Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2804_Библиотеки_им_академика_М_И_Перельмана
.pdf
12
FluidandElectrolyteManagement
MaryamSaleem,StevenCheng
FluidManagementandPerturbationsinVolumeStatus
Totalbodywater(TBW):Watercomprisesapproximately60%ofleanbodyweightinmenand50%
inwomen.Two-thirdsofTBWisintracellularfluid(ICF)andone-thirdisextracellularfluid(ECF).
ECFisfurthersubdividedintointravascularandinterstitialspacesinaratioof1:4.
Example:Forahealthy70-kgman:
ICF=2/3TBW=0.66×42=28L
ECF=1/3TBW=0.33×42=14L
Intravascularcompartment=0.25×14=3.5L
Interstitialcompartment=0.75×14=10.5L
Thedistributionofwaterbetweenintravascularandinterstitialspacescanbeaffectedbychangesto
theStarlingbalanceofforces.Lowoncoticpressure(i.e.,lowalbuminstates)andhighhydrostatic
pressure (i.e., Na+-retentive states) increase the movement of fluid from vascular to interstitial
compartments,whichisanimportantstepinthedevelopmentofedema.
TotalbodyNa+:85%–90%oftotalbodyNa+isextracellularandconstitutesthepredominatesolutein
theECF.Changestothebody’stotalNa+content typicallyresultsfromalossorgainofthisNa+-rich
fluid,leadingtocontractionorexpansionoftheECFspace.
TheEuvolemicPatient
Inaeuvolemicpatient,thegoaloffluidandelectrolyteadministrationistomaintainhomeostasis.The
bestwaytoaccomplishthisistoallowfreeaccesstofoodandoralfluids.Patientswhoareunableto
tolerate oral intake require maintenancefluids to replace renal, gastrointestinal (GI), andinsensible
fluidlosses.
ThedecisiontoprovidemaintenanceIV fluidshouldbethoughtfullyconsideredandnot administered
byroute.Fluidadministrationshouldbereassessedatleastdaily.Patientweight,whichmayindicate
netfluidbalance,shouldbemonitoredcarefully.
Table 12-1 provides a list of common IV solutions and their contents. By combining the necessary
components,onecanderiveanappropriatemaintenancefluidregimentailoredforeachpatient.
TABLE12-1
https://t.me/med1917
COMMONLYUSEDPARENTERALSOLUTIONS
IVSolution Osmolality
(mOsm/L)
[Glucose]
(g/L)
[Na+]
(mEq/L)
[Cl−]
(mEq/L)
Equivalents
(mEq/L)
D5W 278 50 0 0 0
0.45%NaCl
a
154 –
b
77 77 0
0.9%NaCl
a
308 –
b
154 154 0
3%NaCl 1026 – 513 513 0
Lactated
Ringer’s
c
274 –
b
130 109 28
a
NaCl0.45%and0.9%arehalf-normalandnormalsaline,respectively.
b
Alsoavailablewith5%dextrose.
c
Alsocontains4mEq/LK+,1.5mEq/LCa2+,and28mEq/Llactate.
D5W,5%dextroseinwater.
TheHypovolemicPatient
GENERALPRINCIPLES
VolumedepletiongenerallyresultsfromadeficitintotalbodyNa+content.RenalcausesofNa+loss
includediuresis,salt-wastingnephropathies,andmineralocorticoiddeficiency.Extrarenalcauses
includelossesfromtheGIandrespiratorytracts,hemorrhage,andseverethirdspacingoffluidin
criticallyillpatients.
DIAGNOSIS
ClinicalPresentation
Milddegreesofvolumedepletionareoftennotclinicallydetectable,whereaslargerfluidlossescanlead
tofatigue,musclecramps,andposturaldizziness.Severevolumedepletioncanresultinmentalstatus
changes,oliguria,andhypovolemicshock.
DiagnosticTesting
Thefollowinglaboratorystudiesareconsistentwithvolumedepletionbutarenotrequiredforthe
diagnosis:
UrineNa+<15mEq.
Fractionalexcretion ofsodium(FeNa) <1%. FeNa canbe calculatedas ([Urine Na+×Serum Cr] ÷
[UrineCr×SerumNa+])×100.
Elevatedurineosmolalityandserumbicarbonatelevelscanoftenbeseen.
Hematocritandserumalbuminmaybeincreasedfromhemoconcentration.
TREATMENT
https://t.me/med1917
Because it is difficult to estimate volume deficits, therapy is largely empiric, requiring frequent
reassessmentsofvolumestatuswhileresuscitationisunderway.
