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Hyperphosphatemiaiscausedbyoneofthefollowing:
Transcellular shift occurs in rhabdomyolysis, tumor lysis syndrome, and massive hemolysis as
phosphorus is released from cells into the ECF. Metabolic acidosis and hypoinsulinemia reduce
phosphorusfluxintocellsandcontributetothehyperphosphatemiasometimesseeninDKA.
Increasedintakeleading tohyperphosphatemiausuallyoccursinthesettingofrenalinsufficiency,
eitherwithdietaryindiscretioninchronickidneydiseaseorasaniatrogeniccomplication.Thelatter
can be seen when Phospho-Soda enemas (e.g., Fleet) or active vitamin D analogs are given to
patientswithrenalinsufficiency.
Decreased renal excretion occurs most commonly in the setting of renal failure. Occasionally,
hypoparathyroidismandpseudohypoparathyroidismreducerenalphosphorusclearanceaswell.
DIAGNOSIS
ClinicalPresentation
Signsandsymptomsaretypicallyattributabletohypocalcemiaandthemetastaticcalcificationofsoft
tissues.Occasionally,skindepositioncanresultinseverepruritus.Calciphylaxisdescribesthetissue
ischemia that may result from the calcification of smaller blood vessels and their subsequent
thrombosis.
Chronic hyperphosphatemia contributes to the development of renal mineral/bone disorders such as
secondaryhyperparathyroidism(seeChapter13,RenalDiseases).
DiagnosticTesting
Theelevatedserumphosphoruscanbeaccompaniedbyhypocalcemiaasaresultofintravascular
chelationofcalciumbyphosphorus.
TREATMENT
Acute hyperphosphatemia is treated by increasing renal excretion of phosphorus, and as such,
treatmentislimitedwhenrenalinsufficiencyispresent.
Recoveryofrenalfunctionwilloftencorrectthehyperphosphatemiainthepatientwithin12hours.
Saline and/or acetazolamide (15 mg/kg q4h) can be given to further encourage phosphaturia, if
needed.
Hemodialysis may be required, especially if irreversible renal insufficiency or symptomatic
hypocalcemiaispresent.
Chronichyperphosphatemiaisalmostalwaysassociatedwithchronickidneydisease.Itsmanagement
consistsofreducingphosphorusintakethroughdietarymodificationandtheuseofphosphatebinders.
ThisisdiscussedmorefullyinChapter13,RenalDiseases.
Hypophosphatemia
GENERALPRINCIPLES
Aserumphosphate<2.8mg/dLdefineshypophosphatemia.
Hypophosphatemiamaybecausedbyoneofthefollowing:
Impairedintestinalabsorptionoccurswiththemalabsorptionsyndromes,theuseoforalphosphate
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binders,orvitaminDdeficiencyfromanycause.Chronicalcoholismisoftenassociatedwithpoor
intakeofbothphosphateandvitaminDresultingintotalbodyphosphorusdepletion.
Increased renal excretion occurs with high levels of PTH, as seen in hyperparathyroidism.
Hypophosphatemia may also occur from osmotic diuresis and disorders of proximal tubular
transportsuchas familial X-linkedhypophosphatemic ricketsandFanconi syndrome.In acutely ill
patients oncontinuous renalreplacementtherapy, the removal ofphosphorousbyslow continuous
dialysiscanalsoresultinhypophosphatemia.
Transcellularshiftisstimulatedbyrespiratoryalkalosisaswellasinsulin.Thelatterisresponsible
fortheparadoxicalreductioninphosphorusduringtreatmentofmalnutritionwithhyperalimentation
(the refeedingsyndrome). Theendogenous increase ininsulin during treatmentshifts phosphorus
intracellularly, further reducingserum phosphorusinthemalnourishedindividual. Phosphoruscan
also be rapidly absorbed into bone following parathyroidectomy for severe hyperparathyroidism
(hungrybonesyndrome).
