DisElectroLitemii

7/25/2019 DisElectroLitemii

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Fluid and Electrolytes DisturbancesFluid and Electrolytes Disturbances

60% of body consists of fluid Intracellular space [2/3] Extracellular space [1/3]

Electrolytes are active ions: positively and neatively c!ared

Extracellular "luid #E$": 20% of total body &ei!t Intravascular: 'lood plas(a Interstitial fluid

o 'et&een cellso $erebrospinal fluido Intraocular fluid

)in and *istribution of 'ody "luids+ater is t!e (ain co(ponent of body (ass

)dults: ,0% to 60% of total body &ei!t -e&born: )bout .0% of total body &ei!t $!ild!ood: 60% to 6,% of total body &ei!t

"urt!er declines &it! ae

Ci fiziologice de eliminare a apei dinCi fiziologice de eliminare a apei din

organismorganism

otal 2,3, (l//2ore

2000 (l/2 ore

inic!i 1,20 (l//2ore

1000 (l/2 ore

$utanat

. (l//2 ore ,00 (l/2 ore

4l5(n 7 (l/ /2 ore 00 (l/2 ore

8caun 12 (l//2 ore 100 (l/2 ore

Necesar minim lichidian recomandatNecesar minim lichidian recomandat


2/17

reutate # (l//ora (l//9i

110 1201,0

1120 2 ,0100

20

1

2,0

01

2,0

Distributia lichidelor perfuzateDistributia lichidelor perfuzate cresterea de volu( #; esti(ata < ; infu9at x ; plas(atic nor(al/ ; de distributiecresterea de volu( #; esti(ata < ; infu9at x ; plas(atic nor(al/ ; de distributie;i necesar de sol luco9a ,% sau ser fi9ioloic pentru a creste vole(ia cu 2 >? ,% x 2 > / 3 > < 2. >? ,% x 2 > / 3 > < 2. >-a$l 0@A% x 1 > / 3 > < A@3 >-a$l 0@A% x 1 > / 3 > < A@3 >

Compoziia soluiilor volemice n comparaie cu plasma !mmol"l#Compoziia soluiilor volemice n comparaie cu plasma !mmol"l#

-aB

$l C

BD

B

B

$aB

B

a(pon p

$lasma !albumina# 10 102 3F7 0F.F 1F2$G3

2

7@

NaCl %&' ( 1, 1, ,@7

)terofundin iso 1, 127 F, 1 2F, )cetat 2 ,F1,FA

*inger lactat 131 10A , 2 >actat 2. 6@

)olutie gelatina+elofusin

1, 120 7@17@7

)olutie gelatina?elaspan 1,1 103 1 1 )cetat 2

)oluii de amidon,oluven 1, 1, 7

,olulyte 137 110 1F, )cetat 3 7

De(brane 4er(eabilityDe(brane 4er(eabilityDost cell (e(branes are relatively !i!ly per(eable to &aterF De(branes are se(iDost cell (e(branes are relatively !i!ly per(eable to &aterF De(branes are se(i

per(eable to certain anions and cationsF *ifference in per(eability bet&een &ater and dissolvedper(eable to certain anions and cationsF *ifference in per(eability bet&een &ater and dissolvedsolutessolutes

Compoziia ionic a spaiilor hidriceCompoziia ionic a spaiilor hidrice

$lasma -ichid interstiial -ichid intracelular

Cationi


3/17

8odiu #((ol/l 10 1, 10

4otasiu #((ol/l 3@7 3@. 1,,

$alciu ioni9at #((ol/l 1@2 1@2 H0@01

Dane9iu #((ol/l

0@.

0@.

10

"osfat #((ol/l 1@1 1@0 10,

.nioni

$lor #((ol/l 102 11, 3

'icarbonat #((ol/l 2. 30 10

Diffusion*ue to constant (otion of ato(s@ (olecules@ ions in solution

4assive process Doves particles fro( area of !i!er concentration to area of lo&er concentration

$oncentration radient

+ater Dove(ent 'et&een I$" and E$"/smosis"lo& of fluid across a se(iper(eable (e(brane fro( a lo&er solute concentration to a !i!ersolute concentrationGs(otic pressure deter(ined by:

-u(ber and (olecular &ei!ts 4er(eability of (e(brane

Electrolyte 'alance4otassiu( is t!e c!ief intracellular cation and sodiu( t!e c!ief extracellular cation'ecause t!e os(otic pressure of t!e interstitial space and t!e I$" are enerally eual@ &atertypically does not enter or leave t!e cell) c!ane in t!e concentration of eit!er electrolyte &ill cause &ater to (ove into or out of t!e cellvia os(osisF ) drop in sodiu( &ill cause fluid to enter t!e cell

4las(a os(olality


4/17

J seru( sodiu( concentration H13, ((ol/>J represents a relative excess of &ater in relation to sodiu(F

+e define Kmild6!yponatrae(ia as a bioc!e(ical findin of a seru( sodiu( concentrationbet&een 130 and 13, ((ol/> as (easured by ion specific electrodeF

+e define KmoderateL !yponatrae(ia as a bioc!e(ical findin of a seru( sodiu( concentrationbet&een 12, and 12A ((ol/> as (easured by ion specific electrodeF +e define Kprofound6!yponatrae(ia as a bioc!e(ical findin of a seru( sodiu(

concentrationH12, ((ol/> as (easured by ion specific electrodeF

+e define KacuteL !yponatrae(ia as !yponatrae(ia t!at is docu(ented to exist H . !F+e define KchronicL !yponatrae(ia as !yponatrae(ia t!at is docu(ented to exist for at least .!FIf t!e !yponatrae(ia cannot be classified@ &e consider it bein c!ronic@ unless t!ere is clinical orana(nestic evidence of t!e contrary

+e define Kmoderately symptomaticL !yponatrae(ia as any bioc!e(ical deree of

!yponatrae(ia in t!e presence of (oderately severe sy(pto(s of !yponatrae(ia+e define Kseverely symptomaticL !yponatrae(ia as any bioc!e(ical deree of !yponatrae(iain t!e presence of severe sy(pto(s of !yponatrae(ia

)ymptoms

7oderately severe-ausea &it!out vo(itin$onfusioneadac!e

)evere;o(itin$ardiorespiratory distress)bnor(al and deep so(nolence8ei9ures

$o(a #?laso& $o(a 8cale H .

Epidemiology:yponatre(ia is t!e (ost co((on electrolyte disorder

incidence of approxi(ately 1%surical &ard@ approxi(ately F%30% of patients treated in t!e intensive care unit

*rus and conditions associated &it! acute !yponatrae(ia 4ostoperative p!ase 4ostresection of t!e prostate@ postresection of endoscopic uterine surery 4olydipsia Exercise ecent t!ia9ides prescription 3@Det!yleendioxy(et!a(feta(ine #D*D)@ M$ $olonoscopy preparation $yclop!osp!a(ide #intravenous Gxytocin ecently started des(opressin t!erapy


5/17

ecently started terlipressin@ vasopressin

8ypes

ypovole(ic !yponatre(ia Euvole(ic !yponatre(ia

ypervole(ic !yponatre(ia edistributive !yponatre(ia 4seudo!yponatre(ia

edistributive !yponatre(iaedistributive !yponatre(ia+ater s!ifts fro( t!e intracellular to t!e extracellular co(part(ent@ &it! a resultant dilution ofsodiu(!e '+ and total body sodiu( are unc!aned

t!is condition occurs &it! !yperlyce(ia ad(inistration of (annitol

+e reco((end excludin !yperlycae(ic !yponatrae(ia by (easurin t!e seru( lucoseconcentration and correctin t!e (easured seru( sodiu( concentration for t!e seru( lucoseconcentration if t!e latter is increasedF #1*yponatrae(ia &it! a (easured os(olality H27, (Gs(/ al&ays reflects !ypotonic!yponatrae(iaF #not raded

4seudo!yponatre(ia4seudo!yponatre(ia!e aueous p!ase is diluted by excessive solutes #proteins or lipids!e '+ and total body sodiu( are unc!anedF

!ypertrilyceride(ia (ultiple (yelo(a

ypovole(ic !yponatre(iaypovole(ic !yponatre(iadevelops as sodiu( and free &ater are lost and/or replaced by inappropriately !ypotonic fluids8odiu( can be lost t!rou! renal or nonrenal routes

-onrenal loss

o ?I losses: ;o(itin@ *iarr!ea@ fistulas@ pancreatitiso Excessive s&eatino !ird spacin of fluids: ascites@ peritonitis@ pancreatitis@ and burnso $erebral salt&astin syndro(e: trau(atic brain inNury@ aneurys(al subarac!noid !e(orr!ae@

and intracranial surery oss: *iuretics


6/17

Euvole(ic !yponatre(iaEuvole(ic !yponatre(ia-or(al sodiu( stores and a total body excess of free &ater

psyc!oenic polydipsia@ often in psyc!iatric patients ad(inistration of !ypotonic intravenous or irriation fluids in t!e i((ediate postop period Infants &!o (ay !ave been iven inappropriate a(ounts of free &ater

bo&el preparation before colonoscopy or colorectal surery 8I)*

8I)*8I)*$aused by various etioloies

$-8 disease J tu(or@ infection@ $;)@ 8) 4ul(onary disease J '@ pneu(onia@ sarcoidosis@ 44; $ancer J >un@ pancreas@ t!y(o(a@ ovary@ ly(p!o(a *rus J -8)I*s@ 88Is@ antipsyc!otics@ diuretics@ opiates 8urery 4ostoperative

Idiopat!ic J (ost co((on

essential criteria 8eru( os(olality H27, (Gs(/ $linical euvole(ia )bsence of adrenal@ t!yroid@ pituitary or renal insufficiency -o recent use of diuretic aents Orine os(olality reater t!an 100 (Gs(/ t!ou! enerally reater t!an 00,00

(Gs(/ in settin of lo& seru( os(olality #inappropriate Orine sodiu( concentration 30 ((ol/> &it! nor(al dietary salt and &ater intae

8upple(ental criteria 8eru( uric acidH0F2 ((ol/> #H (/d> 8eru( ureaH3F6 ((ol/> #H21F6 (/d> "ailure to correct !yponatrae(ia after 0FA % saline infusion "ractional sodiu( excretion 0F, % "ractional urea excretion ,, % "ractional uric acid excretion 12 % $orrection of !yponatrae(ia t!rou! fluid restriction

ypervole(ic !yponatre(iaypervole(ic !yponatre(iaotal body sodiu( increases@ and '+ increases to a reater extent$an be renal or nonrenal

acute or c!ronic renal failure dysfunctional idneys are unable to excrete t!e inested sodiu( load cirr!osis@ conestive !eart failure@ or nep!rotic syndro(e

$linical (anifestations


7/17

"luid deficit or excess )ltered (ental status

"luid ;olu(e *eficit )cute &ei!t loss

*ecreased sin turor Gliuria $oncentrated urine 4ostural !ypotension

+ea@ rapid@ !eart rate

"lattened nec veins Increased te(perature *ecreased central venous pressure

"luid ;olu(e Excess Ede(a Gt!er clinical (anifestations J distended nec veins@ cracles@ increased blood pressure@

increased &ei!t

ypervole(ia perip!eral and presacral ede(a pul(onary ede(a Nuular venous distension !ypertension decrF !ct@ decrF seru( prot decrF bun/cr O-a no !elp

ypovole(iaF poor sin turor

dry (ucous (e(branes flat nec veins !ypotension incrF ct incrF seru( protF Incr bun/cr ratio 20:1 O-a H 20 (e/l


8/17

$erebral sy(pto(s of !yponatre(ia$erebral sy(pto(s of !yponatre(ia -ausea and vo(itin eadac!e *ecreased consciousness

o >et!aryo $onfusiono $o(a

8ei9ures Duscle &eaness@ cra(ps or spas(s espiratory distress // arrest *eat! #,,0%

yponatre(ia 12613 ((ol/> )lterations of conitive function ?ait stability "alls Gsteoporosis "ractures and inpatient (ortality

+orup for !yponatre(ia:+orup for !yponatre(ia: 3 (andatory lab tests 8eru( Gs(olality Orine Gs(olality Orine 8odiu( $oncentration

)dditional labs dependin on clinical suspicion 8@ cortisol #ypot!ryoidis( or )drenal insufficiency )lbu(in@ '-4@ trilyceridesP #psuedo!yponatre(ia@ cirr!osis@ DD

+e reco((end interpretin urine os(olality of a spot urinesa(ple as a first stepF #1* If urine osmolality 9 2%% m/sm"g@ &e reco((end acceptin relative excess &ater

intae as a cause of t!e hypotonic hyponatraemia.#1* If urine osmolality;2%% m/sm"g@ &e reco((end interpretin t!e urine sodiu(

concentration on a spot urine sa(ple taen si(ultaneously &it! a blood sa(pleF #1* If urine sodiu( concentration 9


9/17

Dild or no sy(pto(s < "luid restriction

)ymptomatic 1ststep is to calculate t!e total body &ater

total body &ater #'+ < 0F6 Q body &ei!t 8odiu( deficit < '+ x #desired -a J actual -a

esti(ate 8-a c!ane on t!e basis of t!e a(ount of -a in t!e infusate =8-a < R[-a B C]infS 8-aT U #'+ B 1

I; "luids Gne liter of >actated inerVs 8olution contains:

o 130 (E of sodiu( ion < 130 ((ol/>o 10A (E of c!loride ion < 10A ((ol/>o 2. (E of lactate < 2. ((ol/>o (E of potassiu( ion < ((ol/>o 3 (E of calciu( ion < 1F, ((ol/>

Gne liter of -or(al 8aline contains: 1, (E/> of -aBand $lS

Gne liter of 3% saline contains: ,1 (E/> of -aBand $lS

yponatrae(ia &it! severe sy(pto(s "irst !our (anae(ent@ reardless of &!et!er !yponatrae(ia is acute or c!ronic

+e reco((end pro(pt intravenous infusion of 1,0 (> 3 % !ypertonic saline oreuivalent over 20 (inF #1*

+e suest c!ecin t!e seru( sodiu( concentration after 20 (in &!ile repeatin aninfusion of 1,0 (> 3 % !ypertonic saline or euivalent over t!e next 20 (inF#2*

+e suest repeatin t!erapeutic reco((endations t&ice or until a taret of , ((ol/>increase in seru( sodiu( concentration is ac!ievedF #2*

1F "ollo& up (anae(ent in case of improvement of sy(pto(s after a , ((ol/> increasein seru( sodiu( concentration in t!e first !our@ reardless of &!et!er !yponatrae(ia isacute or

c!ronic +e reco((end stoppin t!e infusion of !ypertonic salineF #1* +e reco((end eepin t!e intravenous line open by infusin t!e s(allest feasible

volu(e of 0FA % saline until causespecific treat(ent is startedF #1*

+e reco((end startin a dianosis specific treat(ent if available@ ai(in at least tostabili9e sodiu( concentrationF#1*

+e reco((end li(itin t!e increase in seru( sodiu( concentration to a total of 10((ol/> durin t!e first 2 ! and an additional . ((ol/> durin every 2 ! t!ereafteruntil t!e seru( sodiu( concentration reac!es 130 ((ol/>F #1*

+e suest c!ecin t!e seru( sodiu( concentration after 6 and 12 !@ and dailyafter&ards until t!e seru( sodiu( concentration !as stabilised under stable treat(entF#2*


10/17

2F "ollo& up (anae(ent in case of no improvementof sy(pto(s after a , ((ol/>increase in seru( sodiu( concentration in t!e first !our@ reardless of &!et!er t!e!yponatrae(ia is acute or c!ronic

+e reco((end continuin an intravenous infusion of 3 % !ypertonic saline or euivalentai(in for an additional 1 ((ol/>/! increase in seru( sodiu( concentration #1*F

+e reco((end stoppin t!e infusion of 3 % !ypertonic saline or euivalent &!en t!esy(pto(s i(prove@ t!e seru( sodiu( concentration increases 10 ((ol/> in total or t!eseru( sodiu( concentration reac!es 130 ((ol/>@&!ic!ever occurs first #1*F

+e reco((end additional dianostic exploration for ot!er causes of t!e sy(pto(s t!an!yponatrae(ia #1*F

+e suest c!ecin t!e seru( sodiu( concentration every ! as lon as an intravenousinfusion of 3 % !ypertonic saline or euivalent is continued #2*F

=hat if the sodium increases too fast>=hat if the sodium increases too fast>

!e dreaded co(plication of increasin sodiu( too fast is $entral 4ontine Dyelinolysis

&!ic! is a for( of os(otic de(yelination 8y(pto(s enerally occur 26 days after elevation of sodiu( and usually eit!erirreversible or only partially reversible

8y(pto(s include: dysart!ria@ dysp!aia@ paraparesis@ uadriparesis@ let!ary@ co(a oreven sei9ures

yponatrae(ia &it! (oderately severe sy(pto(s +e reco((end startin pro(pt dianostic assess(entF #1* 8top@ if possible@ (edications and ot!er factors t!at can contribute to or provoe t!e

!yponatrae(iaF #not raded +e reco((end causespecific treat(entF #1* +e suest i((ediate treat(ent &it! a sinle intravenous infusion of 1,0 (> 3 %

!ypertonic saline or euivalent over 20 (inF #2* +e suest ai(in for a , ((ol/>/2 ! increase in seru( sodiu( concentrationF #2* +e suest li(itin t!e increase in seru( sodiu( concentration to 10 ((ol/> in t!e first

2 ! and . ((ol/> durin every 2 ! t!ereafter@ until a seru( sodiu( concentration of130 ((ol/> is reac!edF #2*

+e suest c!ecin t!e seru( sodiu( concentration after one@ 6 and 12 !F #2* +e suest additional dianostic exploration for ot!er causes of t!e sy(pto(s if t!e

sy(pto(s do not i(prove &it! an increase in seru( sodiu( concentrationF #2* +e suest considerin to (anae t!e patient as in severely sy(pto(atic !yponatrae(ia

if t!e seru( sodiu( concentration furt!er decreases despite treatin t!e underlyindianosisF #2*

)cute !yponatrae(ia &it!out severeor (oderately severe sy(pto(s

Dae sure t!at t!e seru( sodiu( concentration !as been (easured usin t!e sa(etec!niue as used for t!e previous (easure(ent and t!at no ad(inistrative errors insa(ple !andlin !ave occurredF #not raded


11/17

If possible@ stop fluids@ (edications and ot!er factors t!at can contribute to or provoe t!e!yponatrae(iaF #not raded

+e reco((end startin pro(pt dianostic assess(entF #1* +e reco((end causespecific treat(entF #1* If t!e acute decrease in seru( sodiu( concentration exceeds 10 ((ol/>@ &e suest a

sinle intravenous infusion of 1,0 (> 3 % !ypertonic saline or euivalent over 20 (inF#2*

+e suest c!ecin t!e seru( sodiu( concentration after !@ usin t!e sa(e tec!niueas used for t!e previous (easure(entF #2*

$!ronic !yponatrae(ia &it!out severe or (oderately severe sy(pto(s 8top nonessential fluids@ (edications and ot!er factors t!at can contribute to or provoe

t!e !yponatrae(iaF #not raded +e reco((end causespecific treat(entF #1* In (ild !yponatrae(ia@ &e suest aainst treat(ent &it! t!e sole ai( of increasin t!e

seru( sodiu( concentrationF #2$ In (oderate or profound !yponatrae(ia@ &e reco((end avoidin an increase in seru(

sodiu( concentration of 10 ((ol/> durin t!e first 2 ! and . ((ol/> durin every 2! t!ereafterF #1*

In (oderate or profound !yponatrae(ia@ &e suest c!ecin t!e seru( sodiu(concentration every 6 ! until t!e seru( sodiu( concentration !as stabilised under stabletreat(entF #2*

In case of unresolved !yponatrae(ia@ reconsider t!e dianostic alorit!( and as forexpert adviceF #not raded

8I)* +ater restriction: 0F,1 liter/day *e(eclocycline: In!ibits t!e effects of )* Gnset of action (ay reuire up to one &ee

;asopressin receptor antaonists< )WO)EI$8;asopressin receptor antaonists< )WO)EI$8o Excretion of electrolytefree &atero 'eneficial i(pact on seru( -ao >ac of evidence on lon ter( beneficial effectso )bsence of disease(odifyin propertieso is of overcorrectiono $ost

$ractical therapeutic approach to hyponatremia in 5F$ractical therapeutic approach to hyponatremia in 5F

Establis! t!e dianosis >i(it -afree fluid intae 4rescribe ivFloop diuretics X saline solution 4rescribe vasopressin receptor antaonist Institute O"/renal replace(ent t!erapy


12/17

4ractical t!erapeutic approac! to sy(pto(atic !yponatre(ia in "4ractical t!erapeutic approac! to sy(pto(atic !yponatre(ia in "

)aline solution ? 5ypertonic>

-o &orsenin of pul(onary conestion Increase in urine output eduction in seru( blood urea nitroen -o c!ane in " functional class >o&er read(ission rate >o&er !ospital (ortality

8u((ary of yponatre(ia yponatre(ia !as variety of causes reat(ent is based on sy(pto(s

8evere sy(pto(s < ypertonic 8aline Dild or no sy(pto(s < "luid restriction

Gvercorrection@ (ore t!an 10 ((ol increase in 2 !ours (ust be avoided &it!(onitorin

8eru( Gs(olality@ Orine Gs(olality and Orine sodiu( concentration are initial tests toorder

ypernatre(iaypernatre(ia

-or(al rane for blood levels of sodiu( is: 13, 1, ((ol/literypernatre(iaypernatre(ia refers to an elevated seru( sodiu( level #1, 1,0 ((ol/liter

C.4)E) /F 5@$E*N.8*E7A.1 +ater loss Insensible and s&eat losses ?I losses *iabetes Insipidus #bot! central and nep!roenic Gs(otic diuresis ypot!ala(ic lesions &!ic! affect t!irst function Jtu(ors@ ranulo(atous diseases or

vascular disease 2 8odiu( ion overload

$athophysiology

"luid deprivation in patients &!o cannot perceive@ respond to@ or co((unicate t!eir t!irst Dost often affects very old@ very youn@ and conitively i(paired patients Infants &it!out access to &ater or increased insensible &ater loss can be very susceptible

to !ypernatre(ia

CN) reaction to hypernatremiaCN) reaction to hypernatremia


13/17

)s t!e result of an os(otic radient@ &ater s!ifts fro( t!e interstitiu( and cells of t!ebrain and enters t!e capillaries

!e brain tends to s!rin and t!e capillaries dilate and possibly rupture esult is focal intracerebral Y subarac!noid !e(orr!aesfocal intracerebral Y subarac!noid !e(orr!aes@ blood clots@ and neuroloical

dysfunction

)ymptoms of hypernatremia)ymptoms of hypernatremia

Initial sy(pto(s include let!ary@ &eaness and irritability $an proress to t&itc!in@ sei9ures@ obtundation or co(a esultin decrease in brain volu(e can lead to rupture of cerebral veins leadin to

!e(orr!ae 8evere sy(pto(s usually occur &it! rapid increase to sodiu( concentration of 1,.

((ol/l or (ore

CN) protective mechanismsCN)protective mechanisms Idioenic os(oles accu(ulate inside brain cellsCB@ DBfro( cellular bindin sites

and a(ino acids fro( protein catabolis(!ese idioenic os(oles create an os(otic force t!at dra&s &ater bac into t!e brain and protectscells fro( de!ydration

If t!is adaptation !as occurred and treat(ent involves a rapid infusion of dextrose@ t!ere isdaner of cerebral ede(a &it! fluid bein dra&n into brain tissues

$athogenesis of hypernatremia$athogenesis of hypernatremia

-or(al;olu(e ypernatre(ia:-or(al;olu(e ypernatre(ia: $onditions associated &it! a loss of Zelectrolyte$onditions associated &it! a loss of Zelectrolyte

free fluids #loss of pure &aterfree fluids #loss of pure &ater i!;olu(e ypernatre(ia:i!;olu(e ypernatre(ia: $onditions associated &it! inestion or$onditions associated &it! inestion or

ad(inistration of sodiu( containin !ypertonic solutionsad(inistration of sodiu( containin !ypertonic solutions >o&;olu(e ypernatre(ia:>o&;olu(e ypernatre(ia: $onditions associated &it! t!e loss of !ypotonic$onditions associated &it! t!e loss of !ypotonic

fluids #fluids containin (ore &ater t!an sodiu(fluids #fluids containin (ore &ater t!an sodiu(

Normal?volume hypernatremiaBNormal?volume hypernatremiaB 4ure +ater >oss4ure +ater >oss enal >ossenal >oss