Mild volume contraction can usually be corrected via the oral route. However, the presence of
hemodynamic instability, symptomatic fluid loss, or intolerance to oral administration requires IV
therapy.
Theprimarytherapeuticgoalistoprotecthemodynamicstabilityandreplenishintravascularvolume
with fluid that will expand the ECF compartment. Na+-based solutions are ideal for volume
resuscitationsincetheNaisretainedintheECF.
Intravenousfluidcanbeadministeredas bolusesforpatientswith poorcardiacreserveorsignificant
edema.Oncethepatientisstable,fluidscanbeadministeredatamaintenanceratetoreplaceongoing
losses. In patients withhemorrhage or GI bleeding, blood transfusion can accomplishboth volume
expansionandconcomitantcorrectionofanemia.
TheHypervolemicPatient
HypervolemiareflectsasurplusoftotalbodyNa+resultinginexpansionoftheECFcompartments.Itcan
becausedbyexcessretentionorreabsorptionofNa+.Itisafrequentfindinginconditionswithimpaired
circulatingvolume,suchasheartfailureandcirrhosis.
DIAGNOSIS
ClinicalPresentation
Expansion of the interstitial compartment may result in peripheral edema, ascites, and pleural
effusions.
Expansionoftheintravascularcompartmentmayresultinpulmonaryrales,elevatedjugularvenous
pressure,hepatojugularreflux,anS3gallop,andelevatedbloodpressures.
Becauseovertsignsofhypervolemiamaynotmanifestuntil3–4Loffluidretention,agradualrisein
waterweightisoftentheearliestindicationofNa+retention.
DiagnosticTesting
Laboratory studies are generally not needed as hypervolemia is primarily a bedside diagnosis.
However,thefollowingfindingscanbeseenintheappropriateclinicalcontexts:
Brainnatriureticpeptidemaybeelevatedinpatientswithheartfailure.
Urine[Na+]maybelow(<15mEq/L)inpatientswithreducedeffectivecirculatingvolume.
ACXRmayshowpulmonaryedemaorpleuraleffusions,butclearlungfieldsdonotexcludevolume
overload.
TREATMENT
TreatmentmustaddressnotonlytheECFvolumeexcessbutalsotheunderlyingpathologicprocess.
AlleviatingtheNa+excesscanbeaccomplishedbythejudicioususeofdiureticsandbylimitingNa
+
intake.
Medications
https://t.me/med1917
DiureticsenhancetherenalexcretionofNa+byblockingthevarioussitesofNa+reabsorptionalongthe
nephron.
Loopdiureticsarecommonlyusedforbriskandimmediatediuresis.
ThiazidediureticsareusedforhypertensionandstatesofchronicNa+retention.
Potassium-sparingdiureticshaveacomparativelysmalleffectbutareusefulasadjunctiveagents.
Treatmentoftheunderlying disease process is critical to prevent continued Na+ reabsorption in the
kidney.NephroticsyndromeisdiscussedinChapter13,RenalDiseases.Treatmentofheartfailureis
discussedinChapter5,HeartFailureandCardiomyopathy;andcirrhosisisaddressedinChapter19,
LiverDiseases.
DisordersofSodiumConcentration
Hypernatremiaandhyponatremiaareprimarilydisordersofwaterbalanceorwaterdistribution.A
persistentabnormalityin[Na+]requiresbothaninitialchallengetowaterbalanceaswellasa
disturbanceoftheadaptiveresponse.
Hyponatremia
Hyponatremiaisdefinedasaplasma[Na+]<135mEq/L.
GENERALPRINCIPLES
To maintain a normal [Na+], the ingestion of water must be matched by the excretion of water.
Hyponatremia occurs when this balanceis disturbed by the excessive additionofwater to the ECF
and/ortheinsufficientremovalofwaterfromtheECF.
ProcesseswhichincreasethemovementofwaterintotheECFinclude:
Hyperosmolarhyponatremia.WhenanosmoticallyactivesoluteotherthanNa+accumulatesinthe
ECF, it draws water into the ECF and dilutes the [Na+]. This is most commonly caused by
hyperglycemia,resulting ina fallinplasma [Na+] of 1.6–2.4 mEq/L for every100 mg/dL rise in
plasmaglucose.
1
Waterintoxication. Rarely, theECF water content rises simply because the ingested quantityof
water exceeds the capacity for renal water clearance. This is seen in primary polydipsia, beer
potomania,andtheso-called“teaandtoast”diet.