DIAGNOSIS
ClinicalPresentation
Signsandsymptomstypicallyoccuronlyiftotalbodyphosphatedepletionissevere.Manifestations
includemuscleinjury(rhabdomyolysis,impaireddiaphragmaticfunction,andheartfailure),neurologic
abnormalities(paresthesias,dysarthria,confusion,stupor,seizures,andcoma),andrarely,hemolysisand
plateletdysfunction.
DiagnosticTesting
Thecauseisusuallyapparentfromtheclinicalsituationinwhichthehypophosphatemiaoccurs.Ifnot,
measurementofurinephosphorusexcretionhelpsdefinethemechanism.Renalexcretionof>100mg
by 24-hour urine collection or a fractional excretion of phosphate >5% during hypophosphatemia
indicatesexcessiverenalloss.
Low serum 25(OH)D3 suggests dietary vitamin D deficiency or malabsorption. An elevated intact
PTHmayoccurinprimaryorsecondaryhyperparathyroidism.
TREATMENT
Acute moderate hypophosphatemia (1.0–2.5 mg/dL) is common in the hospitalized patient and is
oftenduesimplytotranscellularshifts, requiring notreatmentifasymptomatic, exceptcorrectionof
theunderlyingcause.
Acute severe hypophosphatemia(<1.0 mg/dL) may require IV phosphate therapy when associated
with serious clinical manifestations. IV preparations include potassium phosphate (1.5 mEq
potassium/mmol phosphate)andsodiumphosphate (1.3 mEqsodium/mmolphosphate). Extreme care
mustbe takento avoid hyperphosphatemia, which maylead to hypocalcemia. If hypotensionoccurs,
acutehypocalcemiashouldbesuspected,andtheinfusionshouldbestoppedorslowed.Furtherdoses
should be based on symptoms and on the serum calcium and phosphorus levels, which should be
measuredevery8hours.
Chronic hypophosphatemia.VitaminDdeficiency,ifpresent,shouldbe treatedfirst(see “Calcium,
Hypocalcemia, Treatment” section) followed by oral supplementation of 0.5–1.0 g elemental
phosphorusPObidtotid.PreparationsincludeNeutra-Phos(250mgelementalphosphorusand7mEq
ofNa+andK+per capsule) andNeutra-PhosK+ (250 mgelemental phosphorus and14 mEq K+ per
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capsule). Contents of the capsules should be dissolved in water. Fleet Phospho-Soda (815 mg
phosphorusand33 mEqsodium per5 mL) isanalternativeoral agent. Limiting side effectsinclude
nauseaanddiarrhea.
Magnesium
Magnesiumplaysanimportantroleinneuromuscularfunction.
Approximately60%ofbodymagnesiumisstoredinbone,andmostoftheremainderisfoundincells.
Only1%isintheECF.Asaresult,theserummagnesiumisapoorpredictorofintracellularandtotal
bodystoresandmaygrosslyunderestimatetotalmagnesiumdeficits.
The main determinantof magnesium balanceis the magnesium concentration itself, whichdirectly
influences renal excretion. Hypomagnesemia stimulates tubular reabsorption ofmagnesium, whereas
hypermagnesemiainhibitsit.
Hypermagnesemia
GENERALPRINCIPLES
Aserummagnesium>2.2mEq/Ldefineshypermagnesemia.
Most cases of clinicallysignificant hypermagnesemia are iatrogenic, occurring with large doses of
magnesium-containingantacidsorlaxativesandduringtreatmentofpreeclampsiawithIVmagnesium.
Because renal excretion is the only means of lowering serum magnesium levels, the presence of
significant renal insufficiency can lead to magnesium toxicity even with therapeutic doses of these
antacidsandlaxatives.
Mild,insignificantelevationsinmagnesiumcanoccurinend-stagerenaldiseasepatients,theophylline
intoxication,DKA,andtumorlysissyndrome.
DIAGNOSIS
ClinicalPresentation
Signsandsymptomsareusuallyseenwhentheserummagnesiumlevelis>4mEq/L.