$entral diabetes insipidus:$entral diabetes insipidus: I(pair(ent in urinary concentration due to partial orI(pair(ent in urinary concentration due to partial orco(plete loss of )* secretion 2\ to $-8 pat!oloyco(plete loss of )* secretion 2\ to $-8 pat!oloy

oo Idiopat!ic #autoi((uneIdiopat!ic #autoi((uneoo -eurosurery or trau(a-eurosurery or trau(aoo $-8 tu(ors$-8 tu(orsoo Infiltrative disorders #eFF@ $-8 sarcoidosisInfiltrative disorders #eFF@ $-8 sarcoidosisoo Gt!ers #eFF@ !ypoxic encep!alopat!y@ bleedin@ infectionGt!ers #eFF@ !ypoxic encep!alopat!y@ bleedin@ infection

-ep!roenic diabetes insipidus:-ep!roenic diabetes insipidus: I(pair(ent in urinary concentration due to inability ofI(pair(ent in urinary concentration due to inability ofcollectin duct to respond to )*collectin duct to respond to )*


14/17

oo $!ronic lit!iu( treat(ent #up to ,0%$!ronic lit!iu( treat(ent #up to ,0%oo ypocalcae(iaypocalcae(iaoo 4ersistent severe !ypoale(ia4ersistent severe !ypoale(iaoo ereditary nep!roenic *I #c!ildrenereditary nep!roenic *I #c!ildren

oo Mlined: defects in ;Mlined: defects in ;22receptor enereceptor ene

oo )utoso(al recessive: defects in )W42 &ater c!annel)utoso(al recessive: defects in )W42 &ater c!anneloo Gt!er #eFF@ sicle cell *9@ a(yloidosis@ (yelo(aGt!er #eFF@ sicle cell *9@ a(yloidosis@ (yelo(a

Diagnosis of hypernatremiaDiagnosis of hypernatremia

8a(e labs as &orup for !yponatre(ia: 8eru( os(olality@ urine os(olality and urinesodiu(

Orine sodiu( s!ould be lo&er t!an 2, ((ol/> if water and volume lossare causeF It canbe reater t!an 100 ((ol/> &!en hypertonic solutionsare infused or inested

If urine os(olality is lo&er t!an seru( os(olality t!enDI is present

)d(inistration of **);4 &ill differentiate Orine os(olality &ill increase in central *I@ no response in nep!roenic *I

Clinical manifestations

o !irsto *ry@ s&ollen tonueo 8ticy (ucous (e(braneso "lus!ed sino 4ostural !ypotension

-o?volume hypernatremia-o?volume hypernatremiareat(entreat(ent

e!ydration is t!e pri(ary obNective in (ost cases reat(ent is best !andled by ivin slo& infusions of lucose solutions If !ypotensive: t!en ,% of total body &ei!t # is needed as isotonic fluids initiallyIf !ypotensive: t!en ,% of total body &ei!t # is needed as isotonic fluids initially ?ive free ?ive free 22G #*,+ or pFoF &ater to correct !ypernatre(ia only after plas(a #and E$"G #*,+ or pFoF &ater to correct !ypernatre(ia only after plas(a #and E$"

volu(e is reexpandedvolu(e is reexpanded

$alculation of "ree +ater *eficit$alculation of "ree +ater *eficit Free ater deficit B 8=Free ater deficit B 8=normalnormal? 8=? 8=presentpresent

.nd& 8=.nd& 8=presentpresentx $x $Na presentNa presentB 8=B 8=normalnormalx $x $Na normalNa normal

/r& 8=/r& 8=presentpresentB 8=B 8=normalnormalx $x $Na normalNa normal" $" $Na presentNa present

)o& free ater deficit B 8=)o& free ater deficit B 8=normalnormal !2 ? $!2 ? $Na normalNa normal" $" $Na presentNa present##

8reatment of 5ypernatremia

"irst@ calculate &ater deficit


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'+ present < current body &ater assu(ed to be ,0% of body &ei!t in (en and 0% in&o(en

8o letLs do a sa(ple calculation: 60 (an &it! 16. (E/> o& (uc! &ater &ill it tae to reduce !is sodiu( to 10 (E/>

+ater deficit < 0F, x 60 #1[10/16.] approx , > 'ut !o& fast s!ould I correct it 8a(e as !yponatre(ia@ sodiu( s!ould not be lo&ered by (ore t!an 1012 ((ol/> in 2

!ours Gvercorrection can lead to cerebral ede(a &!ic! can lead to encep!alopat!y@ sei9ures or

deat! 8o &!at does t!at (ean for our patient !e , > &!ic! &ill lo&er t!e sodiu( level by 2. s!ould be iven over ,660 !ours@ or at a

rate of 7,.0 (>/!r ypical fluids iven in for( of *, &ater

5igh?volume hypernatremia5igh?volume hypernatremia

reat(entreat(ent

DiureticsDiuretics:: re(ove -are(ove -aBBand &aterand &ater *eplacement of ater losses from diuretic*eplacement of ater losses from diuretic

Dialysis if concurrent renal failureDialysis if concurrent renal failure

8u((ary of ypernatre(ia >oss of t!irst usually !as to occur to produce !ypernatre(ia ate of correction sa(e as !yponatre(ia *, &ater infusion is typically used to lo&er sodiu( level 8a(e dianostic labs used: 8eru( os(olality@ Orine os(olality and Orine sodiu( 'e&are of overcorrection as cerebral ede(a (ay develop

)ll )bout 4otassiu()ll )bout 4otassiu(

DaNor Intracellular electrolyte A.% of t!e bodyLs potassiu( is inside t!e cells Influences bot! seletal and cardiac (uscle activity -or(al seru( potassiu( concentration J 3F, to ,F, ((ol/>F

ypoale(iaypoale(ia

8eru( 4otassiu( belo& 3F, ((ol/>

Causes: diarr!ea@ diuretics@ poor C intae@ stress@ steroid ad(inistration@ renal disease Intracellular (ove(ent


16/17

o 'etasti(ulationo )lcalosiso ypoter(iao Insulin

Clinical manifestations:o (alaise@ (uscle &eaness@ fatiue@o decreased reflexes@o faint !eart sounds@o !ypotension@o cardiac arr!yt!(ias@o increased sensitivity to diitaliso EC? c!anes

.dministering A, $otassium

8!ould be ad(inistered only after adeuate urine flo& !as been establis!ed *ecrease in urine volu(e to less t!an 20 (>/! for 2 !ours is an indication to stop t!e

potassiu( infusion 4rincipii de trata(ent in !Calie(ie 1F $orectarea cau9elor care produc translocare intracelular5 de potasiuo 2F nlocuirea deficitului de potasiuo C$l (ax 200 ((ol/l/orao C$l (ax 2@, ((ol/ /2 oreo )d(inistrare pe vena central5o )d(inistrare cu po(pa de infu9ieo

*iluarea solu_iei nativeo Donitori9are frecvent5 a alie(ieio $orectarea !ipo(ane9ie(iei asociate

yperale(iayperale(ia 8eru( 4otassiu( reater t!an ,F, (E/> Dore danerous t!an !ypoale(ia because cardiac arrest is freuently associated &it!

!i! seru( CB levels

Causes:

*ecreased renal potassiu( excretion as seen &it! renal failure and oliuria i! potassiu( intae ypoaldosteronis( 8!ift of potassiu( out of t!e cell as seen in acidosis@ burns@ crus! inNuries@ infections


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7edicamente care produc hiperpotasemie

In!ibitori ai en9i(ei de conversie aianiotensinei

)ntiinfla(atoarenonsteroidiene

'locan_i ai receptorilor pentru aniotensina $iclosporina

'etablocante acroli(us

*iital5 4enta(idina

*iuretice antialdosteronice 4enicilina potasic5

eparina ri(etopri(sulfa(etoxa9ol

8uccinilcolina

Clinical manifestations:o 8eletal (uscle &eaness/paralysiso Irritabilityo )bdo(inal distensiono EC? c!anes J suc! as peaed &aves@ &idened W8 co(plexeso eart bloc

$rincipii de tratament in 5aliemie

1F Gprirea oric5rui aport de potasiu 2F eversarea efectelor (e(branare clorura de calciu 10 % ,10 (l #3@6@. ((ol 3F ransfer intracelular luco9a ,0 B insulina 20 O bicarbonat de sodiu ,0100 ((ol aonisti betaadrenerici F Inl5turarea din oranis( diuretice de ansa r5`ini sc!i(batoare de ioni ad(inistrate n clis(a sau oral epurare extrarenal5

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