Processes which impair the clearance of water from the ECF generally involve the antidiuretic
hormone(ADH),ahormonewhichcontrolswaterreabsorptioninthekidney.
“Appropriate” ADH secretion occurs with a fall in effective circulating volume. In these
conditions, thirst and water retention are stimulated, protecting volume status at the cost of
osmolality. This category is classically subdivided into hypovolemic and hypervolemic
hyponatremia,basedontheassociatedassessmentofECFstatus.
“Inappropriate” secretion of ADH occurs inthe absence of osmotic- or volume-related stimuli.
Because the renal response to volume expansion remains intact, these patients are typically
euvolemic.However,becauseoftheriseinTBW,serumconcentrationsofNa+aredecreased.
Conditions that stimulate ADH secretion independent of volume status or osmolality include
nausea,adrenaldysfunction,andhypothyroidism.
ThesyndromeofinappropriateADH secretion(SIADH)occursintheabsenceofphysiologic
https://t.me/med1917
stimuli for ADH secretion. It is commonly associated with neuropsychiatric disorders (e.g.,
meningitis, encephalitis, acute psychosis, cerebrovascular accident, head trauma), pulmonary
diseases (e.g.,pneumonia, tuberculosis, positive-pressureventilation,acute respiratory failure),
andmalignanttumors (mostcommonly,small-cell lungcancer).Pharmacologicagents, such as
selective serotonin reuptake inhibitors, narcotics, antipsychotic agents, chlorpropamide, and
NSAIDs,havealsobeenimplicatedinSIADH.
DIAGNOSIS
ClinicalPresentation
Theclinicalfeaturesofhyponatremiaarerelatedtothechangeinwatercontentandthesubsequentriskof
cerebraledema.Thepresenceandseverityofneurologicsymptomsdependsonboththemagnitudeand
rapidityofdecreaseinplasma[Na+].Inacutehyponatremia(i.e.,developingin<2days),patientsmay
complainofnauseaandmalaise.Astheplasma[Na+]fallsfurther,symptomsmayprogresstoinclude
headache,lethargy,confusion,andobtundation.Stupor,seizures,andcomadonotusuallyoccurunlessthe
plasma[Na+]fallsacutelybelow115mEq/L.Inchronichyponatremia(>3daysinduration),adaptive
mechanismsdesignedtodefendcellvolumeoccurandtendtominimizetheincreaseinICFvolumeand
itssymptoms.
DiagnosticTesting
Theunderlyingcauseofhyponatremia canoftenbeascertainedfrom anaccuratehistoryandphysical
examination,includinganassessmentofECFvolumestatusandtheeffectivecirculatingvolume.
Three laboratory tests, when used with a clinical assessment of volume status, can narrow the
differentialdiagnosisofhyponatremia:(1)theplasmaosmolality,(2)theurineosmolality,and(3)the
urine[Na+](Figure12-1).
https://t.me/med1917
Figure12-1 Algorithmdepictingthediagnosticapproachtohyponatremia.ADH,antidiuretichormone;ECF,extracellular
fluid; post-TURP, post–transurethral resection of the prostate syndrome; SIADH, syndrome of inappropriate antidiuretic
hormone.aUrine[Na+]maybe<20mEq/LwithlowNa+intake.bSeetextfordetails.cFrom vomiting-inducedcontraction
alkalosisorproximalrenaltubularacidosis.dUrineosmolalitymaybe<100mOsm/Lafterawaterload.
Plasmaosmolality:Mostpatientswithhyponatremiahavealowplasmaosmolality(<275mOsm/L).
Normalserumosmolalitysuggestspseudohyponatremia,alaboratorymiscalculationoftheplasma
sodiumcontentattributedtoextremelyelevatedproteinandlipidlevels.
Elevated serum osmolality suggests hyperosmolar hyponatremia, most commonly attributable to
hyperglycemia.
Urineosmolality:Theappropriaterenalresponsetohypo-osmolalityistoexcreteamaximallydilute
https://t.me/med1917
urine.
Lowurine osmolality (urineosmolality <100 mOsm/L andspecific gravity <1.003) suggeststhat
renaladaptationisintactbutoverwhelmed,asseeninprimarypolydipsia.
AnelevatedurineosmolalityindicatesthatADHispresent,resultinginreabsorptionofwater.
