientswithsevere gastroparesis may require passageof the feeding tube tippast the
ligamentofTreitz.Continuousfeedingshouldalwaysbeusedwhenfeedingdirectlyintotheduodenum
orjejunumtoavoiddistention,abdominalpain,anddumpingsyndrome.
Jejunal feeding may be possible in closely monitored patients with mild to moderate acute
pancreatitis.14 RCTs comparing jejunal and gastric feeding in severe acute pancreatitis showed no
differences in tolerance, complicationrates, and mortality rates. Early initiation of enteral nutrition
within24–72hoursofadmissionisassociatedwithdecreasedmortality,organfailure,andinfectious
complicationscomparedwithdelayedenteralnutrition.
15
ContraindicationstoEnteralFeeding
Theintestinaltractcannotbeusedeffectivelyinsomepatientsbecauseofthefollowing:
Persistentnauseaorvomiting
Postprandialabdominalpainordiarrhea
Mechanicalobstructionorseverehypomotility
Malabsorption
Presenceofhigh-outputfistula
Complications
Mechanicalcomplications
Nasogastric feeding tube misplacement, including intubation of the tracheobronchial tree, occurs
moreofteninunconsciouspatients.Intracranialplacementcanoccurinpatientswithskullfractures.
Erosive tissue damage can lead to nasopharyngeal erosions, pharyngitis, sinusitis, otitis media,
pneumothorax,andGItractperforation.
Tube occlusion is often caused by inspissated feedings or pulverized medications given through
small-diameter (<#10 French) tubes. Frequent flushing of the tube with 30–60 mL of water and
avoiding administration of pill fragments or viscous medications help to prevent occlusion. The
techniquesusedtounclogtubesincludetheuseofa small-volume syringe (10 mL)toflushwarm
waterorpancreaticenzymes(Viokase™dissolvedinwater)throughthetube.
Hyperglycemia
ADA/AACE guidelines recommend a blood glucose target between 140 and180 mg/dL for most
hospitalizedpatients.Inpatientswithseverecomorbiditiesandterminalillness,lessstringenttargets
areappropriate.
16,17
The majority of non–critically ill inpatients will require basal insulin while receiving enteral
nutritiontoachieveandmaintainreasonableglucosecontrol.
18
Long-duration insulin (e.g.,detemir, glargine) canbe used for basal coverage, while short-acting
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(e.g.,lispro™)canbeusedtocoverprandialandcorrectionalneeds.
Patientsreceivingbolusfeedsshouldbe givenshort-actinginsulinatthetimeofeachfeedwithan
approximatedoseof1unitofshort-actinginsulinper10–15gcarbohydrate,plusacorrectionaldose
ifneeded.
Patients receiving continuous (24 hours per day) feeding should receive basal and bolus insulin
whenclinicallystable.
Forpatientsreceivingnocturnaltubefeeding,intermediate-durationinsulin(e.g.,NPH)administered
withinitiationoffeedingisareasonableapproach;however,careshouldbetakentoavoidnocturnal
hypoglycemia.
If tube feeds are interrupted and insulin has been given, an infusion of dextrose-containing fluid
shouldbestartedataratetomatchtheinfusionrateofthescheduledtubefeedsuntiltheinsulinhas
wornoff.
Pulmonarycomplications
Theetiologyofpulmonaryaspirationisoftendifficulttodiscernintube-fedpatientsasitcanoccur
bothfromrefluxedtubefeedingsororopharyngealsecretionsunrelatedtofeedings.Recentevidence
suggests that oral secretions play a far greater role in the development of ventilator-associated
pneumoniathanaspirationoftubefeedings.
19
Gastricresidualsarepoorlypredictiveofaspirationrisk.
20
Preventionofreflux:Decrease gastricacid secretionwithH2blockersor protonpumpinhibitors,
elevate head of bed during feeds, andavoid gastric feeding in high-riskpatients (e.g.,thosewith
gastroparesis,frequentvomiting,gastricoutletobstruction).
GIcomplications
Nausea,vomiting,andabdominalpainarecommon.
Diarrhea isoften associatedwithantibiotictherapyandtheuseof liquidmedicationsthat contain
nonabsorbable carbohydrates, suchas sorbitol. If diarrhea from tube feeding persists afterproper
evaluation of possible causes, a trial of antidiarrheal agents or fiber is warranted. Diarrhea is
common in patients who receive tube feeding and occurs in up to 50% of critically ill patients.
Supplementationwithfiberorswitchingtoafiber-enrichedfeedhasnotyieldedconsistentresults.A
changetoanelementalfeedingformulaisrarelyneededandlikelywillnotresolvetheissueunless
significantimpairmentinabsorptioniswell-documented.
21
Diarrheainpatientswith short gut,whodonothaveother causessuch asClostridioides difficile
infection, may be minimized using small, frequent meals that do not contain concentrated sweets
(e.g., soda). Intestinal transit time should be maximized to optimize nutrient absorption using a
tincture ofopium, loperamide, or diphenoxylate. Low-dose clonidine(0.025–0.05 mg orallybid)
maybe used to reduce diarrhea inhemodynamically stable patients withshortbowel syndrome.
22
Intestinal ischemia/necrosis has beenreported in patients receiving tube feeds. These cases have
occurredpredominantlyincriticallyillpatientsreceiving vasopressorsforblood pressuresupport
in conjunction with enteral feeding. There are no reliable clinical signs for diagnosis, and the
mortality rate is high. Caution should be used when enterally feeding critically ill patients
requiringvasopressors.
ParenteralNutrition
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GeneralPrinciples
Parenteralnutritionshouldbeconsideredifenergyintakecannot,oritisanticipatedthatitcannot,bemet
byenteralnutrition(<50%ofdailyrequirements)formorethan7–10days.Thisguidelineoriginatesfrom
twointensivecareunit(ICU)-focusedmeta-analysescitingincreasedcomplicationsandincreasedoverall
mortalityinICUpatientsreceivingearlyparenteralnutrition(i.e.,within7daysofadmission),compared
withthosereceivingnonutritionsupport.
23,24
Recentstudieshavefoundthatcriticallyillpatientswhoare
unabletomeetcaloricgoalsbyenteralnutritionaloneforthefirst8daysofhospitalizationhavelonger
durationsofstayandgreatermortalityratesthanthoseinwhomtotalparenteralnutrition(TPN)is
withheldforthefirst8daysafteradmission.
24
CentralParenteralNutrition
Theinfusionofhyperosmolar(usually>1500mOsm/L) nutrientsolutionsrequiresalarge-bore,highflowvesseltominimizevesselirritationanddamage.
Percutaneous subclavianveincatheterization andperipherallyinsertedcentral venous catheterization
(PICC) are the most common techniques for central parenteral nutrition (CPN) access. Theinternal
jugular, saphenous, andfemoral veins are also used, although they are less desirable due topatient
discomfortanddifficultyinmaintainingsterility.Tunneledcathetersarepreferredinpatientslikelyto
receive>8weeksofTPNinordertodecreasetheriskofmechanicalfailure.
PICCsareincreasingly usedtoprovideCPNinpatientswith adequateantecubitalveinaccess. They
shouldnotbeusedinpatientsrequiringCPNforanextendedtime(>6months).
CPNMacronutrientSolutions
Crystallineaminoacidsolutionsconsistingof40%–50%essentialand50%–60%nonessentialamino
acids (usuallywithlittleornoglutamine,glutamate,aspartate,asparagine,tyrosine,andcysteine)are
usedtoprovideproteinneeds(Table2-2).Infusedaminoacidsareoxidizedandshouldbeincludedin
theestimateofenergyprovidedaspartoftheparenteralformulation.
Some amino acid solutionshavebeenmodified forspecific disease statessuch as thoseenrichedin
branched-chain amino acids for use in patients with hepatic encephalopathy and those that contain
mostlyessentialaminoacidsforuseinpatientswithrenalinsufficiency.
Glucose(dextrose)inIVsolutionsishydrated;eachgramofdextrosemonohydrateprovides3.4kcal.
Althoughthereisnoabsoluterequirementforglucoseinmostpatients,providing>150gofglucoseper
daymaximizesproteinbalance.
Lipid emulsions are available as a 10% (1.1 kcal/mL) or 20% (2.0 kcal/mL) solution and provide
energyaswellasserveasasourceofessentialfattyacids.Lipidemulsionsareaseffectiveasglucose
in conserving body nitrogen economy once absolute tissue requirements for glucose are met. The
optimal percentage of calories that should be infused as fat is not known, but 20%–30% of total
calories are reasonable for most patients. The infusion rate should not exceed 1.0 kcal/kg/h (0.11
g/kg/h)asmostcomplicationsreportedhaveoccurredwhenprovidingmorethanthisamount.25Arate
of0.03–0.05 g/kg/h is adequatefor mostpatientsreceiving continuousCPN.Lipidemulsions should
not be used in patients with triglyceride concentrations >400 mg/dL. Moreover, patients at riskfor
hypertriglyceridemiashouldhaveserumtriglycerideconcentrationscheckedatleastonceduringlipid
emulsion infusiontoensure adequate clearance. Underfeeding obese patients by the amount oflipid
calories that would normally be given (e.g., 20%–30% of calories) facilitates mobilization of
endogenous fat stores for fuel and may improve insulin sensitivity. IV lipids should still be
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administeredtwiceweeklytothesepatientstoprovideessentialfattyacids.Arecentmeta-analysisof
49 RCTs demonstrated thatuseofω-3 fatty-acid-enrichedparenteral nutrition comparedtostandard
parenteralnutritionleadstoreductionininfection,sepsis,andICUandhospitalstaylength.
26
PeripheralParenteralNutrition
Peripheralparenteralnutritionisoflimitedutilityduetohighriskofthrombophlebitis.
Appropriatemanagementofperipheralparenteralnutritioncanincreasethelifeofasingleinfusionsite
to>10days.Thefollowingguidelinesarerecommended:
Provideatleast50%oftotalenergyasalipidemulsionpiggybackedwiththedextrose–aminoacid
solution.
Add500–1000unitsofheparinand5mgofhydrocortisoneperliter(todecreasephlebitis).
Place a fine-bore 22- or23-gaugepolyvinylpyrrolidone-coatedpolyurethanecatheterinas largea
veinaspossibleintheproximalforearmusingsteriletechnique.
Place a 5-mg glycerol trinitrateointmentpatch(or 0.25 inof 2% nitroglycerin ointment) over the
infusionsite.
Infusethesolutionwithavolumetricpump.
Keepthetotalinfusedvolume<3500mL/d.
Filterthesolutionwithaninline1.2-mfilter.
Long-TermHomeParenteralNutrition
Long-term home parenteral nutrition is usually given through a tunneled catheter or an implantable
subcutaneousportinsertedinthesubclavianvein.
Nutrientformulationscanbeinfusedovernighttopermitdaytimeactivitiesinpatientswhoareableto
toleratethe fluid load.IVlipids may notbe necessaryinpatientswhoare abletoingestandabsorb
adequateamountsoffat.
Appropriate patient selection for home TPN is crucial due to high complication rates ( 50% at 6
months).Riskfactorsforcomplicationsincludetheuseofanontunneledormultilumencatheter,useof
the catheter for blood draws, infusion of nonparenteral medications, use of lipid infusions,
anticoagulation,olderage,andopenwounds.
27
Complications
MechanicalComplications
Complications at time of line placement include pneumothorax, air embolism, arterial puncture,
hemothorax,andbrachialplexusinjury.
Thrombosis and pulmonary embolism: Radiologically evident subclavian vein thrombosis occurs
commonly;however,clinicalmanifestations(upperextremityedema,superiorvenacavasyndrome)are
rare. Fatal microvascular pulmonary emboli can be caused by nonvisible precipitate in parenteral
nutritionsolutions.Inlinefiltersshouldbeusedwithallsolutionstominimizetheriskofemboli.
MetabolicComplications
Fluidoverload.
Hypertriglyceridemia.
Hypercalcemia.
Specific nutrient deficiencies. Consider providing supplemental thiamine (100 mg for 3–5 days)
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duringinitiationofCPNinpatientsatriskofthiaminedeficiency(e.g.,alcoholism).
Hypoglycemia.
Hyperglycemia.Inmostpatients,abloodglucoseconcentrationof140–180mg/dLshouldbetargeted
duringTPNinfusion.Managementofpatientswithhyperglycemiaortype2diabetescanbeperformed
inseveralways:
Ifbloodglucoseis>200mg/dL,considerimprovingbloodglucosecontrolbeforestartingCPN.
IfCPNisstarted,(1)limitdextroseto<200g/d,(2)add0.1unitofregularinsulinforeachgramof
dextroseinCPNsolution(e.g.,15unitsfor150g),(3)discontinueothersourcesofIVdextrose,and
(4)orderroutine,regularinsulinwithbloodglucosemonitoringbyfingerstickevery4–6 hoursor
IVregularinsulininfusionwithbloodglucosemonitoringbyfingerstickevery1–2hours.
Inoutpatientswhouseinsulin,anestimateofthereductioninbloodsugarthatwillbecausedbythe
administrationof1unitofinsulinmaybecalculatedbydividing1500bythetotaldailyinsulindose
(e.g.,forapatientreceiving50unitsofinsulinasanoutpatient,1unitofinsulinmaybepredictedto
reduceplasmaglucoseconcentrationby1500/50=30mg/dL).
Ifbloodglucoseremains>200mg/dLandthepatienthasbeenrequiringSCinsulin,add50%ofthe
supplemental short-acting insulin given in the last 24 hours to the next day’s CPN solution and
doubletheamountofSCinsulinsliding-scaledoseforbloodglucosevalues>200mg/dL.
Theinsulin-to-dextroseratiointheCPNformulationshouldbemaintainedwhiletheCPNdextrose
contentischanged.
InfectiousComplications
Catheter-related sepsis is the mostcommon life-threatening complication inpatients receivingCPN.
The responsible microorganisms are most often skin flora: Staphylococcus epidermidis and
Staphylococcusaureus.
In immunocompromised patients and those receiving CPN for >2 weeks, Enterococcus, Candida
species, Escherichia coli, Pseudomonas, Klebsiella, Enterobacter, Acinetobacter, Proteus, and
Xanthomonasshouldbeconsidered.
Theprinciplesofevaluationandmanagementofsuspectedcatheter-relatedinfectionareoutlinedin
Chapter14,TreatmentofInfectiousDiseases.
Use ofsteriletechniqueduring connectionofTPN,avoiding access ofthe TPNlumen ofthecentral
catheterforotherpurposes,andensuringthatTPNisneverdisconnectedandrestartedcanreducethe
riskofinfection.Microorganismscanformbiofilmsontheintraluminalsurfaceofthecatheterandonce
attachedtheyaredifficulttoeliminate.InpatientsonhomeTPN,ethanollocktherapyhasbeenshown
tobeeffectiveinreducingtherateofcatheter-relatedinfection.
28
HepatobiliaryComplications
Althoughtheseabnormalitiesareusuallybenignandtransient,moreseriousandprogressivediseasemay
developinasubsetofpatients,usuallyafter16weeksofCPNtherapyorinthosewithshortbowel
syndrome.
Biochemical:Elevatedaminotransferasesandalkalinephosphatasearecommonlyseen.
Histologicalterations:Steatosis,steatohepatitis,lipidosis,phospholipidosis,cholestasis,fibrosis,and
cirrhosishaveallbeenseen.
BiliarycomplicationsaslistedbelowusuallyoccurinpatientswhoreceiveCPNfor>3weeks:
Acalculouscholecystitis
Gallbladdersludge
Cholelithiasis
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Strategies to prevent hepatobiliary complications in patients receiving long-term CPN include
providingaportion(20%–40%)ofcaloriesasfat,cyclingCPNsothattheglucoseinfusionisstopped
for at least 8–10 hours per day, encouraging enteral intake to stimulate gallbladder contraction and
maintainmucosalintegrity,andavoidingexcesscaloriesandhyperglycemia.
If biochemicalor otherevidenceofliverdamageoccurs,evaluationforothercausesofliverdisease
shouldensue.
If mild hepatobiliary complications develop, parenteral nutrition should not necessarily be
discontinued. Rather, the same principles used in preventing hepatic complications can be applied
therapeutically.
When cholestasis is present, copper and manganese should be removed from the CPN formula to
prevent accumulation in the liver and basal ganglia. A 4-week trial of metronidazole or
ursodeoxycholicacidcanbehelpfulinsomepatients.
MetabolicBoneDisease
MetabolicbonediseasehasbeenobservedinpatientsreceivingCPNfor>3months
Patients may be asymptomatic. Clinical manifestations include bone fractures and pain.
Demineralizationmaybeseenonradiologicstudies.Osteopenia,osteomalacia,orbothmaybepresent.