Neuromuscular abnormalities usually include hyporeflexia (usually the first sign of magnesium
toxicity),lethargy,andweaknessthatcanprogresstoparalysisanddiaphragmaticinvolvement,leading
torespiratoryfailure.
Cardiacfindingsincludehypotension,bradycardia,andcardiacarrest.
DiagnosticTesting
TheECGmayrevealbradycardiaandprolongedPR,QRS,andQTintervalswithmagnesiumlevelsof
5–10mEq/L.Completeheartblockorasystolemayeventuallyensuewithlevels>15mEq/L.
TREATMENT
Prevention. In the setting of significant renal insufficiency, the inadvertent administration of
magnesium-containingmedications(e.g.,Maalox,magnesiumcitrate)shouldbeavoided.
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Asymptomatichypermagnesemia. Inthesetting ofnormal renal function,normal magnesium levels
willquicklybeattainedwithremovalofthemagnesiumload.
Symptomatichypermagnesemia
Promptsupportivetherapyiscritical,includingmechanicalventilationforrespiratoryfailureanda
temporarypacemakerforsignificantbradyarrhythmias.
Theeffectsofhypermagnesemia canbe antagonizedquickly bytheadministrationof10% calcium
gluconate10–20mLIV(1–2g)over10minutes.
Renal excretioncanbe encouragedwithsalineadministration.With significantrenal insufficiency,
hemodialysisisrequiredfordefinitivetherapy.
Hypomagnesemia
GENERALPRINCIPLES
Aserummagnesium<1.3mEq/Ldefineshypomagnesemia.
Hypomagnesemia is most commonly caused by impaired intestinal absorption and increased renal
excretion.
Decreasedintestinal absorption occurs in malnutrition (chronic alcoholics or anymalabsorption
syndrome),GIloss(prolongeddiarrheaandnasogastricaspiration),andchronicuseofprotonpump
inhibitors,presumablyduetoimpairedintestinalabsorption.
Increasedrenal excretion of magnesium canoccur from increased renal tubular flow (as occurs
with osmotic diuresis) as well as impaired tubular function(as seenwith resolving acutetubular
necrosis,loopdiuretics,andBartterandGitelmansyndromes).
Drugs. Several medications similarly induce defects in tubular magnesium transport including
aminoglycosides,amphotericinB,cisplatin,pentamidine,andcyclosporine.
DIAGNOSIS
ClinicalPresentation
Neurologicmanifestationsincludelethargy,confusion,tremor,fasciculations,ataxia,nystagmus,tetany,
andseizures.
Atrialandventriculararrhythmiasmayoccur,especiallyinpatientstreatedwithdigoxin.
DiagnosticTesting
Low serum [Mg2+] inconjunction withan appropriateclinical scenario is sufficient to establish the
diagnosisofmagnesium deficiency. However,becauseoftheslow exchangeofmagnesiumbetween
the bone and intracellular pools, a normal serum level does not exclude total body magnesium
deficiency.
Theetiologyofhypomagnesemiausuallyisevidentfromtheclinicalcontext,butifthereisuncertainty,
measurementofurinemagnesiumexcretionishelpful.A24-hoururinemagnesiumof>2mEq(or>24
mg)orafractionalexcretionofmagnesiumof>2%duringhypomagnesemiasuggestsincreasedrenal
excretion.Thefractionalexcretionofmagnesiumiscalculatedby:
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Hypocalcemia and/or hypokalemia can often be found as a result of hypomagnesemia-induced
derangementsinmineralhomeostasis.
ECGabnormalitiesmayincludeaprolongedPRandQTintervalwithawidenedQRS.Torsades de
pointesistheclassicallyassociatedarrhythmia.
TREATMENT
Inpatientswithnormalrenalfunction,excessmagnesiumisreadilyexcreted,andthereislittleriskof
causing hypermagnesemia with recommended doses. However, magnesium must be given with
extremecareinthepresenceofrenalinsufficiency.
The route of magnesium administration depends on whether clinical manifestations from magnesium
deficiencyarepresent.
Asymptomatic hypomagnesemia can be treated orally. Numerous preparations exist, including
Mag-Ox400(240mgelementalmagnesiumper400-mgtablet),UroMag(84mgper140-mgtablet),
andsustained-releaseSlow-Mag(64mgpertablet).Typically,approximately240mgofelemental
magnesium is administered daily for mild deficiency, whereas more severe hypomagnesemia may
requireupto720mg/dofelementalmagnesium.Themajorsideeffectisdiarrhea.
Severe symptomatic hypomagnesemia should be treated with 1–2 g magnesium sulfate (1 g
magnesium sulfate = 96 mg elemental magnesium) IV over 15 minutes. To account for gradual
redistribution to severely depleted intracellular stores, replacement therapy may need to be
maintained,often for 3–7 days.Serum magnesiumshould be measureddailyand theinfusionrate
adjusted to maintain a serum magnesium level of <2.5 mEq/L. Tendon reflexes should be tested
frequently because hyporeflexia suggests hypermagnesemia. Reduced doses and more frequent
monitoringmustbeusedeveninmildrenalinsufficiency.
Acid–BaseDisturbances
GeneralPrinciples
ThenormalECFpHis7.40±0.03.PerturbationsinpHcanoccurwithchangesintheratioof to
partialpressureofcarbondioxide(pCO2)asdescribedbytheHenderson–Hasselbalchequation:
MaintenanceofpHisessentialfornormalcellularfunction.Threegeneralmechanismsexisttokeepit
withinanarrowwindow:
Chemical bufferingis mediatedby inthe ECFand byproteinandphosphatebuffers inthe
ICF.Thenormal is24±2mEq/L.
AlveolarventilationminimizesvariationsinthepHbyalteringthepCO2.ThenormalpCO2is40±
5mmHg.
RenalH+handlingallowsthekidneytoadapttochangesinacid–basestatusvia reabsorption
andexcretionoftitratableacid(e.g., )and .
Acidemia and alkalemia refertoprocesses thatlower andraise pHregardless ofmechanism. They
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canbecausedbymetabolicorrespiratorydisturbances:
Metabolicacidosisischaracterizedbyadecreaseintheplasma duetoeither lossorthe
accumulationofacid.
Metabolicalkalosis ischaracterizedbyanelevationintheplasma duetoeitherH+ loss or
gain.
Respiratory acidosis is characterized by an elevation in pCO2 resulting from alveolar
hypoventilation.
RespiratoryalkalosisischaracterizedbyadecreaseinpCO2resultingfromhyperventilation.
Diagnosis
Analysisshouldbesystematicsothataccurateconclusionsaredrawnandappropriatetherapyinitiated.
Oncetheacid–baseprocessiscorrectlyidentified,furtherdiagnosticstudiesmaybeundertakento
determinethepreciseetiologiesatplay.
Step1. Check arterial blood gas. Acidemia is present when pH is <7.37 and alkalemia when pH
>7.43.
Step2. Establishthe primarydisturbance by determining whetherthe change in or pCO2 can
accountfortheobserveddeflectioninpH.
In acidemia, a decreased suggests metabolic acidosis, and an elevated pCO2 suggests
respiratory acidosis. In alkalemia, an elevated suggests metabolic alkalosis, whereas a
decreasedpCO2suggestsrespiratoryalkalosis.
A combineddisorderis present when pH is normal, but the pCO2 and are both abnormal.
ChangesinbothpCO2and cancausethechangeinpH.
Step3.Determinewhethercompensationisappropriate.
Thecompensatorymechanism is anadaptationtothe primaryacid–base disturbance intended to
stabilize the changing pH. A respiratory process that shifts the pH in one direction will be
compensatedbyametabolicprocessthatshiftsthepHintheotherandviceversa.
Theeffectofcompensationistoattenuate,butnotcompletelycorrect,theprimarychangeinpH.
Theexpectedcompensationsforthevariousprimaryacid–basederangementsaregiveninTable12-
2.
Aninappropriatecompensatoryresponsesuggeststhepresenceofacombineddisorder.
Example: In a patient with metabolic acidosis, respiratory compensation attenuates the metabolic
disturbance to pH by lowering pCO2. However, if the pCO2 is higher than expected, respiratory
compensationisinsufficient,revealingarespiratoryacidosiswiththeprimarymetabolicacidosis.If
pCO2 is lower than expected, compensation is excessive, revealing a concomitant respiratory
alkalosis.
TABLE12-2
EXPECTEDCOMPENSATORYRESPONSESTOPRIMARYACID–BASEDISORDERS
Disorder Primary
Change
CompensatoryResponse
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Metabolic
acidosis
↓[HCO32] ↓pCO21.2mmHgforevery1mEq/L↓[HCO32]OR
pCO2=lasttwodigitsofpH
Metabolic
alkalosis
↑[HCO32] ↑pCO20.7mmHgforevery1mEq/L↑[HCO32]
Respiratory
acidosis
↑pCO
2
–
Acute – ↑[HCO32]1.0mEq/Lforevery10mmHg↑pCO
2
Chronic – ↑[HCO32]3.5mEq/Lforevery10mmHg↑pCO
2
Respiratory
alkalosis
↓pCO
2
–
Acute – ↓[HCO32]2.0mEq/Lforevery10mmHg↓pCO
2
Chronic – ↓[HCO32]5.0mEq/Lforevery10mmHg↓pCO
2
Step4.Determinetheaniongap(AG).
Innormalindividuals,thetotalserumcationsarebalancedwiththetotalserumanions.Totalcations
comprisemeasuredcations(MCs)andunmeasuredcations,whereastotalanionscomprisemeasured
anions (MAs) and unmeasured anions (UAs). Certain forms of acidosis are characterized by an
increaseinthepoolofUAs.TheAGismerelyawayofdemonstratingtheaccumulationofthisUA.
> .ThenormalAGis10±2mEq/L.
Becausetotalcations=totalanions:
Rearrangingtheequation:
MCsareNa+;MAsareCl−and .
BecausealbuministheprincipalUA,theAGshouldbecorrectediftherearegrosschangesinserum
albuminlevels.
AnelevatedAGsuggeststhepresenceofmetabolicacidosiswithacirculatinganion(Table12-3).
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TABLE12-3
THEFOURPRIMARYACID–BASEDISORDERSANDTHEIRCOMMONETIOLOGIES
Acidosis Alkalosis
Metabolic Gap
Ketoacids(starvation,alcoholic,diabetic)
Exposures (methanol, ethylene glycol,
salicylates)
Lacticacid(shock,drugrelated)
Profounduremia
Generation
Loss of H+-rich fluids (GI
loss)
Contractionalkalosis
Alkaliadministration
Nongap
Nonrenal loss(diarrhea)
RenalHCO32loss(type2RTA)
↓Hsecretion(type1RTA)
Hypoaldosteronism(type4RTA)
Maintenance
Volumecontraction
Chloridedepletion
Hypokalemia
Type1
RTA
Type2
RTA
Type4
RTA
Serum[K] ↓ornl ↓ornl ↑
Serum
[HCO3]
<10 15–20 >15
UrinepH >5.3 Varies <5.3
Respiratory Depressionofrespiratorycenter
Neuromuscularfailure
Lungdisease
CNSstimulation
Hypoxemia
Anxiety
CNS,centralnervoussystem;GI,gastrointestinal;nl,normal;RTA,renaltubularacidosis.
Step5.Assessthedeltagap.
Tomaintainastabletotalanion content,everyincreaseinanUAshouldbemetwithadecrease in
.ComparingthechangeintheAG(ΔAG)withthechangeinthe isasimpleway
ofmakingsurethateachchangeintheAGisaccountedfor.
IftheΔAG=Δ ,thisisasimpleAGmetabolicacidosis.
IftheΔAG>Δ ,the didnotdecreaseasmuchasexpected.Thisisametabolicalkalosis
andAGmetabolicacidosis.Example:ApatientwithDKAhasbeenvomitingbeforeadmission.He
hasanAGof20andan of20. His ΔAG=10andΔ = 4, revealinganAGmetabolic
acidosis(DKA)withametabolicalkalosis(vomiting).
IftheΔAG<Δ ,the decreasedmorethanexpected.Thisisanongapmetabolicacidosis
and AG metabolic acidosis. Example: A patientis admitted withfevers andhypotension after a
prolongedcourseofdiarrhea.ShehasanAGof15 andan of12.HerΔAGis5andherΔ
is12,revealinganongapmetabolicacidosis(diarrhea)andanAGmetabolicacidosis(lactic
acidosis).
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MetabolicAcidosis
GENERALPRINCIPLES
ThecausesofametabolicacidosiscanbedividedintothosethatcauseanelevatedAGandthosewith
anormalAG.ManyofthecausesseeninclinicalpracticecanbefoundinTable12-3.
AGacidosisresultsfromexposuretoacids,whichcontributeanUAtotheECF.Commoncausesare
DKA,lacticacidosis,andtoxicalcoholingestions.
Non-AG acidosis can result from the loss of from the GI tract. Renal causes due to renal
excretionof ordisordersofrenalacidhandlingarereferredtocollectivelyasRTAs.
Enteric lossoccursmostcommonlyinthesettingofseverediarrhea.
The three forms of RTA correlate with the three mechanisms that facilitate renal acid handling:
proximalbicarbonate reabsorption,distal H+ secretion,andgeneration ofNH3, theprinciple urinary
buffer.UrinarybuffersreducetheconcentrationoffreeH+inthefiltrate,thusattenuatingthebackleak
ofH+,whichoccursatlowurinarypH.
Proximal(type2)RTAiscausedbyimpairedproximaltubular reabsorption.Causesinclude
inherited mutations (cystinosis), heavy metals, drugs (tenofovir, ifosfamide, carbonic anhydrase
inhibitors),andmultiplemyelomaandothermonoclonalgammopathies.
Distal (type 1) RTA results from impaired distal H+ secretion. This may occur because of
impairment in H+ secretion, as seen with a variety of autoimmune (Sjögren syndrome, lupus,
rheumatoid arthritis) or renal disorders. Hypercalciuria is another main cause of distal RTA in
adults.ItcanalsobecausedbyabackleakofH+duetoincreasedmembranepermeability,asseen
withamphotericinB.
Distal hyperkalemic (type 4) RTA may result from either low aldosterone levels or from
aldosteroneresistance.TheresultinghyperkalemiareducestheavailabilityofNH3tobufferurinary
H+. Hyporeninemic hypoaldosteronism is seen with some frequency in patients with diabetes.
Certaindrugs,includingNSAIDs,β-blockers,andcyclosporine,havealsobeenimplicated.
DIAGNOSIS
ThefirststepinnarrowingthedifferentialdiagnosisforametabolicacidosisistocalculatetheAG.
ThespecificcauseofanelevatedAGcanusuallybedeterminedbyclinicalhistory.However,specific
laboratorystudiesareavailabletoidentifycertainanionssuchaslactate,acetoacetate,acetone,andβhydroxybutyrate.(Itshouldbenotedthattheuseofnitroprussidetodetectketonesmayfailtoidentify
ketoacidosisduetoβ-hydroxybutyrate.)Thepresenceofanalcohol(methanol,ethanol,ethyleneglycol)
can also be determined with laboratory assays. Clinical suspicion for toxic alcohol ingestion is
corroboratedbyanincreasedosmolalgap.Thisgapisthedifferencebetweenmeasuredandcalculated
serumosmolality:
IfanormalAGispresent,theGI lossescanbedifferentiatedfromRTAsviatheurineaniongap
(UAG).TheUAGisthedifferencebetweenthemajormeasuredanionsandcationsinurine:[Na+]u+
[K+]u−[Cl−]u.Because isthemajorunmeasuredurinarycation,anegativeUAGreflectshigh
excretion,anappropriateresponsetoametabolicacidosis.Conversely,apositiveUAGsignifieslow
excretion,whichinthefaceofametabolicacidosissuggestsadefectindistalrenalacidification.
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Serum[K+]andurinepHcanbehelpfulindistinguishingbetweentheRTAs.
Types 1 and 2 are typically associated with hypokalemia, whereas type 4 is characterized by
hyperkalemia.
UrinepH is low (usually <5.3) intype4 RTA because the defect is inthegeneration ofthe NH
3
buffer,andthemechanismforH+secretionisintact.Incontrast,urinepHisinappropriatelyhighin
type1RTA(urinepH>5.3).Intype2RTA,theurinepHisvariable.Itiselevatedduringtheinitial
bicarbonaturia,whenfilteredbicarbonateexceedsthethresholdforreabsorption,andlowwhenthe
filteredloadisbelowthisthreshold.
TREATMENT
Ketoacidosis attributable to ethanol abuse and starvation can be corrected with the resumption of
caloric intake through oral intake or dextrose-containing fluids and by correction of any volume
depletionthatmaybepresent.ThetreatmentofDKAisdescribedinChapter23,DiabetesMellitusand
RelatedDisorders.
Lactic acidosis will resolve once the underlying cause is treated and tissue perfusion is restored.
Often, this involves aggressive therapeutic maneuvers for the treatment of shock as described in
Chapter8, Critical Care.Theadministrationofalkali doesnot appear tohaveclear benefitinlactic
acidosisandmayleadtoreboundmetabolicalkalosisoncetheunderlyingcauseismanaged.Itsusein
direcircumstancesorsevereacidosisremainscontroversial.
ManagementoftoxicingestionsisdescribedinChapter28,Toxicology.
NormalAGmetabolicacidosis.TreatmentwithNaHCO3isappropriateforpatientswithanormalAG
metabolicacidosis.The deficitcanbecalculatedinmEq:
However,thisassumesavolumeofdistributionequalto50%oftotalbodyweight.Inreality,the
distributionof increaseswiththeseverityoftheacidosisandmayexceed100%oftotalbodyweight
inverysevereacidosis.Itshouldbenotedthatthestandard650-mgtabletoforalNaHCO3providesonly
7mEqof ,whereasoneampuleofIVNaHCO3contains50mEq.Still,parenteralNaHCO3should
alwaysbeprescribedwithcautionbecauseofthepotentialadverseeffects,includingpulmonaryedema,
hypokalemia,andhypocalcemia.
TreatmentoftheRTAs.Correctionofthechronicacidemiawithalkaliadministrationiswarrantedto
preventitscataboliceffectonboneandmuscle.
Indistal(type1) RTA,correctionofthemetabolic acidosisrequires oral replacementonthe
order of 1–2 mEq/kg/d with NaHCO3 or sodium citrate. Potassium citrate replacement may be
necessaryforpatientswithhypokalemia,nephrolithiasis,ornephrocalcinosis.Underlyingconditions
shouldbesoughtandtreated.
Inproximal(type2)RTA,muchlargeramountsofalkali(10–15mEq/kg/d)arerequiredtoreverse
theacidosis.Administrationofpotassiumsaltsminimizesthedegreeofhypokalemiaassociatedwith
alkalitherapy.
Management of type 4 RTA requires correction of the underlying hyperkalemia. This consists of
dietaryK+ restriction (40–60 mEq/d) and possibly a loop diuretic withor withoutoral NaHCO
3
(0.5–1mEq/kg/d).Mineralocorticoidadministration(fludrocortisone,50–200 μgPOdaily)should
be used in patients with primary adrenal insufficiency and may be considered in other causes of
hypoaldosteronism.
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