Urine[Na+]addslaboratorycorroborationtothebedside assessment ofeffectivecirculating volume
and can discriminate between extrarenal and renal losses of Na+. The appropriate response to
decreased effective circulating volume is a urine [Na+] <10 mEq/L. A urine [Na+] of >20 mEq/L
suggestsanormaleffectivecirculatingvolumeoraNa+-wastingdefect.
TREATMENT
Rateofcorrection
Inchronichyponatremia,thetargetrateofcorrectionshouldnotexceed8mEq/Lover24hours.
Theriskofiatrogenicinjuryisincreasedinpatientswithchronichyponatremia,sincecellsadapt
tothehypo-osmolarstateovertime.
The primary riskofovercorrection is the development of central pontine myelinolysis (CPM).
CPM results from damage to neurons due to rapid osmotic shifts. Inits most overt form, it is
characterizedbyflaccidparalysis,dysarthria,anddysphagia.ItcanbeconfirmedbyCTscanor
MRIofthebrain.TheriskofprecipitatingCPMisincreasedwithcorrectionofthe[Na+]by10–
12 mEq/L in a 24-hour period.2 Other risk factors for developing CPM include preexisting
hypokalemia,malnutrition,andalcoholusedisorder.
Insymptomatichyponatremia,theserum[Na+]shouldagainbecorrectedcautiously.Atargetedrise
in serum [Na+] by 4–6 mEq/L within the first 4–6 hours is generally sufficient to reverse the
neurologic sequelaeandavoid overcorrection.Thetotal dailycorrectionshouldstillnotexceed8
mEq/d.
Typeofintervention
In severe hyponatremia, hypertonic saline should be used to achieve the correction described
above.
Hypertonic saline (3% saline) can be given as a continuous infusion in stable severe
hyponatremia.Avarietyofformulascanbeusedtoestimatetheinfusionrate,butasnoneofthem
account for ongoing free water loss, the risk of overcorrection is substantial. A more modest
startingrateof0.25–0.3ml/kg/hprovidesagreatermarginofsafetyandcanbetitratedbasedon
subsequentlaboratorydata.
Alternatively, hypertonic salinecan be givenin100 mL boluses(uptothreedoses as needed).
Thisprovidesarapidinitialcorrection,idealforpatientswithintracraniallesionsorconcernsfor
herniation,whilelimitingtheriskofovercorrection.
Sincenoequationoralgorithmcanadequatelypredictdynamicfluctuationsinwaterbalance,itis
absolutelycriticaltofrequentlyrechecklaboratorydatatoensurecorrectionatanappropriate
rateandadjustfluidadministration.
Desmopressin acetate (DDAVP) can also be given to prevent overcorrection of hyponatremia,
particularlyinpatientswhomayhaveareversiblecauseofADHsecretion.
Inasymptomatichyponatremia,treatmentshouldbetargetedtothecauseofthedisorder.
Hypovolemichyponatremia. Inpatients with acute hypovolemic hyponatremia, isotonic saline
can be used to restore the intravascular volume. Because ADH is stimulated by the volume
depletion, fluid resuscitation will decrease ADH secretion and facilitate renal elimination of
water.
Hypervolemic hyponatremia. Hyponatremia in congestive heart failure (CHF) and cirrhosis
https://t.me/med1917
often reflects the severity of the underlying disease. The hyponatremia itself is typically
asymptomatic. Definitive treatment requires management of the underlying condition, although
restrictionofwaterintakecanattenuatethehyponatremia.
SIADH. In addition to the correction of contributing factors (pneumonia, drugs, etc.), water
restriction,solutetablets,anddiureticscanalsobeused.
□ Waterrestriction. This is typically the first-linetreatment for SIADH. The amount offluid
restriction depends on the amount of water eliminated by the kidney. A useful guide to the
necessarydegreeoffluidrestrictionisasfollows:
If(UrineNa++UrineK+)/SerumNa+<0.5,restrictto1L/d.
If(UrineNa++UrineK+)/SerumNa+is0.5–1.0,restrictto500mL/d.
If (Urine Na+ + Urine K+)/Serum Na+ is >1, the patient has a negative renal free water
clearance,andanyamountofingestedwatermayberetained.Insuchsituations,adjunctive
therapyisrequired.
□ A high dietarysolute load(using salt or urea tablets) canbe extremelyhelpful, particularly
since water restriction can be challenging for patients. The obligate water loss that
accompaniestheexcretionofthehighdietarysoluteloadhelpstoalleviatethewaterretention
inSIADH.
□ Loop diuretics impair the urinary concentrating mechanism and can enhance free water
excretion.