The precise causes of metabolic bone disease are not known, but several mechanisms have been
proposed,includingaluminumtoxicity,vitaminDtoxicity,andnegativecalciumbalance.
Severaltherapeuticoptionsshouldbeconsideredinpatientswhohaveevidenceofboneabnormalities.
Remove vitamin D from the CPN formulation if parathyroid hormone and 1,25-hydroxy vitamin D
levelsarelow.
Reduceproteinto<1.5g/kg/dasaminoacidscancausehypercalciuria.
Maintain normal magnesium status because magnesium is necessaryfor normal parathormone action
andrenalconservationofcalcium.
Provideoralcalciumsupplementsof1–2g/d.
Considerbisphosphonatetherapytodecreaseboneresorption.
SPECIALCONSIDERATIONS
Monitoringnutritionsupport
Adjustmentofthenutrientformulationisoftenneededasmedicaltherapyorclinicalstatuschanges.
Whennutritionsupportisinitiated,othersourcesofglucose(e.g.,peripheralIVdextroseinfusions)
shouldbestoppedandthevolumeofotherIVfluidsadjustedtoaccountforCPN.
Vitalsignsshouldbecheckedevery8hours.
Incertainpatients,bodyweight,fluidintake,andfluidoutputshouldbefolloweddaily.
Serumelectrolytes(includingphosphorus)shouldbemeasuredevery1–2daysafterCPNisstarted
untilthevaluesarestableandthenrecheckedweekly.
Serum glucose should be checked up to every 4–6 hours by finger stick until blood glucose
concentrationsarestableandthenrecheckedweekly.
Iflipidemulsionsarebeinggiven,serumtriglyceridesshouldbemeasuredduringlipidinfusionin
patients at risk for hypertriglyceridemia to demonstrate adequate clearance (triglyceride
concentrationsshouldbe<400mg/dL).
Carefulattentiontothecatheterandcathetersitecanhelptopreventcatheter-relatedinfections.
Gauze dressings should be changed every48–72 hours or whencontaminated or wet.Transparent
dressingscanbechangedweekly.
Tubingthatconnectstheparenteralsolutionswiththecathetershouldbechangedevery24hours.
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A0.22-μmfiltershouldbeinsertedbetweentheIVtubingandthecatheterwhenlipid-freeCPNis
infusedandshouldbechangedwiththetubing.
A1.2-μmfiltershouldbeusedwhenatotalnutrientadmixturecontainingalipidemulsionisinfused.
Whenasingle-lumencatheterisusedtodeliverCPN,thecathetershouldnotbeusedtoinfuseother
solutions/medications(apartfromcompatibleantibiotics)ortomonitorcentralvenouspressure.
Whenatriple-lumencatheterisused,thedistalportshouldbereservedsolelyfortheadministration
ofCPN.
RefeedingtheSeverelyMalnourishedPatient
Refeedingsyndromemayoccurafterinitiatingnutritionaltherapyinpatientswhoareseverely
malnourishedandhavehadminimalnutrientintake.
Hypophosphatemia, hypokalemia, and hypomagnesemia: Rapid and marked decreases in these
electrolytesoccurduring initialrefeedingbecauseofinsulin-stimulatedincreasesincellular mineral
uptakefromextracellularfluid.Forexample,plasmaphosphorusconcentrationcanfallbelow1mg/dL
and cause death within hours of initiating nutritional therapy if not adequately replaced. Suggested
replacementguidelinesarereviewedinseveralsources.
29-31
Fluid overload and congestive heart failure are associated with decreased cardiac function and
insulin-induced increases in sodium and water reabsorption in conjunction with nutritional therapy
containingwater,glucose,andsodium.Renalmassmaybereduced,limitingtheabilitytoexcretesalt
orwaterloads.
Cardiacarrhythmias:Patientswhoareseverelymalnourishedoftenhavebradycardia.Suddendeath
from ventricular tachyarrhythmias can occur during the first week of refeeding in severely
malnourished patients and may be associated with a prolonged QT interval and electrolyte
abnormalities.PatientswithECGchangesshouldbemonitoredontelemetry,possiblyinanICU.
Glucoseintolerance:Starvationcausesinsulinresistancesuch thatrefeedingwithhigh-carbohydrate
meals or large amounts of parenteral glucose can cause marked elevations in blood glucose
concentration,glycosuria,dehydration,andhyperosmolarcoma.Inaddition,carbohydraterefeedingin
patientswhoaredepletedinthiaminecanprecipitateWernickeencephalopathy.
ManagementofSevereMalnutrition
Carefulevaluation ofcardiovascularfunctionandplasmaelectrolytes(history,physical examination,
ECG,andbloodtests)andcorrectionofabnormalplasmaelectrolytesareimportantbeforeinitiation
offeeding.
Refeedingbytheoralorenteralrouteinvolvesfrequentorcontinuousadministrationofsmallamounts
offoodoranisotonicliquidformula.
Parenteral supplementation or completeparenteral nutrition may be necessaryif the intestinecannot
toleratefeeding.
During initial refeeding, fluid intake should be limited to approximately 800 mL/d plus insensible
losses. Adjustments in fluid and sodium intake are needed in patients who have evidence of fluid
overloadordehydration.
Changes in body weight provide a useful guide for evaluating the efficacy of fluid administration.
Weight gain >0.25 kg/d or 1.5 kg/wk probably represents fluid accumulation in excess of tissue
repletion.Initially,approximately15kcal/kg(containingapproximately100gcarbohydrateand1.5g
proteinperkilogramofactualbodyweight)shouldbegivendaily.
Therateatwhichcaloricintakecanbeincreaseddependsontheseverityofmalnutritionandtolerance
tofeeding.Ingeneral,increasingby2–4kcal/kgevery24–48hoursisappropriate.
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Sodiumshouldberestrictedtoapproximately50mEq/m2bodysurfacearea/day,butliberalamountsof
phosphorus,potassium,andmagnesiumshouldbegiventopatientswithnormalrenalfunction.
Allothernutrientsshouldbegiveninamountsneededtomeettherecommendeddietaryintake(Table
2-7).
TABLE2-7
MAJORMINERALDAILYREQUIREMENTS,DEFICIENCY,TOXICITY,ANDDIAGNOSTIC
EVALUATION
Mineral Recommended
DailyEnteral
Intake/Parenteral
Intake
33
Signsand
Symptomsof
Deficiency
Signsand
Symptomsof
Toxicity
Diagnostic
Evaluation
Sodium 1.2–1.5ga/1–
2mEq/kg
Encephalopathy,
seizure,weakness,
dehydration,
cerebraledema
31
Encephalopathy,
seizure
Sodium
p
(correctfor
hyperglycemia)
Sodiumu(will
oftenonly
providea
roughestimate
[i.e.,toolow,
toohigh])
Potassium 4700mg(47)a/1–
2mEq/kg
Abdominal
cramping,diarrhea,
paresthesias,QT
prolongation,
weakness
QRSwidening,QT
shortening(sinewave
morphologyinextreme
cases),peakedT
waves
Potassium
w,b
Calcium 1000–
1200mg/10–
15mEq
QRSwidening,
paresthesias
(Trousseausign),
tetany(Chvostek
sign),osteomalacia
Encephalopathy,
headache,abdominal
pain,nephrolithiasis,
metastaticcalcification
Calcium
w,b
,24-
hcalcium
u
(correctfor
albumins)
Magnesium 420mg/8–
20mEq
Tachyarrhythmia,
weakness,muscle
cramping,peripheral
andcentralnervous
system
overstimulation
(seizure,tetany)
Hyporeflexia,nausea,
vomiting,weakness,
encephalopathy,
decreasedrespiratory
drive,hypocalcemia,
hyperkalemia,heart
block
Magnesiums,
magnesium
u
Phosphorus 700mg/20–
40mmol
Weakness,fatigue,
increasedcell
membranefragility
(hemolyticanemias,
Metastatic
calcification,theoretic
higherriskof
nephrolithiasis,
Phosphorus
p
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leukocyte+platelet
dysfunction),
encephalopathy
secondary
hyperparathyroidism
Subscript:b,blood;p,plasma;s,serum;u,urine;w,wholeblood.
a
Note:Adequatedailyintake.
Body weight,fluid intake,urine output, plasmaglucose, andelectrolytevalues should be monitored
dailyduringearlyrefeeding(first3–7days)sothatnutritionaltherapycanbe appropriatelymodified
whennecessary.
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