□ VasopressinantagonistspromoteawaterdiuresisandmaybeusefulinthetherapyofSIADH.
Both IV (conivaptan) and oral (tolvaptan) preparations are approved for the treatment of
euvolemic hyponatremia. However, giventherisks of overcorrection, these agents shouldbe
initiatedinacloselymonitoredinpatientsetting.
Hypernatremia
GENERALPRINCIPLES
Hypernatremia isdefinedas a plasma[Na+] >145mEq/Landrepresentsastateof hyperosmolality
(see“DisordersofSodiumConcentration”section).
Hypernatremia maybe causedbyaprimaryNa+gain or awaterdeficit,the latterbeing muchmore
common. Normally, this hyperosmolar state stimulates thirst and the excretion of a maximally
concentratedurine.Forhypernatremiatopersist,oneorbothofthesecompensatorymechanismsmust
beimpaired.
Impaired thirst response may occur in situations where access to water is limited, often due to
physical restrictions (institutionalized, handicapped, postoperative, or intubated patients) or mental
impairment(delirium,dementia).
Hypernatremiadue to waterloss. Theloss of water must occur inexcess of electrolytelosses to
raise[Na+].
Nonrenal water loss may be due to evaporation from the skin and respiratory tract (insensible
losses)orlossfromtheGItract.DiarrheaisthemostcommonGIcauseofhypernatremia.Osmotic
diarrhea(inducedbylactulose,sorbitol,ormalabsorptionofcarbohydrate)andviralgastroenteritis,
inparticular,resultindisproportionalwaterloss.
Renalwaterlossresultsfromeitherosmoticdiuresisordiabetesinsipidus(DI).
Osmoticdiuresis is frequently associatedwith glycosuria andhigh osmolar feeds. In addition,
increased urea generation from accelerated catabolism, high-protein feeds, and stress-dose
https://t.me/med1917
steroidscanalsoresultinanosmoticdiuresis.
Hypernatremia secondary to nonosmotic urinary water loss is usually caused by impaired
vasopressin secretion (central diabetes insipidus [CDI]) or resistance to the actions of
vasopressin(nephrogenicdiabetesinsipidus[NDI]).Partialdefectsoccurmorecommonlythan
completedefectsinbothtypes.
ThemostcommoncauseofCDIisdestructionoftheneurohypophysisfromtrauma,neurosurgery,
granulomatous disease, neoplasms, vascular accidents, or infection. In many cases, CDI is
idiopathic.
NDImayeitherbeinheritedoracquired.AcquiredNDIoftenresultsfromadisruptiontotherenal
concentrating mechanism due to drugs (lithium, demeclocycline, amphotericin), electrolyte
disorders (hypercalcemia,hypokalemia), medullarywashout(loopdiuretics), andintrinsicrenal
diseases.
Hypernatremia due to primary Na+gain occurs infrequently because of the kidney’s capacity to
excretetheretainedNa+.However,itcanrarelyoccurafterrepetitivehypertonicsalineadministration
orchronicmineralocorticoidexcess.
Transcellular water shift from ECF to ICF can occur in circumstances of transient intracellular
hyperosmolality,asinseizuresorrhabdomyolysis.
DIAGNOSIS
ClinicalPresentation
Hypernatremia results in contraction of brain cells as water shifts to attenuate the rising ECF
osmolality.Thus,themostseveresymptomsofhypernatremiaareneurologic,includingalteredmental
status, weakness, neuromuscular irritability, focal neurologic deficits, and, occasionally, coma or
seizures.Aswithhyponatremia,theseverityoftheclinicalmanifestationsisrelatedtotheacuity and
magnitude of the rise inplasma [Na+]. Chronic hypernatremia is generally less symptomatic as a
resultofadaptivemechanismsdesignedtodefendcellvolume.
CDIandNDIgenerallypresent withcomplaintsofpolyuriaandthirst.Signs ofvolumedepletionor
neurologicdysfunctionaregenerallyabsentunlessthepatienthasanassociatedthirstabnormality.
DiagnosticTesting
UrineosmolalityandtheresponsetoDDAVPcanhelpnarrowthedifferentialdiagnosisfor
hypernatremia(Figure12-2).
https://t.me/med1917
Figure12-2 Algorithmdepictingthe diagnostic approachtohypernatremia.BUN,bloodureanitrogen;↑Ca+,hypercalcemia;
CDI,centraldiabetes insipidus; DDAVP, desmopressinacetate; ECF,extracellularfluid;GI,gastrointestinal;NDI,nephrogenic
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана