เวชบำบัดวิกฤตพื้นฐาน Fundamental in Critical Care

clto j

L'rlJU'rLin?nrlfl ug1u

AKt fi:l1ufl,: nq'rro,r1lnfifinr:non,na'rvfirfito' norirorfiulra-us"ooteq;rflurJnotnnt:

rildurrrilnorrirfr (functional changet prerenal) vionrrt duuttln n:tntrt (struclural change)
roilnflld lou AKt fioldd.rlulnilnfinia1ufi1rudr'lnmut{oi.r 1ct<o1 o;iiodunrr: mt rfiafi

Ln rdfl1l1auaaauuflv0 qto?uavui {a-{frf,l \tu.{u.,'-

t. finr:rfildurardl creatinine tu65l > o.s mg/dL (> 26.5 mol/l) nrulu +e d'rTil''

z. finr:rfildurorri.r creatinine lud*r > t.s nircrndr creatinine rdunru'll z iud

nirurr
3. r.lirrruflaamvriaunjr o.s mt/kg/h Geroiflriuu'ru o drfu':

o"rruun AKt oonrflu 3 :;a:60 stage 1 fio stage s 1or:rtfi t 1 lnrL'lfinr:urlduuurJa,r

na{Fi'r creatinine lufi*rnSonr:aoa*na.tlir.rrruioan; lun:ninornrudvY,:oorifiqflu::u:firLfin
9t1\:nu [fin1yuf] stage gt'l tnruTT n?l ?uul\tr]1nn11

1nr:rofer- uont staging ot acute kidney injury [or"o tttJo':tr n ton nrr dr't 6,t z-+1

'1 1.5-1.9 time baseline OR < 0,5 mykg/h for 6-12 hours

] > 0.3 mg/dl {> 26.5 mmol/l) increase < 0.5 ml/kg/h for > 12 hours
|2 < 0,3 ml/kglh for
[g 2.0-2.9 times baseline >- 24 hours OR
Anuria for 2 12 hours
s.o timJasetine oR
I
toIncrease in serum creatinine I
OR> 4.0 mg/dl (> 353.6 ttmol/l)

Intiation of renal replacement therapy
OR, in patients < 18 years, decrease
in eGFR to < 35/min per '1 .73 m?

.[1ui{n rufdrr-6rf<rnr:d!rfluro.rln\l rilur.ln6*nynr:n:rlni': tl?nfl serum creatinine > 4

:rmg/dt (> 353.6 mout) rt:{rItida..::-nb'td1u FRT bj'jrc:d'rEr{oilt{i'lnfinr cynne-oaulu

!stage 35a lu{ilru rfinfiarqriounir tB flfis!:rr estimated glomerular filtration rate (ecFR)

< 35 mumid1.73 m'6,: rytfiuTfru'ld creatinine clearance (CrCl) fif{'tuxru'ta1n Schwartz
lormuta r:'ldirnrrific{i'u AKI staoe 3 niun"us

r,rulr{:Jrudfi stage flo{ Rrt iiq,rduo;finl rdu,:ro.:nr:rfi!6ioulo:nrrrdarnr:nrr

fnumouvrulo (RRT requirement) lndu

Clinical Presentation of AKI

{rJru nrt o'ree:lrjfiornr:tn"l (asymptomatic) fir nn riulripu:.: Toflet:revtun't:niirl
duraJ autl ttn: creatinine lnu:r".lrdq a1n']:lla:olnr:lloo.riirir4irurlnruuurntitdud nr:fi

iawia.Management of Acute Kidne)- Injury tau'!*g? 547

volume overload [nr uremia {ilrufifi uremia o'lae: 1diuo.]n1liiaa1yT oduld oliuu fi'u
fi:cTnuz lmetallic tastel fi:.r lrffcornr:d'u {lru nK fifi metabotic acidosis :uu:,:l;noldn
(Kussmaul breathing) firJraafiafi hyperkatemia ?u!r:\role ldruornr:rilun (syncope) exl aiu

lnfinoir lnypotension) nianrr*r'rtlvqnrdu (cardiac arrest)

alcurj.rln?rfl tfll,l nonoliguric (rloRrrvunnir 400 mL n'oxiu) otiguric (100-400 mL sio
rTu) via anuric (< 100 mL daxiu)

nr:fnil:cr-f,

nr:'iin!::ifi nr:rfi urdoutnorruqaat AKt oon rfl u 3 ndil60

1. Prerenat cause: rJ::i6nr:qryrdurir un: rn6ou:' niu fra.,trdu n6o1:nd,lf,r.nrudnlnr:fi
renal perfusion nno,i niu congestive heart failure r'rianrrcfran

2. Intrinsic renal cause: oreq:fil::ifinrrqqrfiudtRny rn60u:njurdurfir prerenat AKI

:l::ifildiuor:frd (contrast dyne). n1rldixu1fiifiBsio.ln 1nr:r,,rfi z;. ornr:uao.rrolnr:fi

lrlproteinuria trju flaorr;rflur',lo,t [nyornr:!tf,f,],ua\: glomerulonephritis 50 vasculitis lriu

palpable purpura nr:lorflur6on (pulmonary hemorrhage) uncfloorr:fif1dr,:rdo 1n"r"trriul
3. Postrenal cause: rJ:;ififi uansflrt:n::lunrsrdufloare: rdu benign prostatic

hypertrophy T:nr:Fryrrouir':n niofi':tunrr rhu:Joorr; 01nT rfid1d'qAanlrlriiilflflrry (anuria)

ornr: rgri]oarr: rrrdiloom;Iiloon (urinary retention) nrrrfio potyuria oair.tri:.r otiguria,/ anuria

ri.:d'fi.:nrr: intermittent obstruction roorr.:r6l:Jootlv

n,l?nfledl\tn1il

nrrn:rcir.rn r u d'o,: ri,: nhtul':v rdu rnrird

r. {il':ufidori,rdto.onr:inurdtu Rnr a rirl ri o oiruni olri

1.1 alfl'tllla.l volume overload (edema, hypoxia, acute pulmonary edema LLfl:

volume-related hypertensive emergency)

1.2 aln'ltnsn uremia ltiu nr:r:Jduuu nr cognitive function, alteration of

consciousness. flapping tremor (asterixis) [tn; pericardial friction rub

1.3 01n1:10{ severe hyperkalemia Lg1.l syncope, bradycardia, heart block, cardiac

arrest irrnirnr:t deruu:Jo,llat Et<G

2. nT :nrrejrrnrufirLanfi,o1:nfirflufllltE?otnrry AKI niu arnr: hypovotemia tufi:Jru

prerenal AKI [[fl; ischemic ATN :aflITnUir?ruftttlir livedo reticularis, palpable purpura'lu

{ ta glomerular disease

3. o:ro ro'nuruyrarl:nlnmur{ai,,rrdarruncrn AKt on too cxo n5o ESKD [d n?1rJ

faro . ad c ysofrt?!frdnfdru uremic frost firyf,rulfir nrryfin
nq=frrfru

548 retlhrjoinqnfrugru

2mfl.tf, u6[o{ Drugs Associated Wth Acute Kidney Injury6'

:'''t: ' NSAIDs, ACEls, ARRS. cyclosporin, tacrolimus.
radiocontrast agents, amphotericin B.
Prerenal interleukin-2, diuretics

I - Reduction in renal pedusion through Aminog lycosides, colistin, rad iocontrast agents,
amphotericin B. cisplatin. antiretrovirals
tI_I alteration of intrarenal hemodvnamics (adefovir, cidofovir. tenofovir, foscamet),
Direct tubular toxicity (acute tubular necrosis)

t_
Rhabdomyolysis
Intratubular obstruction by precipitation sultadiazine, foscarnet, indinavir. tenofovir,
of the agent ethylene glycol. triamterene, large-dose
vitamin C

Allergic interstitial nephritis Penicillins, sulfonamides. ciprofloxacin.
vancomycin. macrolides, NSAlDs, omeprazole,
lansoprazole, ranitidine, phenytoin. allopurinol

Hemolvtic-uremic svndrome CNls, mitomycin. cocaine, quinine, conjugaled
estrogens

[I"'"'*- intravenous immunoglobulins, starches,
mannitol. radiocontrast agents

dsrnln.:crnranor:dr{6$ o *nt z
fialrfllfi4 : NSAIDs, nonsteroidal anti-inflammatory drugs: ACEI, angiotensin-converting enzyme inhibitors: ARBS,

angiotensin receptor blockeG; CNls. calcineurin inhibitors

Differential diagnosis
n1i'r{fi 3 afl nrrifilduuunl:nraynl?:ili d1t qlro.! AKI

Approach to Acute Kidney Injury

lurrtilfr ffi fi drdrprfl urirn"r u:nfi ado,,rot;ufnfinnx1t.td16'rpta,rnrrl nrc 6o Tquda.,rrilr

r:iurr:dlu{rlrufrfiI:ndugrui #EJ''reionr'rc nxr :T rrf.:tu{r-t':ufir-hudruT:ndrurjaujrrflu
f,rrfiEra\: nnt lmrm,ri +y ua:fia,rifioaunr; AKt ifi1d6stttrirvu;fi t udrrirnr:frr.Lduuocufilr
d1lflE riio{?1nd1R'r?r AKt lullrnillnrauerEj{fidn:rnrl6lafiinrrndu ;rLi 1 udnnuu?vr1\)n1l
ifiqouun;inurnrr; AKI

i\'lanagement of Acute KidneI Iniury tr,:njr? iauyia 549

gsrr:rnfi rLf,n{ Differential diagnosis of acute kidney injury

PRERENAL AKI Possihle Caus€s
Intravascular depletion
Effective circulating volume Sepsis. hemorrhage. vomiting, diarrhea
lvledications Congestive heart failure. cinhosis or hepatorenal syndrome,
INTBINSIC AKI nephrotic syndrome
Acute tubular necrosis Angiotensin-converting enzyme inhibitors, nonsleroidal
anti-inllammatory drugs
Glomerular disease
lschemia (similar to prerenal AKI)
Vascular disease Toxins: drugs (e.g.aminoglycosides), contrast agents, prgments
(myoglobin or hemoglobin)
Rapidly progressive glomerulonephritis: SLE. small vessel
vasculitis Wegene/s granulomalosis or microscopic polyangiitis).
Henoch-Schonlein purpura. immunoglogulin A nephropathy),
Goodpaslure's syndrome
Acute proliferalive glomerulonephritis: endocarditis,
streptococcal jnfection. pneumococcal intectjon

Microvascular disease: atheroembolic disease (cholesterol plaque
microembolism). thrombotic thrombocytopenic purpura. hemolytic
uremic syndrome, HELLP syndrome. or postpartum AKI
Macrovascular disease: renal artery occlusion,
severe abdominal aortic disease (aneurysm)
Allergic reaction to drugs. autoimmune disease (SLE or mixed
connective tissue disease), pyelonephritis. infiltrative disease
{lymphoma or leukemia)

Benign prostatic hypertrophy, prostale cancer, cervical cancer.
retroperitoneal disorders, iniratubular obstruction (crystals
or myeloma light chains), pelvic mass or invasive pelvic
malignancy. intraluminal bladder mass. neurooeni0 bjadder.
urethral strictures

fil'lUlt'ltl : AKl. acute fenal failuret HELLP. hemollsis. elevated liver enzymes. and lorir platelet counti SLE. systemic
lupus eMhematosus

550 r':trirriainqorfrunru

4n1:1'tfi l!flo\l Common causes and risk factors of acute kidney injury

Sepsis Dehydration or volume depletion
Critical illness Advanced age
Circulatory shock Female gender
Burn Black race
Trauma CKD
Cardiac surgery (especilly with CPB) Chronic diseases (heart. Lung, liver)
Major noncardiac Sx Diabetes mellitus
Nephrotoxic drugs Cancer
Fladiocontrast agents Anemia
Poisonous plants & animals

!0ne'tn6o.idnlT;r6rrarq:rqd'r'rnruorir':nvt6ro llfir nt:yt6douri1.r r:n'tr (clinicalies0
tdu nr:'l"n cardiac output fllTj:ttfiu preload ttflv preload responsiveness n'l?59 intra-abdominal
pressure Ltfl;n1?n:revrrtfio'r:Ji:j6n1: nju creatinine, BUN, calcium, phosphorus. albumin,
uric acid, complete blood count [!a: liverfunction test [[R: creatinine kinase flu rhabdomyolysis)
fi rJ::1uflilunr:6iududlrrnrrn;inb1n'r'l: AKI

Urinary index

nl:gn'tg urinary indexes lntr"o sodium ttnt creatinine lunaralr ttn;:Jad1x:cidxu

fil lfiunr:vti*t'tufl0.Ififloodafin (renal tubular function) 'h prerenal failure evfin'l:oon,llo't

renal perfusion ttfly GFR ua:n::{unr:qnnn'l (reabsorption) flo{ sodium tto:frlotu renal

tubule o-.niu6.lllo'rtmoiru::ui'r.r creatinine lu:Jdfl't?:LLflslln1dtJ't [urinary : plasma creatinine

ratio) fid1{,:n'j1uR;virnttrrfirdusat sodium tuianrr;fi"rn'jr rfiorrliu!tfitrlfiifltJru intrinsic
axt lnrsrsfi s;

5nrmad uf,o\r characteristic urinary indexes in patients with acute kidney injury due to prerenal

or intrinsic renal cause

Urinary sodium concentration (mmol/liter) <20 Rcnal causes
Fractional excretion of sodium (%) <1 >40

Ratio of urinary to plasma creatinine > 1.5 <20
Ratio of urinary to plasma osmolarity >20 < 1.1
Plasma BUN to creatinine
Fractional excretion ot lithium (%) <35 < 10
>20
Fractional excretion oJ urea (%) >35

.Itanagement of Acute Kidne)- Injurl' rff,lrt? imaia 5Sl

Continue to monitror if

high-risk

tunaqfri ttfiBn approach to acute kdney injuya

552 rruriljnrinqnfrugru

dafio::itlunrlr aatn urinary index

. afiFractional excretion of sodium lfelta; d,rn'rurruo1n ([UN, / Pnl / [Ucr / Pcrll

riurldrorr:lu{:-lrrfitflu otisuric nKl rvitiu rirdc;drilr'ldttilannhjldlu{neudri1d,il6ud':r
flna'rr;. {rJrufifi glycosuria un;{rhu cxo f,rfi sodium transport finrJnfiaqjrrd':

r !Intrinsic renal AKI arnul\:fl'ltfiE ?v FeNa riaun'ir t X 16 niu lurcu;tt:n1a':

glomerulonephritis io tubular lunction tftilnn' uiolu{rhu contrast-induced nephropathy rlnl
pigment nephropathy (myoglobinuria) lfio,lmnluflotnm:dllfi renal vasoconstriction tflu

nn.[n dr druddrtrirfi o nxt

. Fractional excretion of urea ([U," / Pu"] / [Ucr I ec4 firJ:vTutritu{rhufildilur

rhiocrr; ua;lu non-oliguric AKI tdo.lorn urea o:qngon6'1fi proximal tubule i'tltrilutr n",l

riu'lu prerenat state urea rv4nqnnffilrnrirtrifirir reuru rioun'jr gs% tfiaaernurlTufloarrv
rfior4nnro;oonqldfi Hente loop ttfl: Nacl cotransporter o'.triuo:Li:lnrudr FeuN dauntiu

dhinur:ntddr FeuN ld donm:fi fi nr:rtfi uuu:Jo,:nrrqerndlfi proximal tuoute rriu {ilru1d
osmotic diuresis rra:{:Jru cfo

Urinalysis

' "n?lnt'te:1fl fl'r1:ou'lnfl J [0u6 lu$" ijru AKt rnflu fiil:;Ttrrrilunr:'1fi[und1! frlrs{ AKI

Tnu rarrvorir.:ti,rh intrinsic AKI

1. urine sediment lu prerenal AKI dxutJlnoi nfi (bland) uiofi proteinunia tfinriau

rroni,:oreflu hyaline cast

2. Intrinsic renal disease

. !fiiaGlomerulonephritis alyu dysmorphic red blood cell. red blood cell cast

Proteinuria

o Rapidly progressive glomerulonephritis (RPGN) 13ti{u telescopic urine sediment
. Acute tubular necrosis 01?r,lu "Muddy brown" granular cast un: tubular cell

cast

. n1rfi eosinophilluflao1.]:vrulfirfttu acute intersiitial nephritis !!a: atheroemboli

3. Urine sediment'lu postrenal Art lvrJn6 uaooio"lqornu crystal 6lpJdr.:rar crystal
arldrtltl o nor rrqtrs,:fir'lurr,r rdufl ooll:1d

Radiologic study

1. Renal ultrasonograptry lsgilnfilnevfitu'rou11 10-12 tr. nr:nu.lnturotfindmrir

cortex :r1{ un:fi hyperechogenic rj.:d6.tnm;lnrrutisit renal ultrasonograpny rflunrrfrr:du

Ilanagemenr (f Acute Kidney Iniurv tn?qgj inuvin 553

fififianlunrriflrii'u obstructive uropathy lnuc:r,rrirfi ditatation aosnrrrfiurlodrryl?rfioda

1nfi fi nr:oofi'u (hydronephrosis, hydroureted

donr::yir'lunrrld renal uttrasonograptry rdoiricdu obstructive uropatny fin-lri

o r.lnflun1{ (false-negative) dolrhrllnr:rurura{ collecting system'lun:rf,{irflu acute

obstruction, retroperitoneal fiOrosis via{rJrufi hypovolemia irr.tdru

o o'tQe:vt hydronephrosis'luntrvdul tdu reflux nephropathy, nr:n&,:nr:fi, papillary
necrosis riafi rufifl Rorryrjirrruuln Ldil rltiildiuulrTlflcRrrt

Z. 'lufirirUd,rfl! hydronephrosis arqfiqr:rurni spirat CT without contrast media rdo

rjrvrfiuurfirtunrnrdxlldfll?! rra:ol"rrru .:n"finr:qoniu nr:ni intravenous pyetography (tvp)
ovjier':rrrfiutdon'i:rfio contrast-induced nephropathy rn:nr:fior:nn inurdnuunyttirr.,: t6u
lJflfl']1; tl\t9t'lutftUtO lyoU't{8\'[ufr ']Uf.trdfr anuria U5o urosepsis irldtu

Renal biopsy
lou:Jno'{rJru AKt hjdl rilildo.rlir renat biopsy unr{un:nifin,,offtri.ld1r qna{ AKt !flu

tfo intrinsic renal uay'lri}i ATN nhl RpcN

Management of Acute Kidney Injury
tttlutflu general managemenl lrfl; renal replacement therapy (RRT) efrrflnr:

fl ar niu uo v nr:fn u1 AK I In utd u1e cn on rird,uy".ldo rYo'l:i

General Management

:J:cnoudru

t. nr:inr*r rfi a*filtI:nii rfl uRr mqtaln'r.l; AKI
't.t rrfilzn,r: urinary obstruction nr:tdgruCrui6ld1,]y (bladder calheterization)

'lu:ruiiosdunrr: urethrat obstruction rdu fir.l::i6:J.rniaom:*siriruliloon flr.Jrufi anuria nllq

{vlx futt btadderlouranr:'tufiilrun{ilrdu,: niu rurltrmu {rJruiifil:nuioqrsrrqfrbdura-.:

lun:h{rruq.ro, adfi benign prostatic hypertrophy nr:'ldRruo.tuilanrryrird.rg'lfirJ:yrfirrJilrru
iosrT :lduriudr uavfineruelnnr:inurlu prerenal AKt 6nd?u

t.z ufiln hypovolemia 6?afi1i1.!Y1 isotonic saline n1?:yfin'lirffl0,fi{ilrufifi otiguria

ttio anuria Totrrovlrcfi ruinqn a'refirJ?r'rru votume (sodium) r.trir.lnrurfjildu udtl n:refltl
edema dlrn"ufi intravascular votume ngnnld ri',rr?upr::*fi1:rnunlun niu'lfitrr inotrope/
vasopressor lufiilrfl CHr rfja rdr.r effecrive intravascular votume turrmjfrrjnyrn :;rftu
intravascular votume 'ldlrid'qrquorrna.flri isotonic satine luo'nfl eo-t zo muhr ltnyfionlrJ

554 rrrnirfolnqmfrugru

:J?l'rruflcott:dr BUN ttn:dr creatinine n't:li'l invasive monitoring rtju nr:io central venous

pressure (CVP) tio pulmonary capillary wedge pressure (PCWP) nrrrirlun:rfldnrrr.l:: rfiu

intravascutar volume lrinur:nrirlddrui66ur

lu{rLrufifi hypovotemia rfroQrnnr:lfinr:rir firvruir{rJrrfirloarr;rfrrn*u BUN unv

creatinine ona.:nru'lu z4-aa drlil{ 1finr:ified'u'ir{:huiinms prerenal AKI rroiflr{ilrald$t

cr:rirodr.lrfiurvroudr rir euNl uflY creatinine ti.rn,rrfilq.rdu nr:ifiqoufio ischemic ATN

t.s nqnurfifiritdolm (nephrotoxic agent) (61?1,ifi 2)

1.4 'lfi specific treatment niu lu hepatorenal syndrome nr:fnlrd6dqn6onr:

:Jgnrirunir lu lupu" nephritis nr:ltinr:insrdru corticosteroid Llnt immunosuppressive drug

2. inBTrl?r llvnndautal AKI 1nr:rlii o)
2.1 inbln'r?vfiltrirrn'ullvnon r6ao (iniravascular hypervolemia) Tou furosemide

80-100 mg lrrrdurfionrr'r vSofiunarir{siorfjo,urtrdurfiooo'rtuo'n:r 1o-+o mg/nr flrrJilrrnt

isa, r:rT.'rlriuiu.,,l,ratu t f':Ilflfifierlrulrfirrt 10 lurosemide tiJu 200-2so mg iorildurfiooo'r
firri,lfi:loarrciou nia{:-hua{'lunrrrinqfi niufi hypoxemia da.:rfier: rinurdru RRT n:rfi

dlrjnrorouotsia furosemide ?Ju'tgg.inxlfiqou't tdo,rlrnnr:tti furosemide lrnn'j't 1 gm oioiu

.[d"

arcfialfirfin sensorineural hearing loss

2.2 lr/letabolic acidosis nllinulfiru Sodium bicarbonate nr:ldrfiofi metabolic
acidosis ?u!r?\: 6o fi pH ntrni'r t.z via zzd:: uco,- turfiaonhnil 10-15 mEq/dL daa?rr:i{

fion,:'hi sodium bicarbonate vr.:rftut6anra'rcvri'rlfifinarrvnndoufidrd'qf,a elfi sodium tir

ddronrurjirrru:.rrnfi volume overload un;rir'lfi ionized calcium oontld

2.3 inu1nl?i hyperkalemia o-tuon,'tlunr:r.'1fi 6

2.4 drl'ruiifi calcium phosphate producl (ca x P) 1nn'jr 72 o;fin.).l:J tdu':danr:
rnn metastatic calcification n-rrfu'lufi:-hu nrnirdnr:tilnn:cd! phosphates lns aluminiu.

hydroxide riou rda ca x p riounir ss 6,,rr?r.r1fi phosphate oinoer fifi calcium ttju calcium

carlconale y3o calcium acetate

lun:rfifiinnrruaur:ndorzor nrt Ieuuilil16eln fio.,:fier:rurinurfnu RFT

3. l"lonr lnuldrir{nrnriln rriu urr.l!6ru: lunre: AKt q:fidr creatinine lrinid

fi''.'niu'lilnrridorJnr:oirr1 uiu MDRD equation ria Cockcroft-Gautt equation rrtflunr':r{rurn-r

nrdr crR [sinr:fiafin"n'ir'lu AKt ri'] cFR a;nno{cufiac.in'ir 10-15 mumin adr.rrduunaiu ua:
ldd'rd'lun1r:liJonturourdrtl fini{nrndr.rnramrrln fld.rornfirhuldiunr:fnr*rdru RRt dar
fi nr:!iu rfr murn urrJfr fi ru:6neri,,:1n u11.r1o11 0{ u1a sdu nt rtfi ato,: RRT

+. lnturirrinlufiilra nrl

I\'Ianallemenr of .{cute Kidney Injury trtrji? iauyin SSS

6n1:1{fr [flo,] Supportive Management of Intrinsic Acute Kidney Injury

l\,letabolic acidosis Festriction of salt (< 1-1.5 g/day) and water (< 1 Uday)
Consider diuretics (usualty loop diuretic)
Hyperphosphaiemia Ultrafiltration
Hypocalcemia
Hypermagnesemia Restriction of oral and intravenous free water
Nutrition
Restriction of dietary potassium
Drug dosage
Discontinue K supplements or Krsparing diuretics

K.-binding resin
Loop diuretic
Glucose (50 mL of 50% dextrose) + insutin (10-15 U regular insutin) tV
Sodium bicarbonate 50-100 mEq lV (only with concunent acidosis)
Calcium gluconate (10 mL of tO% sotution over 5 min)
Hemodialysis/ hemof iltration

Restriction of dietary protein
Sodium bicarbonate (if HCO3- < 15 mEq/L)
HemodialysiV hemofiltration

Flestriction of dietary phosphate intake
Phosphate-binding agents (calcium carbonate. calcium acetaie)
Calcium carbonate (if symptomatic or sodium bicarbonate is to be
adminisiered)

Discontinue magnesium-containing antacids

Restriction of dietary protein (< 0.8 gr,4<g/day up to i.S g/kg/day on

continuous venovenous hemodialysis) 25-3O kcal/day

Enteral route of nutrition Drefened

Adjust all doses for glomerular filtration rate and renal replacement
modality

Clinical evidence of uremia
Intractable volume overload
Hyperkalemia or severe acidosis resistant to conservative management

556 renirrjainqnfrugrr

4.1 d.'r,r'ru 20-30 kcal/kg usual BWday loufidodrutotnriTulauorn 3-5 (q{qo

7l glkg/d rroJhrJiu 0.8-1 g/kg/d lnuinrt::o'l serum glucose :lx'jr',: 110- 150 mg/dL

4.2 n6n rduonr:l'rriororrr:'[:J:6urdo:]o{niuvioncnonrrinurrn nnuln (FRT1 lou

111 tU:9U

o 0.8-1.0 glkglday lu{ilru nypercatabolism dhifi hvpercatabolism ttflv'lrifi

rio:t,ldlo,: nnr

. 1.0-1.5 glkglday {:-hu moderate hypercatabolism frinurdru intermiilent

RRT ['iiu intermittent hemodialysis

. 1.5-1.7 (fl,lqn 2,5) gr/kg/dav {:-hafifinrt severe hvpercatabolism unvinsr

d?u continuous renal replacement therapy (CRBT) il30 peritoneal dialysis

Renal Replacement Therapy (RHT)
nRr fidori,rdtln:di:-nurrunun:nfioulo{ AKI louulrtn:nr:insr :vA'url:vno.t'lrildzun

Prevention of AKI

rvnaudru nr:rrfillrlo{ufre:rio'hitfio prerenat faiture ttdoflotn"unllrnn ischemic ATN

'leudo.rrl:vtfiu volume status uo:finr:'lfiar:rirod'l{! lYfl (adequate hydration) duriun'r:

tdurn{r vasoprssor/ inotrope lururofitfltJ't;ffN Toufi rflltrrurdo'lfifi renal perfusion tfiutno

drr rYur ouSoldar: un; uT d rijuliudolnrioud4n

1. Hydration

nT rtfrnr:rirergjrutfil renal perfusion ttavt4oc'tt nephrotoxin tutloarr; tdo':crn

n.ro'rrcr:rir (votume deptetionl rfluflol"u rdu,:dra'rpoianr:rfin AKI ttfiilriilfi RCr d,rflnrr

nnro.:nr:'lliflr:u*ruJiu!rfiut-rTousn,'triu placebo 'tunr:ilo,rriu AKI finru rroirflufruslfirYudr
nr:lfinr#rttirfiu',rroun;rnrr;srfi:J:;ltmrilunr:io.,tniu AKI dftd1tflq 1qlnu1 aminoglycosides.

amphotericin B. cis-platinium. trflY acyclovir truti'o nru dfinlrn lodinated radiocontrast,

rhabdomyolysis, ufl; tumor lysis syndrome

orirrl:fioutuioXriufirnngrunri:-rar1u'ir {rJeuinqfirrrnvt{r|ru AKI dfin1xv fluid
overtoad finruf,irfiuidn:rnr:rfludiardo.rdu*'o d',,,:rfudoulfior:rir uri{:-l'ra nr:n:'loi'}cn1ulrflv

dldu'ir{rlruin, ry AKI sfiofioo!fius.:sianrrlficr:rir (volume responsive AKI) xia1ri rdu

n'llfrl'le jugular venous pressure (JVP), skin turgor, CVP :tlvt',1 fluid r€sponsive test nr:tt{
or:rirlu{rlrUfio{tun'r'r! euvotemia ia hypervolemia arcoldr}i{r-hurf,on1,)3 fluid overload

ruarfi nrr rdu.,rsionr:rfr udinrfildu

-uanagement of Acure Kidne.i' Inj\ry ttfrv,g1 inwin 552

duirrfienotorthfrl'fi ornnn'nSrurr{nr:urrrrfluflclriuvruirnr:resuscitation Tnu

tdar:rirsfin corroio dsarosioo'n:rnr::aoiinLiunn{ir.,rorn crystaroidl- 6.:n.::1fi isotonic
lactate solution (RLS) 'l nr:[fillun;:"nBrnrrvlr9l
crystalloid ttiu normal rstrarlfinioefl'oliroriuRnirn:grfeior's
AKt lu{rJrun{rrdu.,r unv'lunrr:-nrrfi rufifi nrr l:L
nr:rir'lunaao16oon "

ludr uoncrnf'[rinr:lfi atuumin 'lu{:-hrouTrrquronlar,, unyr6n rdu,:nr:id cottio n{r nydro-

lilxylethylstarch 1ues1 rfu 10%o pentastarch (HES 200/0.s) r!R! 6%io tetrastarce (HES i30/0.4)

{:Jru6orrdo'lun::uoTnfin lsepsis) rfiamrnnuirrirlfirfiqnrr: AKt rr..rfifu fiRrrrrda.:nrrnr:inur
drr Rnr grrsu *arfioh:rnrlfiufiinrfiildurfroulliu!rfiurrirnr.linurlou isotonic crysraroid,d'5

2. Maintaining renal perfusion pressure

rlo{unn'n z rh;nrrfinir'hi renar perfusion aoor ldrrri systemic arteriar hyporension

(shock) ttnc abdominar compartment syndrome da uu:ritrt'rIil rfiafnurtrtfi renat perfusion fi

lfitJ'1 :5[ ]J:J^-6 {UI

. urnqrr vasopressor fiqrnfiidrtdurdondr d'\:riudari,rdfidrn'eg6o nr:tdurn{ild

drrfiunr:'lficr:rirluftJra oistrtbutive shock lrirr septic shock rfiolfifi intravascutar votume fr

tfiu.J oun: perlusion pr"""ure dmrr:fl louorqehuiudo,:hfiurn{doi,:uoid.l,rrL?n1 xo,tnlt

:"nurlu{ilrudfiarrloulnfimntrrrn fir:;o'nlllRro'jr vasopressor iiruro6..:rfiul:ifinarirtrirfin

severe vasoconstriction llnt poor tissue oerfusion

o 11fl fi a"n31uyl1lnr:rrrlltJ'luio?illkiarrlrrnol1[d'ir vasopressor rfi nlofi

:Jt;RrBnrrq.l4ntunr:flordu nKt un;tunr:inurfirJrt septic snock fifinmc AKt nr:finrr
FCr rurotrr!r'rJiaurfiulnr:inurnrr:6ondru dopamine un; norepinephrine rr:.t'ir6'n.:lnr:
ritu6in:uyi,,:nrdrlrum n (renat function) lrirrnndrrrYulounuRrr;ul:ndouda arrhythmia
lu{:hd:hurdru dopamine'tfln'j.r norepinephrine'u

. tTrlrifi{oXn'irnrrlo-uTafinrrirloioqyrfiu.r aeionl:fla,lriu renat hypoperfusion

{rdrrrrrgm.,rrirurrutrirtfi mean arteriat pressure rJtlru 60-65 mmrq tufuJrurfrlluo:

aro g.rndrdludrhuq.raru uov{dfi I:nnruo-ulnfi nc,,roei rGr

. n1'tv intra-abdominal hypertension o:drTrifi renal perfusion noal rra:rfio AKI

n-{usue'.ldo.rrHrry{,rtu{!rudrdrl.:rionm;d '[qunr:innrr dulunrrrrr;floom: nr:uflbod'r,:

:rorSro;drlfi nrirdto.rlnnn'urrrfl uiln6ld"

3. Nephrotoxin-specific prevention
lnur,r''rlilar:rfinldu,:ar:fiiourfiuiuriurYuln (nephrotoxin) n:rfiifierruoirrflu fiuur

lrlnr:fl arnju nephrotoxicity gtnltun:drturinvtfinrilrd

3,1, Aminoglycosido nephrotoxicity

nr:tfi n16u.:nr:'ldu't aminogtycoside tu{rhafi fiflt{urdu,rsionr:rfi o nephrotoxicity

558 rrmirrinlnqmCugru

lduri {rLrudfi votume depletion fiT:nfrugrurflul:nlsr, lrnd!iliaI:nrielo. 'td aminoglycoside
irrdrarrTlfloorrrturngtnsolddrrfitt nephrotoxic agent 5u1 tun:rfldfinrrl.l'irrfludo':ldm

n{ld nr:rfiofiudalrleraenflfianr:fla,lriunrr; volume depletion 'lu{rhu un:nr:rirn-o:;l:

irlrT arnr:inurtr{rioun'j'r 14 nrarfiusiolstq'tn aminoglycoside rfinernurgn endocytosis ttns

d;flrtu proximal tubular cell [flctfio,ic']nnnlndrflunnlndfinrl6rdr (saturable process)

dhiuluvrrovrqtfi nrtld aminoglycoside {ua; 1 ni': (once-daily dose) c:Ran1:tfiel nephrotoxicity

ldlrnn'jrnliurj.:'lfiriun: s n*i (multiple dose) ldomrnovnorlirirruur:rlfio;o u trbular
cell nlr rvdun1rfinurd,,r njiul rfiuun1:'lfiurfi".t z ttu:: lnunrair meta-analysis vl!'j1n1:'hi

uTri.r e uuu'lfinrohiunnrir.,rnlunl ::fininraluntidrulniu un: fiuur}ir.riinr:}iu'r!!:rlr once-

'daily dose c:fifiudolniaun'jr'u

3.2. Atflphotericin B nephrotoxicity

vrrnrrvfldgtfi''r t ls to.r{rJrufi'Lfrfu amphotericin e lounrr ldu,t'lunrrtfie AKI e:

qrdufir$lur n ar oc ail r'iiildu nr:tti volume repletion i'lltn'u potassium supplement qvn0A'l'u.l

l6iu,,rto,:nr:rfin amphotericin B nephrotoxicity nrrfinur Rct uJiiu:irfru! nr:inurTould liposomal

fl!amphotericin A lu{rlrufifi persistent neutropenic fever tYl conventional amphotericin B

drrfinlerlurdurndu tgo/o lunajr tiposomat amphotericin B un: 34% 'lun{riinurdru

conventional amphotericin B (p < o.oo1) Iauil:vRrina'lunr:innrtaturvl',i z nell lrlrrcrnoir,r

nu" 1oun"r1:Jnr:1f liposomal amphotericin g n?o urfirurdo:lnci echinocandin u3o azoles

riaitfiolnril lu{rhudfi renat insufficiency renal tubular dysfunclion adudr 1nldoro"rfi.rfi.,r

cost-effectiveness dru rda{ernurfr'',inairrfi :rnr gt

3.3. Contrast -induced AKI (Cl-AKll

Badiographic contrast agent rfluorrfiqruttloo nxt tub'tnur::rn ylurBrir tfiqoro tfin
qtnnttfi renal vasoconstriction via rfl1lfiuleru'l:,0uD,t iodinated contrast media (CM) tdo renal

tubular cell nrrfl o':liu!::nolfi ru

3.3.1 tl7slfuJ'"71nliluJE/o,tnntfinnt2t cl-AKf

nrrrrdurddr6'ryd4n,uornr:fin Ct-nrt 6onre:lnrruriai.l lcro; uiafirir ecrn ii

nhurru1nuflJnr: MDRD fiaunir 60 ml,/min/l.73 m' riorfiuurvirn":-r creatinine > 1.3 mg/dL'lu

{rruuw > 1.0 mg/dt 'lu{n{'r nrurdu.l6u1 ldud {rJruu-rrueruiidlnmur{ai,,1 T:nnruo'u
Infiorq,: I:nrfttrdtJrfiflr (congestive heart tailure, cHF) {q.ta1q fififinrrsroorfl.llnia hemo-

dynamic instabititv {rl'rtlfi'L{urfififiuriolertfiodu1

nr:ri'rrinnnr:fifinr:6o cv rfi',rmn{:jruldfrlnr:ufi.lrnrr;rronr#r n'rry6on cur

rac AKt udr unvfi'rfinrtrc'rriurfro.l'Lfrir ct'l rflun{odnararrvirtornni.:u:nodr,:riou +a drfu.r

tu{ftudl!fiildurdu.o drrfi{rJra cKD lriorutnrunr:rir{crnn*'0u:nod'rrriau :rrzz nrr1r.r.:

\{anagemenr of Acure Kidnev Injuff ro?yg? inwin 559

r:fr.,rar:rnqorurdfiriueialn6ul Toura NSA|DS. aminogtycoside, amphotericin B, high-dose

loop diureric rioufr {r-truc;1d'ir: cv

nrrrfinrdurnrr: Ct-AKt lnu'l$n1?qi.t? magnetic resonance imaging (tl|Rl) jxrl

nirdq cadotinium chetates (cd) eyfio.,:::u"n:rfi'lufi{radrflu cKD rru:ri1u.l Taurourylu

firjru oiabetic nephropathy rds,rcrnfilu,,t.tunr:rfin Gd-induced AKt., uonorndu-.,rfi:ru,rru

Rr?; nephrogenic sysremic fibrosis (NSF) lu{ilrufifi AKt :uu:.,:un:'lufi:hu cKD:;u;fira

Tou eo fidofiriltfitu{rJru cro dfi "ern < 30 mumin/1.23 m, uo:'lu{rJru AKt fifid.trfinrr.r
{:Jrudlifinr:drfi'oilgnrirufi'l Ferioperative liver trans-
qlfl hepato-renat syndrome:urft

plantation)'z3

33,2 nfrnuf,il.E r'rd,Jaan iodinated contast media (CM)

nr:iintrvtl'jr bw-osmolar contrast CM fi nephrotoxicity lisfln,j1 standard CM

lnu:i:ylurfc;rioudroriautu{rt':afrfinrirfilqiln6ilrriou nrndlrr8'orautu{:Jrud..rfi chronic kidney

disease oqjtdr.rTauravrrvadro0.rlu{rhuturrnrufrfr renat insufficiencfa arir.ol:finrl tow-osmolalar

CM thnrfinnreiunliju hypertonic (ZO0-800 mosm) infinr:nrfifi iso-osmotar CM fi,,rfi osmotatity
200-300 mosm nr:6nur uliu! rfiu:Jfl"u iso-osmotar !!ny low-osmotar CU 'lu{r_hun{uoir,:1 u-r

lrigrrrrnn:rld'i1 iso-osmotar 6n'ir tow-osmotar CM 'lunrrooo-anrnr:rfin Ct-AKtru2.

leuoplrn{o4aluflo1iu uuvrirtfrld cM rfie nonionic, tow-osmolar r6a iso-osmotar
iu:Jtmrufrriaudqo drrrfunr:'lricr:rirtfin isotonic crysraloid turf,:Jrudfinlrrdu.iri0nl:rfia

ct-AKl

s.e.s nlfrffiflI1 (fluid adminstation)

rfluraa'ndrn"rglunr:flarrru crnn tu{:J.:adfinrurdu.r lorulfiar:frrfiq isoronic satine

tia1ruSS1 isotonic sodium bicarbonate (NaHCO") > 1-1.5 mUkgr,rh g-r Z drTrJo (arir,rrjot

r t'r1lr; riou{:JruldirL crvt un;siordo.rl:Jou o-rzrirturnn-l{r-huldi! cr,r rflrrr.nu'lfifiilosrr:

:rrnn'jr 150 ml/n nr:duit'rn.l (force oral fluid) Iildxuflo,rriunrtvdlu{:J.:rtfifinrr rdurgia

ct-lxt *n;hidrrfludo.rlfiorlirludrirudlilfinrrilrdurrdufiilrrfifinr:rirrruuo. nrflulln6un:

oai'lu euvolemic state

3.3.4 N - acetyl -cystei ne (l,lAC )
rfio'rcrnnr:rli dula.J o, fre€ radicats 'lu'[n orcq: rfluilc{'ufifj.:'lunr:rfio nxt 6tfi

nr:rjtor runc d,rrflu thiot-containing antioxidant 'lunl?flalrYl ct-nxt Tsulunr:finsrti,Jrfio

RCT ufl; meta-analysis dlu'lilqjuifilT tuc irilriunr:hff,'Ddl1fin isotonic saline (NSS) il50

isotonic sodium bicarbonate (NaHCQ) lr!.jrfiri:;Turilunrttirunonl:rfio Ct-AKl (serum

creatinine rfrrdu o.s mg/dt ifta 2ayol rrrilrinna'fl:rnr:rfiafiiflun:nrttda.rnr:nr:inurrnlmuln

(RRT requirement) lnaun'aynr:6fnrrfinllunnrirlniurYrnrju.h;mn:diinr*r ll'nnnr:dtdii.r ru.rn

:r1o.r NAc yrs,:rfiquaclitrrura,onr:fr Tqunlrlrj:flutriro,l NAC Elilri.i'qreil urirdoocrnrfltl

560 rrtrirrininqodugru

urd:rarlrjuvr.:unvfinnrrr:nfouriou 0m1d NAc d?tJfi'x hydration'lunr:fla.:dunllfin AKt tflvrls
'[ufi rhufr fi n'rurfi u'rsio clnxtn

drfifrsurn lrnviiui lr NAc finrtr unndrrdluri ooo mg fir 1,200 mg r-un: 2 n:s.t
lnudrurJrnfiurflfi{:-l'ruiurj::vrru NAc 1.200 mg iun; e nft rir t turiaurirfinnnr: siolfio,,t

qu 24-48 :irlil,rndtriT riqnnr: n:rfitd.:drl niu emergency coronary angiogram {rfiurtrcp
urtyiruuu:ri'r'hi NAc 600-1,200 m9 tv riaunirinnnr:urunrriurl::rmu ttsid:-huarorfinnrr:

anaphylactoid reaction Q'ln intavenous NAC ld

s.e.s ntlf,a,tfrudu?

lProphylactic hemodialysis/ prophylaciic hemofiltration, furosemide, mannitol fi

ilr :lunilun rrfl o,,rniu c | -AKt'

3.4 Heme-induced AKI
nr:dfifir*oiolortunrr;dGa rreme pigment drd,orrorn myoglobin'lu{rJru rnabdo-myotysis

rioln'urmn hemogtobin 1u{rLruiifi hemolysis uanrnfiol mnnr:fnurdtrnra,r rhabdo-

myolysis !ro: hemolysis ra"ndrdrpllnr:ila':njunm; heme-induced nxt 6snr:}{or:ri:rfr lrlu,)

nordoufillnm; votume deptetion tto:nr:flotfiunr:tfio intratubutar cast 1oufi1o{..:tr.r'ra
niotril renal perfusion nondun:tuqrnntr:trn t6on (ischemic injury) rfiuJlrrzuflaorr:rdo
'lfi intratubular cast fl4fl{[nJflonr:rfionr:qon-uturioln lintrafubular obstruction) :un'trfir.r

nrrri *rrarEo*rrr,:inarrc

nt:lfi normat satine (NSS) oi,,r ursir*illfoduT:nun:tfiria rda.:eunirnrlynr:daruro.l

ndtrrdarro: hemolysis nralil lnuo'nlnr:1fi4r:rt*rdauJiunlrJnll ?uu?{1ro{n11: vorume
depletion loalidl{:-hufifi massive hemotysis c:flonraoyrfiqn'r?: volume overtoad !!flv

pulmonary eoema irrnir{rhu rhabdomyotysis tdo,iorn'lunrrc rhabdomyolysis c;fior#l

irlrrurrnoonqrn rdu16oolroqjlundrr.r rdaii gnnhoru

lnaafl urur,rfl arrYr heme-induceo nf r fi d,:d

3.4.l rl7ytfrua11 tiitnsa.fl/'tefia heme-induced AKI

fi ru rhabdomyolysis fiidr phsma creatinine kinase (CK) Hrnnir 5.000 u/L" ylo

fi cr drdln*uadrroioriia.:nr:ldilnr:flo.rriunrr; heme-induced nKt lnunr:1fiar:f1rr,r

rnoa 16on

a.+z ntsf,atffu heme-induced AKt ifrflLnryrln rhabdomyotysis
{rdurmcyuu:rirlrilfi ttss t-z finrsiad'rfurlutirrn:nno,:nr:fnur rYrdda.:rilr::1,,r

}nr,rnuvrtndoufrrfioernnr:triar:rir l5r 1fiulil rdu putmonary edema lnurar{rc'[u{r-huo.,rorq

rtr'lcrrur{ofr u5o{:Jrulnrrar{ofe oiorrtriaorJ?rrruar:rlr1nufirflrylrutfildfiil?ilrruflooms

zoo-aoo lo.riarirll,rotirociarda,r unvvunnr:'lfior:rhrfiarir cx nrfiun:fioun'jr 5,000 u/L

trfanagcmenl of Acute Kidne,r lniury rn?DJ? inutia 56L

9.4.9 n1tilo,tin heme-induccd AKt ifrffifirilfrm hemotysis
ri{dTnunr:trlor:rhrdufi'ulourtr'[:lnr:i*rtfi uss luo'm:r roo-zoo la.siod,rlrr.]

3.+.1 nttitiJamzzlfifiuoitt (atkatanization of uine)
luvrrrnqufinr:drflaorr;1firflurir.,:oyasnr:rfln cast oen-u'lu renat tubute [fl;ao
nr:t figu hemoglobin rflu methemogolbin un:nanl? riounrqrufinooncrn myoglobin uo{lu

fitflo1triuti.ililfinn"ngruufiuauo'lrnr:rir:loamvlfirflupir.ildilnq'nirnr:lfiorrrirvrauyrlfira r,rss
tuntnuz'"

otiril:fintrtu{rJrtrfifi rtrabdomyotysis iuui\r arorlorrrurm:rirrloat:lfirflurir.,r
yn'{ornlfi ruSS uri{ilruoufiflocrryoonfi udr Toutd z.sx NaHco3 150 o. (3 amps) Blfl fiu

i5o/o Dlw n3o sterite water finr'ludn:rritdu zoo ln.piorirll.r.r runyrrrrdulnfiqo'rrin.:.t

uSs lnun'rflrnr, ulfiTle a,t?:fi pH r.rrnnir o.5loudofiru?oda.rlqn alkatinization of urine rfio

t ) {rhtfi hypocalcemia ruu:.ltiofi symptomatic hypocatcemia rriu g'nrn5,: n::qn eT

protongation z1 rfiandrJrurflud'tn (pH > z.s1 niofi Hcq- rJ1nn.j1 30 mEq/L 3) {d?uiirI.lfi

anuria rlo oliguria :'r vrs.r'luntnin"lfi uaHco" uluMnfr.jr g-+ t'r1lru&rtir'l*jgrlr:0u".r1fi

:lnorrvfi:-hufi pH > 6.s .lfi

9.4.s nliinffidu.t

lrifiuo'ngruirnr:tri bop diuretic rro: mannitol fi :;tuuilunr:floon-u neme-induced

AKl" do{tfir:cr"'l hypercalcemia lrflc hypocalcemialnunr,:insrlnu'ld calcium gluconate fiio
calcium chloride 6oyn.:rduTafing'rrl'ofirJruorntr rdu yrl eT prolongation fiornr:t-nnia'l$
tunr::"nurntr severe hyperkalemia frfinr:r:Jduurulaola.:ndu}{ffrri'rtcwirriu

4. Pharmacologic strategies for AKI preventiona
urynrutfinfrnr':f,nrr'lufin{nnnoluo;nr;finrr'lu{:-hulru& urn r,ir.l'jri :yIerfi:lu

n1?io'lil.rrLflyinul nxt urinri'rcrnldi!nr:finurlu Rcr turn'lnqihirr.r.jrfirJr:lunjlunr:flaon-u

lrt lrinonrufis.rnlr RBT unv'hiooa-n:rnr:r6lu6in ulildrfldrri tow-dose dooamine

(1-3 g/Kg/min), fenoldopam (selective dopamine- 1 receptor agonist), atrial natriuretic peptides

(ANP), recombinant human insulin-like growth {actor-1(tcf-t; :rui.lnrdfr runC 'lu{:-lruinrln
fifin'nlo'uTafiod, un:nr:td nnC lu{rJrund,,riroin drniu toop diuretic (furosemide) bifi

rl:rluttilunr':fl0*rn-uua;inur nrt fito:-i':dlonrytdlunr:inurnn: votume overtoad Mrriuo

laflfi11d1.t6\t
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23. Kanal E. Broome DFl. Martin DF. et al. Besponse to the FDA s May 23, 2007. nephrogenic systemic fibrosis update,
Radiology 2008;24611-4.

24- Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J
Med 2003:348:491-9.

Managemeff of Acure Kidne-y Irryry itftefl inu:ia 563

25. Lask€y U Aspelin P, oavidson C. et al. Nephotoxicity ol iodixanol ',,ersus iopamidol in patients with chronic kkjney

diseass and diabetes mollitus undergoing coronary angiographic procodures. Am Heart J 200s;1s8:822-8 e823.

26. Heinrich Mc. Haberle L Muller v. et a]. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-

osmolar conlrast media: metaanalysis oI randomized cortrolled trials. Radiology 2009:250:68_86.

27 Ve€nstra J. Smit WM. Kredlet RT, Arisz L Belationship between elevated creatine phosphokinas6 and the clinicat

spectum of rhabdomyolysis.Nephrol Dial Transptant 1994;9(6):637.

2S Huerta-Alardin AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis-an overview for clinicians. Crit

Care. 2005:9(2)1 58.

29 Brown CV. Rhee P. Chan L et al. Prevertting renal failure in patients with habdomyolysis: do bicarbonate and

mannitol make a differBne? J Trauma 2004;56(6)t191-

30

Sodium and 'Water Disorders

x(uv4,1 xnuvxn

rnnrrrdfilorrjrrrre'rtdolfiorrr:n rdr'le lfinr:ifico! ttn:insrnrr:fi,: tfinornnrufior

r.lnfirarqnrir (abnormalities in total body water) ludr.tnru {i.iloarJn6l:ificdu1drnrtnfif,n

ernnrrfinfl:rfio n6lo.:nru tdl{uto.flt16a lulo'rol'l (hypernatremia lrnv hyponatremia)

n?1 * vn't1il txsrql lflrEil3"ru
tJtuf,

1. Hyponatremia rrfl: hypernatremia rfiocrnflrrtJfio nfito': total body water ffBW)
kihiarrrrfi ailnfi ro.r:Jilnrult rdur.rluir.,,:nr u'

"natremia" 6onmr rdlduto t tds!tianrlx du{ulo.:rir'tuvi nrom

d',lrfu hyponatremia = low serum [Na] =Jamount ot Na in ECF

HrO

(ECF, Extracellular fluid; [Na]. nr,')t.Jttuduta''tTtrda luunrolr;
ttfl: hyponatremia + Na depletion (hypovolemia)

hypematremia = high serum [Na] = J amount of Na in ECF

H,O

lrnv hypernatremia * Na excess (hypervolemia)

ri.r hyponatremia r!fl: hypernatremia luvr.rnfifinovn:r{rLrurfrofrfi Na depletion

(hypovolemia), normal Na (normovolemia) ttflY Na excess (hypervolemia)

Sodium and Warer Diserde$ ttfrtgt iawin 565

z. tufirj'rr n:ru 1:rrrft{rJruinqn) frfinrr; dysnatremra Lruxyrl{nlrfi.rfl1[]18 ufl:

inurrirrflufio'rq "rjiurruTsrfisr" {i.:fr60 "vorume status" flo.id.r{nlu.jroeiiunejr.rlnuo'rfind1
lrudrludo t

nr:rrri':fitirstflu Na depretion (hypovoremia), normar Na status (normovoremia) t|fl:

Na excess (hypervoremia)1d'lrnflo4ovnoer6finrrn;n1:n:mir{nrurfio:J:;rfiu ECF vorume status

rrirtiu 1nr:r.rfi t1

rnnd lecr Votume status)

1. Clinical : heart rate, BP, postural hypotension. jugular venous pressure (JVp). conscious_
ness. urine output, skin (turgor. edema), central venous pressure (CVp). pulmonary cap_
illary wedge pressure (PCWP)

2 Laboratory: urine [Na]. urine osmorarity & specific gravity. serum BUN,i creatinine ratio,

albumin. acid-base balance, hematocrit

n'T nlr, dorafi ldrio tun:fi rJr;lurrilurirhuinrln

3, Osmotic Actlvity
6a solute activity rion11$ldudu (concentration) ra.:oitnna:otu (sorute particres)

luf,r:n;nrrl.olution) tfionfi.:1 osmotic Activity o: rt:J:nrnnriuriu activity yio concentration
rotfurnnnrir (water morecuresl lunrrn:nruriul Tou sorute activity 'lufl.rrfl;flrrqyfir rs
ufi6,rtfl! osmoles losm) o-,:usu osmatic activity ltrtrora.ror:n:nratrinufirl c:fi{drMrniu
fln 5'rtJ?o\r osmotic activity flo.J sotute lnrfiodoqjluor:n;arurfu dTrir monovatent ion (rriu

Nat' K-, cl-) osmotic activity ii'ruco.:drur ruu:! milliosmoles (mosm) rio unit volume eylyi.r
njunrrrrdlduto,: ion d.lfirrirurflu mi iequtvalents {mEq) Fia unit votume triu

Osmotic activity no{ isotonic saline (NSS, 0.9o/o NaCl):

0.9% NaCl = 154 mEq Na /L + 1S4 mEq Ct /L
= 154 mOsm Na /L + 154 mosm Ct /L

= 308 mOs m /L

Osmolarity 6o osmotic activity ria ilrrudr:nr01uyt''r tn (solution yYtylno:ryird!
solute rltn water) l'trjrttflu mOsm /L'

osmotality 6o osmotic actjvily doliil1rufr luotrr. of water) fiylrurflu mosm/

xg H.o lorr'r'"rl:h-nq: ttflo{ osmotic activity 10,rfi.]rf1'luirrnrutnutfi osmotatity rrn:rflo,:crn
:jirrruro':utrtud'r.:nrufi 3rt.trurrnn'jrrlSu'rruro,: sorure rJln ri'.,rriui.rorrrrnldldnvr .osmctatity'

![nr "osmolarity"llnr:lono'.: osmotic activity lo{fl lt;,]t d,lnm u

Osmolarity = Osmotic activity / volume o{ solution (solute + water)

566 rrnirriainqorCugru

Osmolality = Osmotic activity / volume ol water

o"rniu OoOy lluid : Volume of water >> volume of solutes

n-lu&u Osmolality = Osmolarity

4, Tonicity

rdofiar:a:ara (solution) z lfin dto{nun: compartment 1ou0nfi'udxu membrane

{irfiqruolrGuailfirirrjruusilriBotJ'lfid'r0nnYn'ru (solute) r.jru{i,ilou:-lnfirir lwate4 e;rituqtn

o'r:n;arufifi osmotic activity o{{ldd.rfr osmotic activity gtnil tiun osmotic activity fitflu

u:,:drlfifinrrun6outooti1:vv'jrt 2 compartment (2 solutions) d'j't ""rr*rlu" osmolality" vio
"loniciiy" or:n;aru'lo1 fi osmolality g.:n'lT,lnrnlr n6 q: tiun'jl hypertonic solution ttj! 3%
Nacl d1?aca'rufifi osmolality n'ln'jrrnrf,lttiun'j1 hypotonic solution nju 0.45% NaCl tLn:
cr:acnrufifi osmolality tndt6u{n"llyrfl16llJ1:lnfi tiun'jr isotonic solution ltiu 0.9% NaCl (NSS).
Ringe?s lactate solution (LRS) 1nt*1Jnr:lndoutoorir (water) tfitttacoanctntrod tuir.rnru

c:nnrilvun1au effective osmolality lio tonicity :vu'jrlnlair'lursffd (intracellular fluid. lcF)

Ltn;uon cell (extracellular fluid, ECF) (iilfi 1)

TBW:6,0 .1" of BW

E( F

!o%l w

ICF

loy.BW

IT rv\ -rl"v"r,r-\
orx ECFI
!9t ileff Cirpulatory Vol

:sxECF) ,"::::::,-/

'-rr-t-f

LOrssmmooiicllc sSrtaor'lling

distribution Forc€s

llr-ta 1 $f,n\1f,7U117:n8 g17U11l1U11, \tn18

ruif,lfl1Tn:fl'ru z lfioqnnudrl membrane fruolbin",,,:rir (water) rrn3 sotute oiruld
drfinr:rfirdula',r solute rfurir{lu compartment ud.,t (solution fi.,,:) solute tfuo:erm:nrirun:o

membrane rdrl:lautu6n compartment (solution)ldod1,JAfl:vr!0Y1i{fiiflloo1:u'jt'ldt?n:ntuvt',:
z il.,r riuarnnhhirYr 2 compartment fi osmolality godurrdnrtrrrmnrdl{:vfi'j't.J osmolality to.t 2

itutinScrdium and \X'xter Disorders r{frl.ag't 567

compartment Lirildluuilnl ei'triui.rlrifiqlntfirfin water movement tsx'j't{ 2 compartment
dradrttar sotute dfinrud tt'fidlduri ur"" rdofinr:rfjmrsuro,r ureaTu ECF (BUN rfirJ) urea e:
n:cqtuor.i'r'Jrrori?yr".ruanun;lu ce (tcF) l.i'trfu{,rlrifinnrirtrirfiprnr:lnatauro',rrircln tcF 00n

{ fCf ri'.:rfu azotemia rflu hyperosmotic condirion lleil]i[flu hypertonic condition

5. Plasma Osmolality
lqurJnfir:rnr r:nia osmotatity ?fl.r eCrldloun:,:Torulvrnfin freezing point depression

mahod'luvrr.,rilfri6r:rorrr:nn'rulru osmotatity so{ ecr ld'lou'ldarrur{rduta.: Na, ct, gtucose

un: urealurntf,rrrfio,:lnor:rtrirdrflu sotute airubrylu rcr

6'rarjro Plasma osmolality = (2 x plasma Na-) + glucose + BUN

'18 2.8

= (2 x 140) +90+ 14-

18 2.8

= 290 mOsm / kg HrO

rnrur{rduro.:It16urds,:rjrrrnru 2 rfiarqrnrfir:xzuacrnnnol:d'lidru n$Tndun;
,rea 'lurnrorr'ldfi 1rJ mg/dl drurn''rlar 18 ufli 2.8 rcrnd't fnoymori (atomic weight) 't:
dru to rfiorilduu mg/dl lfirflu mosm/kg H,o

6. Osmolal Gap

tirfi sotute 6u1 uanwfioorn Irrduil. Fraal:6', nBInf, un: ,rea rfi dulu ecr e:
finrnri'rtfi ptasma osmolatity dinlnuorxfir4urnnir ptasma osmotatity dtficrnnr:rirur : osmotal

gap = Measured plasma osmolality - calculated plasma osmolality (dr:Jnfiao\: osmolal gap
riaun'j't to mOsm/kg H,O)'?3

fl! osmotat gap or 1r:rnn-Jr zo mosm/kg H,O) lun?riifiilfl't:rlulr,ratirtrfjr.rdu'lu

n?3$dlfian nju ethanol. methanol, ethylene glycol uc;lu{rJrulnr, ur{oi.: (unknown toxin)'

7. Plasma tonicity
tflo,:11n urea drrr:neitur:n cell membrane ld'or.ir,r6cr;fr,tfi.rnr?ri,r lru effective

osmolality uia tonicity ra{ ECF 6\rn"q eUN aana'lnflx.tR1:

Plasma tonicity (effective osmolality) = (2 x Plasma Na+) + Glucose

18

= (2 x 140) + 90 = 285 mOsm/kgHrO

18

d{fin'rdr{eln iorat osmotatity rfiu.:5 mosm/kglro rfiuldit nrrlrfilriuto,,r urea
rflurh{ufifizuoriou lnrianlrr duuu nr ptasma osmotatity ua;ornornr:{rtduc;rfiur'orcu

'jrnml rir.rduto.rltt6u ,uvrnrcrr (tt',tal1 liud'rufinfi'rflun'rrirnuo effective osmotatity (ptasma
tonicity) o,:liu 1t'tal 6.,:ufluflco-uln-nfie;rirfiuqnr:rodaudrauir (water) rd't uR:0onalntrnd

568 rlruhrioinqndugru

Iqualil tttal 'lu pta"r. rfiuitiundndcvrirruonl:rndoufilro.:rirtdruavoanerntsad

rrnvrflun'rdrrtunn?l rrnnd't{tro\t volume to\t lcF ttnJ EcF n"rarir'lniu 'tufi;Jru hyponatremia

ovfi ptasma tonicity di o''-rriurirovrndoufiunuan ltadrdr{'lurtadfizuorir'lfi lcF volume {n
(mndlli) riaujiulrfi ur.rrTu EcF volume

Hyponatremia

fi uu 6onrr:dinrurdl{uta$trduu'tuunrarr (tNal) fioun'jl 135 mEq/L (mmol/L)

Normal physiologic r,esponse of hyponatremia
lnuiJnfiriia rfinntc true hyponatremia (hypoosmolalaty fi30 decreased tonicity) rir

a: rndaurdr{rtnd louronrvadroij': osmoreceptor cett rflunnlfidr,rnrufinr:nounuo,lq'ld

t. d tnirst center acl flt:fi1urir unliulu:rtfifi psychogenic polydipsia

z. rda:vniu osmolality tii'rn'jr zzs mosm/kg HrO l:tit-rtilnr:nd.:ua;nr: eisuto.l

antidiuretic hormone (RoH) o'rnrior'ldgr.raflflunrnrir'lfifin.lrtit-t free water urndudlt rfrar-nurhi
osmotatity o{d zzs-zso mosm/kg xro n-.:riurdofinr:rfirto,l water rf,rqid'rtnrudruin''lo1 1tvr,

filrirlrnt) lnc;furJrdrurfiuaanrirbifirlsalivcrl io urine specific gravity riaun'irnio rvirril

i1.005. urine osmolality 20-90 mOsmikg HrO ttnvfi lrufloorrvlrnfiqo (Jr: 1nr 1 Uhr)

zfi'rlrilflunlr :vnr:drtfiuuao'r'lrfio,:iiryurdln tdu finm;lqrru (cFR < 10 mu

minl niofin-rnr{ududfi6ninnmnn'J'm1r; hypoosmolality fid1tfifinlrrn'o noH niu nr:on

n{so\t effective circulatory volume (tdu e1n hypovolemia, heart tailure, cirrhosis), syndrome of

inappropriate ADH secretion (SIADHI, nx1 [5 r.ho, ndu'ldorriuu tln:sttlt,ttfin

o:tfi uld'irfiT n"on{u pseudohyponatremia (normal plasma osmolality) rravnsjl hyper-

tonic hyponatramia oanl:Jud?c; ttrjr{dru hyponatremia (hypoosmolarity) ldrflu z nriltrqi

lnu'ldnr:m':rcdr*rnluodron; rdunirrnir{oXarrtn6fln ttnvldioqorr'rrio'rrJ!rifinrrrnaullarlu

l. Primary Na loss, secondary water excess donsj#finr:gqrfultrdal 6a loss

type) LtnJn4ildfi arterial volume nnnl 1mrfllfr z {o s. nr:r':fi s1

Inur,r'':}lrdo effective circulating volume tlio arterial volume netn{stin'it:lnfilrn

n'jr 10yo rrfiornrirtfifinr:n:;{uhict, ',run:nn-,r noH crntiouldmrotd':und.r rfirdurfluarnrirtrt
finr:gnnft-r tree water nildudlnu?rrru oistal lubule uav collecting duct rroifi hyponatremia

0rltJtJ't

n'r:fi:.rdulrrntnqlun4*rd ddra'rgdqo6odoryndldlrnri'nsruvrt.:nfifinunrnt:n:rr

d'r.,,:nru qrnqr:r.rfi 2 {D 3 (a) 6anr!1fifi hypovolemia finT:gqr6lu Na ernf,rtuqdrtl nr:onrl

dr{nruqcr! poor skin turgor. JVP, cvp nio PCWP d'1, arufio1jnrutfirrEu, orthostatic

Sodium and \irarcr Disorders zfivn inwin 569

hypotension rldrl finr?:uxrJ (eoemal n{rdl:rrLi,lfll nonrenat Na toss d,rcyfi urine [Na]
[[aJ/ iO urine tcl {oun'jl 20 mmol/L !!fly renal Na loss 6,nnu urine [Na] rJlnn'j1 20 mmoy

3L (Sn'rr1{fi r;no )

2n1?lnd rrdu{f,rr}19rso{ hyponatremia

| 1. Hyponatremia with a normal plasma osmolality

a. Pseudohyponatremia: hyperlipidemia. hyperproteinemia
b. infusion of sucrose and maltose-containino immunoqlobulin
c. Absorption oI isotonic glycine (urological or gynecological procedures)

2. fi solute flio particle drfir, rnduua:a.:aa1u ror lptasma osmotatity aro)

II a. Hyp€rglycemia

b. lnJusion ol mannitol

a. EcF volume contraction 6oi hypovolemia nianr:grprdultrdaralni1{mu (n'l:'l..ld 3)

b. Low arterial volume ttrifi venous volume rfildl rdu heart failure

c. Low arterial volume *n:fi interstitial luia ldlrdu6onT;dfi hvooalbuminemia niu

cirrhosis. nephrotic syndrome

4. Primary water galn
Syndrome of inappropriate ADH secretion, SIADH

a. iaaflu ADH aifln posterior pituitary gtano lnullildgnn::{ulnu tonicity

(u'r?J hyperosmolality) ua:llifin1iflna,tso.1 "eflective circulating volume"

i, ar 1nr:rrd +;

ii- c"?n:sfiu ADH 6u1 lriu nrrurSt-r rnluurr. nre;niuldorriuu. vagat nerve stimulation
iii. 1:a:::rlnlo,:drunnr': tdu stroke, hemonhage, infection. trauma
iv. l:ntrquofin tdu porphyria
b. fi ADH lrcrnurdo6uli.rl ldoiollfisrJo.t

i. tdaoonrrttf,o triu cA lung (esp. small cell cA). cA pancreas, CA duodenum

ii. nir]lir4TlU'lu1,rtf,o (oxytoxin. dDAVP)

". urdnirqtrdtao ADH dtn (n'm{d 4)

Hormonal changes
d. Adrenal insuJficiency (secondary and tertiary)
e. Hypothyroidism

f. Pregnancy

570 rrtrirrioinqndug,u

gntnrd ltfis,Jfllrfiqto\t extracellular fluid (ECF) volume contraction

Ff"l *" renal sodium loss (urine INal and/or urine Icll (2o mmoyL)

l, Gaslrointestinal tract (vomiting, drainage, ileus, dianhea)

ll. Skin (excessive swealing, bums)
(b) Benal sodium loss (urine INal (20 mmol/l)

l. Diuretics: hydrochlorothiazide (most common), osmotic diuretics (glucose. urea)

ll. Salt losing nephropathy: tubular disorders with low aldosterone bioactivity
lll. Cerebral salt wasting syndrome
lV.Addison's disease (primary adrenal insu{ficiency}

qrnelrl.rfi 2 da 3 F) aonr! fifr effective circulating volume n't ttrifi venous volume

rfrdu niu{lrudfinrr;rir'lodlrrn? (heart failure) ni,ltiunr:ot:rldr,,rnluolvuLnnuru;to',: poor
tissue perfusion nil llnrufiorlalurfirrfiudrlrYu JVP, cvP fl50 PcwP 4.1, f,tlfiulrlootvru'irfi

crepitating 2 {1.: (left-sided heart failure}, 01cfl! S3 gallop xiaalel; :.Jo1n'lllo'r right-sided
heart failure niu edema, ascites n1l1nfi 2 {o 3 (c) 6an{ffifi4'a:;fiu1ufiiloit:iu cirrhosis,
nephrotic syndrome d,,rrfunr:n:':odrlnluaYflxn'l?ru'ltl, JVP cVP vio PCWP lli{.t. amuu
ascites [[R! pleural effusion 'lu{ ra cirrnosis oleq??er! sign of chronic liver disease ld

tur[r-hufifi edema vi.l z n{rii ttfi urine [Na] uflv urine lctl n'r firnr:n:rnflanrrv

vrlrriouc:ldiuarfirfl fl fl 'lx: (diurelics)

ll. Primary water excess

Syndrome of inappropriate ADH secretion (SIADH) 60{thufifid"rn:;{udupon
ryfioorn "nr:nero.rn0{ arteriat votume' drirtfifi noH va'{crntiailficlo,r rdriduviafinr:nd,'r
ADr ernuyd.:6u.i rdu rdo,ron (mr:r',rd z f,o q) urrr':rfin 1nr:r,rii +1 noH d1:rndudq:d.r0rn
tfifinr:qonn'u free water dlnrfirdurflonre: hyponatremia ua; rflo,:crntto 6lfiu1rifinrrno
fl,Inan effective circulating volume d'lriu{rJrun{lde:o{tulnr normovolemia n'tin?miNnlu

skin turgor r.lnfi, JVP, cvP ttfl: PCWP lrin'1tteJ'lriurntrvru (edema) odr.rl:finrl{rJru
n{rdfi "ri,rfiu" luunrarr r3ofi 'telative hypervolemia" q',:rYuq:vr! urine [Na] > 20 mmol/L

{ilrclfifinmrfie:.lnGta,:safllu tdu hypothyroidism. adrenal insufficiency ttn:n1r
ns.,ro::fi e:fi hyponatremia drrfiavrn '\t'r tfiu" lns volume status rlnfi nrrrrunf,1-hun{udaon

c1n stADH rir'ld'lnsn'nd'n :;ih n:redr.rnru lrdu rrarnr:mrtn6finflon hypothyroidism) [Rr

nr:flrdum,,:fiot:Jfrrj6nr: rriu serum cortisol t!flv thyroid function test

iofrltnn: primary adrenal insufficiency (Addison's disease) fi hyponarremia 6':do
o{lunq'u renat Na loss tfio.tqrn'vrflrionrnd adrenal gland d'lfu{{finrrc hypoaldosteronism

ir dril nr:n:roirnn'tue: rL hypovolemia fotcu niu fi postural hypoiension jrlfii skin

SodiLrm and r*'ater Disorders rtftt*fl inutil 571

hyperpigmentation tlnyii hyperkalemia drnil secondary uflc tertiary adrenal insufficiency fn
es.[ tldnurutns.t volume deptetion doiooglunejt water excess uflJhiy{ll hypokatemia rdaoorn

'lrifi nrrtrprsoSluu aldosterone

nr\rii 4 uoo.rurdfirunrtrlfi nDH aaivitv ntir.rtru 't
| 1. Centrat Stimulation of ADH reease

Nicotine, morphine, clofibrate. tricyclic antidepressants. antineoplastic agents such as

vincristine and cyclophosphamide may act by causing nausea.
2. 'ADH-like" agents (oxytocin. dDAVP)

3. Drugs promoting ADH action on the kidney by increasing cyclic AMP

Oral hypoglycemics (e.9. chlorpropamide), methylxanthines (e.9, caffeine. aminophyltine),

L analgesics which inhibit prostaglandin synthesis (e.9. aspirin. indomethacin)

nlt2uQgt Ugnf tlnf,1lilnI1o{n1?g hyponatremia
uflnndirurr nifi 1 rrnruH nfiii 2

Hl'ponatrsflla

I'm<0iItrr-ll-l-| Hypg,rolsrL ; r > Euvglgrnlg HyF Yo|dnkl
|
IrV?l t_--__-!.__-._-...| V!]
u 0bl i Rsnal loss E(farefEllo€Bl <20
tl >m
ntEq/L Adrt€ d chro|llc E&mahls ltete (cHF,
| ----------------
i Il- cttntcat equtr/ocat rsnal bilur€ llvsr cdrosb. NS

Iri l(hypo{ sul,olamb) |
i!------":-----n-e-rp-o.niss
b r,rss'

l.--r'-

Grrooortffi dof.

Hypothirfoldism

SIADH
OrWs, str€6s

' L, ttl.l r.? i:!bt l-2 a4!

t x4frii I ttso,tuuautiluntt awroach ilqnl hyponatrema

572 nrnitioinqndug, u

ls Na lN lr the

. Dlurotics . snd spdcs . Low albumin
. Gitsact .Haaft omuem
.fEgh mnd anion . Skin . Endocrine prcblem
. Remots diursllcs
exc|etion as in vomillng

. Renal Na+ v!€sung

.CerehEl Na waslirt

.Addison's dls€asa

..flugfiii 2 uda,Juuln1nlun1l approach fl{Atn hyponatremia

lounpJnr:ifiodaLLflflI:Fd'rrfiEtonnl'l: hyponatremia fidrn'qda o'1fl'ttltflq,! 1{nAfin

lo u ra lc vot ume status to{{ilx u rrdri.flfi annr:q:r?r'l{fi 4{ilifi6n1*nfl u-xdl.{uttunl:n

Ptasma osmolatity ldf,uuiunr:ificdu'jr{ilruoglunm; true hypoosmolality ria'[ri

urine osmolality frrrnnr'r 100 mosm/kg H,o riwanirfinrtli'tn1urro.tao{l u ADH
dru::d'uddrn'jr 100 mosm/kg uro n:rmldlu{:l'tu primary polydipsia, malnutrition fifi low

solute intake (ttiu beer drinker potomania) uflY reset osmostat

Urine sodium concentralion tdttEnn'tr:dfi effective circulation volume depletion (rios

ni1 20 mmol/L) nitlntcfifi normovolemia ttio renal salt wasting'tu StnoH 1:1'l! urine [Na]

1nni1 40 mmol/L

Sodium and V'ater Disorders ttfivy iawia 573

n1rifiedunms STADH

1. Low plasma osmolality
2. Inappropriately elevated urine osmolality (> .100 mosm/kg H,O) d?!:J,tn{; .tnn,j1

300 mosrn/kg H,O

3. Urine [Na] > 40 mmoVl
4, Low BUN [td; low uric acid concentration

5. rit plasma creatinine tt'nl: nfi

6. Normal acid-base ufly pota$sium balance
7. Normal adrenal uflr thvroid function

O1R1:UAcO1n1:Ufn{fl A{fl 1?C hyponatremia

rfluornr:ro,t lradfl on:Jx r+ e1neiourfldu nfiilft o1L6u! xod:Bt lflunrnir cv6n

duou drornrrtrn?yfiil lilifrnd'? fn uncfi respiratory arrest rY.oarnrtyrrlnfifin un;nr:

riorrrurorrrt rd.,rei?uro\rnllinulaydria{n-ld'n:tirto{nllrnont?: hyponatramia ns:::fiJfiil

lztdur rru;16urriufirufibnrr;f,rirrfiul:J louroilrc chronic hyponatremia qlfinrlc ur:ndo!
rlntsndorattfiur tiun'j't central pontine myelinolysis tlio osmotic demyelination syndrome5'

1. Acute hyponatremia vrltu:rufirflupurif,occfi:ya'udirlnduiln"rn.jr 1 i 5 mmot/L
nrulur':nr so-aa drTrJ-l r:iu 1u{r-l.rrun',or.jrm-oirnlfiilar:rirsfin hypotonic 3urrurrn'

2. chronic hyponarremia :;ollfiiilndalnernldrl lurrnulnn'j1 48'ij'rl*:rir1fi

rrndoro,lfinnr irn'r slo.,rlriurrmnnnrl"ncylrifiornrr orir.il:fiorutr.huorcfiornr:ldfir::o'!
[Nal riorn'ir 105 mmot/L y5olurrsiifi chronic hyponatremia otiun;'ldcr:rirdrflu nypotonic
3rrrumn

n'rtinrfl Rt2! hyponatre m ia

nzinat'luSttndfr Na toss nlafinteafranyan effective circuratory votume

t, :u q n nr: d ur'hn?o er'lrirlfi ria s nir rJirrrui c nrr

2. inuln'ttJfltr rl
2.1. 'ht NaCt niu o.g% NtaCt lufi:-hufifi EcF votume contraction
2.2. lutil?udfi heart faitura ftiur:iuflacmyrfrona pretoad, lfiurd.ru rfiilnr:itld'r

lo.:rirl,r linotrope), [Rran afterloao
2.3, yl@rtrllEoflilufrlrn t:iu gluoocorticoid, fhyroid hormone

nteinuilu{thadfr pimaty water excess tfiuna-n (normowremia)

t. ulnnr:duirniodlrir'tfirioun.irrlilrruics'n:

ftz. insrrfiotfifinr:ldr 1rua1 o.s mmol/uhr rdo,:ornlunu 70 kg eyfi x zo = az

literes of water drriudo.r'lfi 2i mmot of NaCt lu r drfu.lrfrorfir Nal 0.5 mmot/t/trr

574 r':rniljoinqndug'ru

a. tfirnr::iu free water Iou
s.t. lfiflrriuilaarr: furosemide dlr:fiHnlfifinr:4rgrdu Na un;ri-rluiacrr:iurY:t

lfi NaCt rouru Na loss
o.z. rqnu.dfiq"d'rdrnr:nd,r nol n?ouil:.rqufra{ ADH dler
3.3.'1fi vasopressin receptor antagonist ril mixed V2 ufl3 V-a receptor anlagonist

!1i1-t conivaptan r!n: selective V2 receptor antagonist niu tolvaptan, satavaptan

nttinal hyponatremia laa intravenous fluid therapy\

t. fir{:,hrfiornr:quur,r rriu r-n. it'urJin (coma) ohrflufiotinutfiahifinr:rfiu [Na] otjl{

lorSr rrju nir tl't.l t-z mmot/L'lu e-q rhTrl.'ru:nlou'l$ hypertonic saline
nr:iruru: rfiac;rfiil [Na] 3 mmol/L'lufi,r-hu zo rg (* 40 L of wateo
dartfi lta 3 x 40 = 120 mmol - 230 ml of 3% NaCl in 3 hr

z. dr{rJT ulrifiarnr:niaiornr:rfiuouddaulrdu iiu,,,:.r nSoduourfinriaur:uribnrrv
hyponatremia athrdrl 6orJ::rrru 0.5 mmol/Uhr drifiu 10 mmoUUday) 'luriuu:nuov'lrirfiu
18 mmol/L iu +a d'r1nr

s. nr:rt unudrnrrer rdr 1tta1 lounr:lfi tta ({ftud'nn?ofi EcF votume contraction)

uian?:cyinurlounru'rtifi negative batance tor water dunrridut fi{rlrulrifiornr:pu:.l

ttflc'lrifi hypovolemia)

a. iu{rJrudrutuqifililrd,rphuuialrifiornr:nr:fierrrurfnur un:no water intake rr'rn
n'irnr:inu{ounr:'hlnrlirvnlvnoarfioo iurYr-rnr:nmliarjsilrrurlruoc l"ta fiaanmrr,oflnamv
ruachi Nt. dgryrfi urrvnriacrr:vrnununn"r r{rqi{ilru

s. nr:fnur{ilruiifi EcF votume contraction or:fiq'r:rurnr:1fi tvF dfi tonicity !fifiou
riura'rou{r-hu urunr:'lfi 0.9% NaCl (tonicity etJlru 300 mosm/kg H,O) rdo.rornnr:'1fi

normat satine ufiovufinrr: hypovotemia ld:rotirudorco: "1'lfifinT :nir ttt.l r5rrfiutf

vr ro. firfio,:finr:'1fi}JsriflrdsrJa.J'luar:frnr:no:Jtrrnr na'[u un:lfi uvrurfioyfin

rdu,rn'r:r druurJn\: tonicity lo,:ar:rirdl:lfi{rJru'

z. nr:drurruua:ufib hyponatremia d'ru tvF n4o}4 tr.ral rfirdu o.s mmotrutrr ritd

3 ttuuu" 6o
z.t n:nidfi:J?rrruilonrryriou nr::h":l tonicity r0,I tvF fra:llTbidrvrTurin-l tnal 1u

plasma

tuf,:Jru zo kg fi TBW 6ovo = 42 L

rirdornr:nfu Na 0.5 mmo rio t 6n: ta{ TBW
tu t d'rImrfiorlfi Na r{mr'r tvF 0.5 x 42 = 21 mmotlhr

Sodium and Warer Disorders ttfrvg1 ifruzifr 575

2.2- n?rfi d ilrhufi potyuria do,,r'lfi fi 1:r.lrlo ayro uru rn 6 o udfi gnfiL o on rrnl,Ji fl d.tx y
ud}ifi n r::iurJrlfi :lilrrud rru r y su dl o'r a dr.,r

{rhu zo rg nt?tyru [Na] 120 mmoyl fio.,rnr:lfifi p,,t4 r$ildu 0.5 mmot/Uhr

d'rriu fioo'lfiinr:qrl r6lufr p"te, toss) 0.5 = o.4o/o 1)Bn TBW'lu t hr

120

=0.4x4,200 = too mL'lu t dr1r.r.:

100

dr{:-tru:radfiflaorr::ir1rray go0 mL ua;'lufloem;fi 1Na+6 = 100 mmot/L

'lu t rirllm:fi 1Na+t{ luflaortl = 30 mmo
dtriunr:hi NF r{fi tNa+{ 30 mmot 'Iil (so0-160} = rqo mL lurror r drlilr

o;higrgrfru Na !!ni K rrnyfi water toss 160 myhr

z.a ntfl{rJrufi chronic severe hyponatremia usilrjciriuilrirurdo.:lrn{r.hulrifi
arnr:fi:uur,r nr:'h4 hypertonic satine orcdrlfifinr:nijrdu:ro,: 1t't"1 rrnlfiulil 'luvrrr:Jfrrlfiorrtfi
loop diuretic (furosemide) urif,:lrurfr atrirJilrruiact:rfirlrnrsr.

nfiiccrryfi'oonrnornqudto.l {urosemide ryfi [Na] 100 mmot/L ua;i 1q t o-
15 mmoyl rir{rJru ZO kg (TBW - 401) fi [Na]'lu ptasma .t00 mmot/L m!

da,,lnr:nir [Nal 0.5 mmot/Uhr niorfil [rual 1u ptasma o.solo ria 1 rirTlr {il

fifiorfi}|nrr:ilrJroonlrnirlnrs 0.5% = 0.5 x 4.000 = 200 ml/hr

100

fi r {rJru:r rdr n',ild f urosem id e fi f, oarr; aanlrtirl { fl c soo m L
qyfi Na loss rroflaotr: - 50 mmol/hr Lta: K loss rr,rflao,],]c 7.s mmot/hr
olfutu{rhu:ruf,1nn' dfi turosemide) n'rflltfitdrna'rrir{ir.,rn.ruToufi p'ra1
50 mmot uo: [14 7.5 mmot 'luor:rir 300 mL (s0o-200; 'lurrar t rirTnr
fioli o.g"z" Nacr 1 L + KCt 20 mmot 'hifirJranou'hjtudn:r 3oo mLnr

e, ld'jro;i.fi61nlunr:'hior:rir un;n1irf.tu.l do.rfifl1l6tx1 [Nal finorulutir,r u:nr1n
1- 2 hr r!flyflfl + nr'lutir$ro,r

9. donrr::i,r iufufrafifi EcF votume contracrion yn'{crnl6dlorrd.lcu EcF naiu r
rJn6frtr{d'rn:;{unr:yn',: eoH firultlnr;no:.touo,,rodr,::rnrir lom:finrrr'udh lwater oturesisl

vrriacrr: Tnuinorr:c;fifl'nr*ru:r6oorurn (sp.gr. rioun.jr 1.003) lmy!'il?!.rruiltnldfin 1
yrrr arryir'lfi lual rdr.rrfuadr.r:rar5rfiuJ::lrru 2 mmot/L ld n-.rriulu{:-t.:unsjld nn.rmnlfi
orzutrrsruilurda rehydration udr rfioruiriirj::lrruflaorr:rfitdulrn un::Jogrr:fidnuzuv
16oqr,:qhriufr'a.:srmq nny rflr::r",r::d'r 1wa1 ilnarorr unclu:.lr,r:ruareda,rhl convp d.rrflu

57O tllJU1UO?nqnXUj'rU

nor dfiqrd'eir lnutdlurnfiriordqoiirirlfififlanrr;tiaua.ottnvo'trr:n'hfifr1d 1oln;atddio

fl olfiunrr: osmotic demyelination mnnr:ttiiulo{ tNal t51[fi ulLl

t o. 'lu:rudfi nyponatremia d'rtJli! renal failure otqdooficr:rurinurfnu renal replacement

therapy

Hypernatremia

f,uril 6snrr:dii [Na] 'luvrnrfi 'ulrnn'jr 1q5 mmol/L fito fintt; hyperosmolality tu

I'tfl'lfllt1

Normal physiologic response of hypernatremia

:J? rn:1a{rrnd'evnna,: qmodrdurl rda,oornrir'turrndgnfi.u.nogluvrnT orrrsndona.r

rr iuoi'rlouo:or osmote (ion) 'lumadrfrarlorrYurrndrfiHrdodsntdnnr'lunr::Jiusr'':niuriu

1. R11s hyperosmolality ?sn::qu thirst center rir'lfi {rhun::nrrti.r unrdr,ti'ru.ndu
nr:rva;r?ufirlrr{:Jrunrrsdlfiroorli'r{ilruusufiiqnld thirst center viohi nju finu'rBnnrvr
fr ora.:airunnr.:vSoiiqnrdrunrrdoorlfl u stroke

2. n'ny hyperosmolality q:nonrldtl.rrnynrrnn.:aoflr.ru AOH rrndo fiq or riuHo
rirtfilnqerrirnn"rurndu r'rlfiinnrr: r{rdudafi osmotatity lrnn'jr 1.000 mosm/kg H,o nio

r;urine specific gravity rJ1nfl'j1 t,ozo un;fi irrruflnnrr;rioafiqo ( 1ru 400-5oo mL riaiu)

fi'rlrjn:inr:no:rcuoon'.r 2 r.l:vntlduan.r'irlorfiilqrr6ohjau"r':nrfirrirlilfi (renat water toss)
dr{rJrrnnlldoroll,uunntldra:lqrr potyuria drficrlnqdru'lnqi 6al:nruria (diabetes insipidus.
Dl) rnyn4ilfrfiif,d,']xv rncrnfifior:dfi osmol rlrnaqjtuflenrrr (osmotic diuretic)

q'r! 4ra{ Hypernatremia mcuurrr.iifiq{urrunlrn 1uuaru{fifi 3 rrns 4)
ttiutdurfflnr?y hyponatremia nr:Frdumnrtrqro\: hypematremia 6snr':m:roircnrB
rfroq votume status rjirrruiloorr:, nr:6fudurnrrriaulfrfbnr:frdr6'q lduri urine specific gravity
rufl! urine osmotatity louurit{rJrtlldrflu s n{r 1unu4fifr 3 LLo! 4)

1. Na sain 6o{rlrufinrrllftnrJnfiydn 6o fi:J?lrrulrrdulrfiuludr.,rn'mdrfioHnrirlfifi 1na1

trirdunrr.rurcvn:2e ECF volume expansion (hypervolemia) niu lvp nia Cve g,r $Jrl

r;n:cfiruri1lrn;finr:nornuorddr6'rgfiln6ai]ocr?lrcrirt (urine sp. gr. > 1.020. urine osmotatity
> 1,000 mosm/kg H,o) unvfi srJlruriarorrrqlun{rflfrurili'fu NaHcoi t.r1nrfiul crnnr:rir

CpR niaufill acidosis fi:h oxa yn',oldirnrrr'nurdru o.g%Nact, nlili'l peritoneat diatysis

lrio hemodialysis dldrirurtfiernrurdr.rduq.,r rro: primary hyperaldosteronism

2. Non-renat water toss fiofinr:grprfiurir llrnn'irgcpr5la1trduil) ilr.Jotu.l dll'tdvrr.,:1n
rtiu nr:rfiarntooril{ 'rfl. gastroenteritis !'l\:tfin nt:o:tqd't,Jntuqv EcF volume contraction

'.l

Sodiurn:rnd \vaLcr l)isofders ztfiwt't istulin 577

Assess ECF l'olume stfitus

Hypovolemin Normovolemia Eypenolemia

IBwll,rBNa*l TBwl , TBNa-- TB$'1, TBNa: ll

-f.fITllU lNal > 20 <20 Llspgr low high I
IU [Nal > 20
Renal Erh?renal Renal Ertrarenal Sodium
losr los$
wloss loa$ gain
t=
@@
Isotonic + Ht?otoDic Ilroreplacement Diureiics

NaCl rcplacement HrO replacement

3usu4frfi tif,ann11 approach f,q\1 hypernatremia

ls lhe ECF
\olume €xpanded?

ls there 1068
otwelght?
th€ ulne osmolaliv
al its maximum and volurne

Urlne osmolality <200

osmolality Bxceed 300

4u$uliii LLsannlt approach flrynt hypernatremia

578 rrttirrinrlnqndugru

!1iu JVP. cvP, PcwP oirun:n"nrru;6u1flon hypovotemia lnufrlororfinr:nolouar nfito',r
hypematremia 6afloolrv il'rrufiouun: rdrudurrn drrn"rfinr:narou0{:Jnfinonn1?; hypo-
volemia 6an:1{ u urine Na < 20 mmol/L

3. Renat water toss fioriar]rrJirrruunvnolnrvurilrflu z nq'illilr!

3.1 Diabetes insipidus (Dl) fiolnlriaur:nrfrruacnonn-!frlfludl\m'ruelnnr?fifi?'tlJ

fter:Jno'dtilfinr:yn'o ADH (central diabetes insipidusl niolnlilcreuoua.:sio noH (nephrogenic

diabetes insipidus) nr:n:redr.rnrac:uudr{ilrufi volume status :ln6 1rdo,.:ernlro[ririrlrilrn
Tttdur; flnorr;rJSrrruun (polyuria) uflta1.l (urine osmolality < 200 mosm/kg HrO r?a urine

sp gr < 1,005)

3.2 Diuretic induced water loss niu lu{:-hufil{ loop diuretic (furosemide), osmotic

diurefic e1n glucose ttiu dd?U hyperosmolar nonketolic diabetic coma flio osmotic diuretic

?1n urea ttju diuretic phase of acute iubular necrosis (ATN), post-obstructive diuresis {dru
n{,rflirrfinarrge1rf.iur&',tllrr6auruo:u:ifrA Ln dg o"rriunr:q:rqir,rnruc;nu ECF
,i d
lqrlrfiarhrrnn'irltlfiur.r)

volume contraction n;2lylU urine osmolality lJlnn?1 200 mosm/kg H2O !!fly urine spgr. 'tn

n'jr t.oos lou urine osmotatity LLas urine spgr. o; lrnneir,: udrrrsidnuru;Tloogr:dogj'lu:)oom:

niu lu{r.hadfi glucosuria evfi urine spgr. rtnn'it 1.020, f,il':u ATN fi urine spgr. rJ:tl1nl

1.010 lfludu drrir urine Na o:urnnir 20 mmoUL rdomrnfi renat Na toss illdlu

a. finrr:iior:-.rriouun:lir1fifi hypernatremia dafinr: shitt rotfrqrn EcF rfid rcF
rdu tu{:Jrud'n (convutsion} unvfi:-huifi rhabdomyotysis li{iifi particte frrirtfi rcr osmotatiry

g.,:'flud',rriu water c'nrndaueln EcF rdld lcF

iafsrnn

. Hypernatremia tuyrrra6findT u:.rrnc:finrrgryrdrrfr (water toss) irln-l4rgrfiu thirst

. drurrnrr.,rnfi inTou rarvr:lu'lof g c:fl uf, 1 rfi qyR'ruf, r ryndufiu

0'ln1lllf, !O'1fl 'l:Uf, q\ttO{R'l1V hypernatremia

tfioornrtadclorrdu'rrTnnrtu{rJruiifi:vriu 1t',tay rfilduodr'l:rnr5rrir'lfinr:rliun-rra.,r

llafdlonrfiolri?riu ornr:il'uq:fi1finu,1udadu-Ifi arriuu:Jro6:rc fiinu il'u dn ua;nrnf,fi

ntrllrdroiruro,onrrinuro;rruo{fi'rarn'rtJrlt*r',nrurotn {:Lrtranriuntfi:1qnr'lurrrrJf116
o;nilu{:hadfibnnr.rolatdtgeprfianr:n::yrurir, firhudoldiunr:drmn pituitary gtand (central

iior1 r5 o'tu{rtr ut'.:ld:"u NaH cO" r n:rru : ntr nr:fr ufi n

nTinuTn?; hypernatremia

t. inr*rsrmnrdoilqnn'ngqldlf1 niu nrr'lfi noH tu{:Jru centrat Dl

Scdium and \Itater Disorders ttftvgt inwin 579

5n.}fl# Rfln\r6l'lt]1nton diabel€s insipidus

Central Diab€tes Insipidus

a, Trauma (especially basal skull fractures)
b. Neurosurg€ry (hypophysectomy, oiher)
c. Space occupying lesions

l. Neoplasm
- Primary (craniopharyngioma pineat cyst, pituitary tumors)
- Secondary (metastatic)

ll. Granuloma

- Sarcoid, histiocytosis X

d. lntection (meningitis, €ncephalitis)

e. Vascular (aneurysm)

f. Fost hypoxia

g. Drugs interferjng with ADH reloase (e.g. phenytoin)
h. ldiopathic (may be famitiat)

Nephrogenic Diabetes Insipidus

a. Compromised ADH induced cyclic AMp rise

Orugs (lithium, demethylchlortetracycline)

Congenital nephrogenic diabetes insipidus

b. Loss of medullary hypertonicity

L Renal medullary pathology
- Infiltrations (amyloid etc.)
- Infections (pyelonephritis)
- Drug induced
- Hypoxic damage (sickle-cell anemja)
- Obstructive uropathy

ll. Drugs compromising medullary hypertonicity

- Loop diuretics

lll. Generalized kidney disease

- Polycystic disease

lV. Electolyte abnormalities

- Hypokalemia
- hypercalcemia

r. ldiopathic

580

2. inurrfi onor::ri'r ltrtal'luunrclr lnufier:rurcrnnrrrtd'rriru larnr:1u*:': niu dn
Mio coma) tlfl: volume status fla.i{lxu

z.t tu{rtrudfi nypovolemia dtufiut:fion do':tfiar;tih isotonic saline (0.9% NaCl)
rufibnrr: hypovotemia riou eunrrrdulnfionJnfi i.rfitr:rurrtfi'hrntv "trorir" nioon::nir.r

lrr6u:.rsiolil

z,e {rhrfifi ECF volume contraction ttrilrifi nypotension fio.tttfi-hvs'J water deficit
run:uflbnrr: hypovolemia d"ruor:rirtfia hypotonic saline ([Na] 38-77 mmoyl crr:'rtd o1 rir
fr'urlinnr'r?fi1 urine etectrotyte ld nr:r6on'ld NF dfi tNal sirnir [Na] lurlocn: rfiaflasnlu
Iritfifi nypematremia urndu uo:firfier:rurlfi lJfi'orfiuil ($ lu lvF o:fl"{fi tonicity io'r lvF
rfi#u o'trildo.otfi tvF fi tonicity rjosn'irrloorrv (tNal+tKl)lvF < ([Na]+[K])urine 6,:f,rlrr:n

tlfll1 hypernatremia.[dB

z.s {r-hufiriu "water loss type" uns volume status n6 nr:tririrnorrvru drlnonfiu
fiqe1fi6lrirvrr':rJrnriam.r NG tuoe n:dfrlriol.n:n'lfivr, .::hnld nr:'lriarlirnottnurflu sr.

6rr:rtfi ttflof distribution of one liter of Intravenous therapy to treat dysnatremia

Hyponatremia 1. Expand ECF lsotonic saline . Raise [Na] 0.5
volume (154 mmo|il)
Hypertonic saline L+2.1 '2.1 L mmol/Yhr to avoid CP[4
2. Coriract ICF (3% 513 mmoli )
r Glve ADH (dOAVP) if
volume
Water diuresis starts to
Hypernatremia 1. Expand ICF D5W 333 667 avoid a rapid rise in [Na]
Do not use in a patient
vorume with hyperglycemia
Limited use in 0.2-0.3 l/hf
2. Expand ECF Half-normal Fisk of hyperglycemia &
and also ICF saline (77 mmol/l) hypokalemia

volume 2/3 D5W + 1/3 'nillilNal il its tonicity is

normal saline 500 higher than udne
Risk of hyperglycemia
On*third normal
saline (51 mmol/l) Possible hemolysis if rapid
Quarter normal infusion into small vein
seljne (39 mmol/l) Good if [Na] in urine
> 50 mmol/l

Sodirrm and W'ater l)isorders tlbT.t fqurit 5gl

dextrose in water firrvfido"irrioTasoin:r metaborism ra{nefnfl ri'rriuifildhirfiu 300 muhr

(nr:r,ld o) ntr lSlpirus 0..: nr:inurlsua { rilornr:r ot firha "

z.a.r tu{lhuiifiornlTtuul.r niu rn,6rrrn yio coma ayRa [Na] rfr6o luo-m:r r
mmol/IJhr rl:vrrru 3-4 mmot/L 14i0 nn [Na] lhJrl1ru zozo (niardmiiurfu water 2zo) rflu

il?rrru ui u':llafi dr}1y qonr rt4'n

tu{il.ru zo ks r' TBW 60% = 40 L, ?% x 40 = 0.8 L

n-.ru'ufi I r: rur}i',water,' rrri {,r-h urh yrJ 1 [u 8oo m L

2.3,2 ludil?ufifiornr:riouyialrifiarnr: lun:rfidtrifi{ofir n'::riqr:rurhirirrr,,r
rjrnriauriJurfrsrjuu:n rflrvrlrflrfionar [tta; l,urnromao'ludn:r 0.5 mmor/hr udlrjrfiu to-tz

mmoVUdayq'o

iifrrorirtnrrnhurru water deficir rdrl6 z

rru# r Otra{nr{u3ru'irannruto,r TBW rlny [Na] '[u ptasma a'drn,rfi

TBW, x [Na], = TBW, x [Na],
TBW, = 1e121 body waler tun,]?y'Ijnoryirriu 0.6 x BW rjnfi
[Na], = 11qr-rn.1 serum sodium lyilfi! 140 mmol,/l
TBW, = 1e1q1 body water to,rfi:-Jru ru rrnrfi'lfi desired [Na]

[Na], = 6eg;r.4 ttt

or"rod'r,lrtiu fiilrur'rrin z0 kg fi tNal 160 mmot/t fiotnr:urilt'hii [Na] mn'o
150 mmot/t lu z+ ii"r1u

0.6x70x140=TBWzx150

TBW2 = 0.6 x 70 x 140 = 39.2 L

150

.'. dadrtrrir 4z-3g.2 = 2.8 LU 24 rtrlrll z,goo = r 1z mUhrluiuu:n

24

uul# z tu{rhu Zo kg fi tNal 160 mmot/L darnr:no [Na] 0.5 mmot/Uhr

.'.dornn [Na] llfnairu o.s llrrnr t drTt,:

tou

{rJru zo t<g fi rew- +zr .',r{a,:tfirhud{dr u o.s x 42 = 130 muhr

160

582 rrmi'rrininqndu5ru

doofic'nzur:liurufl acrr:tot{:Jrufi fi hypernatremia dlu

a1 firrfi:J'rufi:)nor':vrioa nrrlirirLifi ltta1 nornt 0.5 mmol/Uhr 6o:l:trru 130 ml/

nr 1n'.rrirurru{rfiu)

o) fiTfiilrufi polyuria niu {rJru ot, nio {rhuldiu lurosemide

li. fis,rvnunu water loss rr{ilonrrcfira }i6fi insensible loss ttiu tv$o :rc

rJirrrufioul niu hhirvrorrvru = urine volume in t hr + 130 ml/hr

ii. rir{ ru polyuria uo:f,nr:4qr6larndouinlricorrv (furosemid€) n?nififl1tJto
tn urine etectrotyte ldi nr:q [Na] ltny Kl 'luflanrrvrrsinvrirl*: ir:.rn"ln:rrdrrnraq volume

status uns 16on'lfinr:rlrrnurud rflu hypotonic saline dtv rcfl ddrd'rp6ofio':lfi [Nal 10,0 lvF

iic:'trleir n'jr 1na1 luflonrr:

3. do,:finrrrfir:ci,o rJ:: rfiu nr n nr:inrr n:redronruq volume status in ?r.rrruflosmc

unr6ernr fla16ofirflurcu:ttn:6o,1fi; lfiufl:-huTnunr:n:roir,onrudrrlnniortdildflnr6oe ltrulu
'lu
chronic hypernatremia nr:lfi::oitt a1fl 'tnon.ilrirfiu to-tz mmol/lJday
[Na]

a. fu:rufrfi hypematremia d't:.tti:t renal failure iiluurl grcdo{ficrrminr*tlou renal

replacement therapy

Sodium and \\,'arer Disorder.s ttfrvfl inuy{E

'ta
]anmrdfia{

l Rose BD. PostTW The totalbody water and the plasma sodium concentration. In: Clinical physiology ofacid-base

and electrolyte disorders.5* ed. New york Mccraw-Hill. 2N1.241-57.

2. Gennari FJ. Current concepts: serum osmolality: uses and limitations. N Engl J t\4ed 1ge4:310:102_5.
3. Turchin A seift€r Jr- seery EW. crinicar probrem-sorving. Mind the gap. N Engr J Med 200gi349r468-g.
4. Rrrssell HA Lynd LD. Koga y. The us€ of the osmole gap as a screefling test for the presence of exogenous

substances. Toxicol Rev 2004:23189-202.

5 Norenberg MD, Leslie Ko' Robertson AS. Association betr4een rise in serum sodium and central pontine myelinolysis.

Ann Neurol lgS2:11:128-35.

6 Lin SH HsU YJ. Chiu JS. et al. Osmotic demyelination syndrome: a potentiatty avoidable disaster, eJM 2Om:96:

935-47.

T Gross P' Reimann D, Neider J, et ar. The treatment of severe hyponatremia. Kidney Int suppr rggg:&:s6r'r.
8. cadotti AP, Bohn D. Mallie JP, Halperin ML. Tonicity balance. and not eloctrolyte.tree water calculations, more

accurately guides therapy for acute changes in natremia. Intensive Care Med 2001:27:921_4.

9. Rose BD. Post TW Hyperosmolal states hyponatremia. In: Clinical physiology of acid-bas€ and electrolvte disorders.

5" ed. New York: Mccraw Hitl. 2001:746-93.

'10. Adrogu'HJ. lvladias NE. Hypernatremia- N Engt J Med 2000;G42:1493-9.

Potassium Disorders

7tfu91 Fnwin

nrufi orJnfilorqnlnurctsutflunrrlduuriou'lurrmJfi:ifi dmrctlnmeuu tfi utRru
ftnrJnfirrrrtoo'rJirihnrtlnu{rlrulrif,ornr: filoorctfiuoluqlolrTrlo tf,ufin{lm; lcardiac
anhythmia) r5o cardiopulmonary arrest tu{ilruinqn urnrudfilorlotnuhlt{rlc v:ruuurfirl
nr:lfiedu unvarrr:nlilnr:inurnr'tgfin nfilooqn1nrrvrmfiul lqulonrvodr'rii,:'lun:rfid{:.hu
oglunrrvqnriu

fi?1xvinI il31u
dnfi'luirrnrmvftlilrrulnunctfiuuJ:rtJlru 50-5,5 mEq /kg loraiauav sa rvagtutlnf

1d'ulrnoglunftnrdo dnrfioo{tufu tfintfionum unvnicen) tauav z nio os-zo mEq otiuon
rtnd 13rJfi t1 uovfirf,ur 0.4% (1s meql rrirriudo{'lunnrstJr d{dunr:1{'tvq-unlrtdriuls.t
lyrulErdullunnrorr 16 d..:rfluartrJruonrto{ (extracellular fluid, ECF) lruonfi'rrl3lrrutsl
Iilursrdurt'luir{nru ii':fiiooirn"nnntu:Jrvntl'

loun"dilrlnfi Rurvfurhsu'tuotnr#!:Jimruluuvrctiuu 5o-1oo mEq/kg tounr 90 m.t
lnuvral6u#ii,lrhrwrurvr'uaonrr.:lndtndscvduoanr'ritqrel::1grJfi t1 firir,:nrulfifulnrrvra-

rilurrdrtlnrllo1 finu dt,:urnrvinolnrirluuvrsriutrdrlJoglurtnfr nd{mnusu e-a drlrr ln
r;l-:.rl urarfifl drufiuoonmnitntu rdaflorrYul*jtfi p<1 lunarm.rrgufiul:Jrufinoun:ruld'

nnlndnrqrnttndsui:rstlnrtrrorfuiltdlttnv00m']nt$nd (transcellutar shift;''"lunrr;
rlnficcordunrfliNrulo.tao{lu insulin rrn: p.-adrenergic catecholamine aoihuvY.rgo,rinv

Potassiun Disorders flivy1 {nurin 585

(RBC, Muscle, Liver, Bone)
250 2635 250 300 In_Eq

ICF 1osxl
Kidney 90%

t@l -e'6i5emE-q[ex.-'Fti*l
mK E-sq0/d-1a0y0
(2%) Colon l0%

1flt.nJ uf,n,JnaflBnl unfiLfratJ[ui.tnn.tu

fnryfiunr:rir.,lruro\r Na-K-ATpase fi,,:ogifinni.rrrnd drtfi rodouiirdlzod uoncrndnmv

hyperkatemia fl.rfi zunlnan:rririfih uvrnrfi trrnfi oudrdr rrari':.trndu

Iiluila16urJ'luvlnrorriin:0.:rjruniruln (gtomerutus) e;qngana'1fr proximat tubute (60-
70 %) ufl: thick ascending timb of Hente's toop (20-30%) ritfilnunar6urirydaluyiolrurf,l
?c6"! distal tubule !?:}l.lru j 0%o rSrrn-rvnoodoUlrldrurlaruii6rn,jr cortical collecting tubule

(ccr) ivfi principar cerr rirr.rfrfiva"n'hnr:nruqml::mrulyrrMorfirJrJfioonHl'luiJnorrv.iroc

rrnriafior f;:jd z1 louo:ir;uogjrYu e r]o{urn-n' 6o

1. [K lurnlflr1 fi'rqoo;dr1fifinr:rTilyr uyrorfirrynrln 1fr cc1 rfiirulrndu un:flro'r
o:nanr:rlir unarfitrr d ccr

C CT= c.rllc6l
colleding tubule

Mrin Eit6 ofnd

10
%

20-

5o,100nEq/day

i za uaal renal potassium exrj'.etion, ion transpon in pincipat ce at cortical collecting tubule

586 remirrinlnqnfrugrl

2, Aldosterone hormone evtli nr:1ilTflttrf,t6uu (K secretion) lou aldosterone o;
dlfii aldosterone receptor fi principal cell nr;{utr{ epithelial sodium channel (ENac) tflq ln
l*u ua:qonn'r:1tr6uilrfiildu rfluzuntrltu tubular lumen rflunlrrndu uavfinr:d':-r1n uvrol6ut

To! passive transport oafl {uflflf,Tt;tJrndu uonornd aldosterone titrir'lfi rua-r ATPase fi

basolaterat membrane ri, ,rrurfrldu drlfifilnrrnorfur'lu principal cell lrndu ttn:orrr:ot'tl

oonernrr'tnru'Ifi rniiu 1;rld e1
3. Distat flow v6or.lir.rrrufloomv (Nta uac ;1) dlvnoonrrtuviolnriru aru (distal tubule

ruo: ccr) drfi ilT ruurnfilvfi Na 'lu lumen tLitrru cct rrn rfluarnrir'hifinr:gnndultrduu

(fl1'r ENac) rro:d nunarfiuraanvrnt*ud'odnrir,'hl{rudu n:nifrfi ecr volume contraction Q;
finrrgnnn':.rro,r1zrfiur un:frtl'rn ri'.:riu6tfi distal flow riou vritfi:lil'rrul'r rm n 16 uld g nrilo a n
hirfimr*u *r('irrirlrunairdc:fi aldosterone q-r lulrulfi{rhufiddiJrd'!ioorr: (diuretics) ttfl:fi
volume depletion {itfi::d'r aldosterone g.':dxx]nil distal flow ilrn lflus,ladrlfifinr:rTl K oon
ornirrnrad ccT rl'rn myfi hypokalemia nr x'l

loaofl::n'l 1q lunnrnrr o:duo{rfr.rnr:ladouto,th urotiurtfitoonorntrad ttacntt

rl vrrmc16urvt't.:oqcr::Lto;dtn Tnudtmnalnrrvou6une:nnnrt-rn fi principal cell d.toqjlu ccr

foruordu:lodu?a-n B r;n'n6o t I ::arl 16 lul'rnrf,Nr 2) {il?uoglunm;fifiaofhu aldosterone
qn (rdu votume deptetion) uialri ua; 3) {ilxafi distal flow ( 5 1ruflaom;1 rf uotirol: drnrll

nrrfiuTvurvrorfitlt.t (K intake) evfiflodrllirfin hyperkalemia frrio riia{:-hufiiftyrrlunr:t"tt K. vrr,:
lsrooa.xdrHdiuM'ru*u un;rda{crnTflurdt6fltJfioH'luo'tflr:rfr}J {rrflunr:srniie:tfio hypokalemia
crnn'r:!3TnnI fl oufr s''rodr.rt6ur

10
(7o k9 Aduk)

Serum K*
(mmEcy'L)

K+ Deficit (mEq) K- Excess (mEq)

Ttii e u*ntanxdxriuizninlnunatfiue.fiudaauazntttJdtnwJavnr[wunat6uxlui^,ntu'

Potassiua I)isorde$ atfrvy1 inuiin 587

fidrn''rg uotdo,:r:rilurrm.Jf,l-fi6o nrrldur{uf,::n.jr,::llilrruTvr ffiou6u:rtuir.,rnru ltotal

bodv potassium) uocnr:!:Jduuurjnmv6'u 1q lunnrorriin"nururflu "curvirinear" o 6rJfi s) lu
nu;r-Jdr,r:Jnfid.:fi::o'l 1q ,rJnfifi 3.5-5.s mmol/L e:finTc [6 l,uvlorolrann,! 1 mmo/L lddofi

totat body potassium noo{ 200-400 mrq lrtru;fifir'ludr,rnrufrlvr rryrolfirrtrlrnrsurfiu.r too-

200 mEq r:rirlfi 16 tu prasma rfildu r mmovr uiowlrnTuursriurrflurnfiauiiifiri?mru

rrn'lurtnd d'rriu flri'rtnrufinrrvlroTflurra16E r.J (potassium depletion) q; lfinnr:undours,r K
ornturrnfaanlrrortmanrrnd 'lurruvro'EJri'uf,r'ldfrl K+ crnarfirflfiscr:utrlult?lrrug.: 1r

tr;:ra:u:n :ymnr5aun: solo,ITntlriarqulfildr-ll:qnt"uoanlr.rrlcort;tunm 4-6d{ ,1 .tru

Souny 80-g0 r0{firn6ocvrnfl'oufrLdrrrndrfjo.:o.rn 16 fig,::t8uo;n:v{utfiy6'.r insutin ufidu Ins
:vrr'uzo':luuvrcrful'lugnf c;rflufirrirrun'irfndrula.flvruno16urd'ldfuoyrndouir{rmndtd

llrnriouudlru

Hypokalemia

fi srr fionmyiifi nlr.r rdrduto.:lvlursr6urltunaralr 1Kl rioln.ir 3.5 mmot/L

Normal physiologic response to hypokalemias
rfiafi nypokatemia iioirunrjr CCT roolnctoqndr:Tvrlmnrfiurg,:norflunadrtfi
1) K excreiion < 15-20 mmol/day (K. excretion = urine [K] x urine volume

dadrn"nfi odo.:rfi ufldd1?: 24 d'rT rrrirusu rdolornnrurdldurot K tuiasrr:lu

rusin;tir,:trarq;lrjrvirriu lirlfiluurrlfiri6ri1il1d1u{urudfi hypokaremra luu:.r

2) Iianstubutar [K-] gradient (TTKG) < s

TTKG n'rurruldqrnan,r

TIKG tKlu4Kpl
lU/Plosm

Ioufi 1rc1u = urine potassium concentration
= plasma potassium concentration
tKlp
Osm = osmolality

TTKG (transtubular potassium gradientl 6a Truvrnrfialfirirloontto:ou'hrinorrydarilmj.r

rJnraqo ccr 6:lii z1 il'.rrfluaommnnr:rir,rrumlaoflxu ardosrerone rdomrn ccr lflunhrrmj.r

un'ntunr:nrrnrnr:riu K. ornirrnru nn-rornflaatr:airucrn ccr lfid meduflary coflecting

duct (l\rCD) tsfinrrr filuurjo.r K'flux dou rn uriddruvlir McD ?:fin1?oond'urir rdrddr{nrfl

(lou6nivrnro,,,: anridiuretic hormone) {iuflunodrlfi 611ur)oorr:diold4.rdu lrdouJiurrfiurnir
[Kl 'lu tumen uinrudru:Jnrsta,0 ccl
louti'dilfirfinrrrir.:rurao ddosterone o:trLir 'tu

1K1

588 rtnirriainqmdugru

tumen iirirrrudru muto{ ccT o:fin?r rtu'fiug.,rrflu 7 tYi1rro.t 1xl'lurrrnror.n d"rriurfiori'o

6rinato.,:nr:gonO':Lrhfi r,,lco 6,,rdatriT (ulp)osmolality tJ1fi't:elno'n:rdru6',:neirr rl:vTani

flo\r TTKG doldnrrrfiri1aRrrvn{trdur (spot urine) lrn'ruru dodrfi'ofidrn''ry60 rirdo:rirrr
'atu'ftirlddfisitorfdio urine osmolality frrirgtnir plasma osmolaliiy tviltiu

3) Urine potassium-creatinine ratio (UK/UCreat) < 1.5 mmol/mmol creatinine
'ld soot urine'lunr:q:rqtdurGurn'! TrKG tdo':ernnrfl{o creatinine Tln'lu (creatinine

excrerion) fidrdoudr.rn':fi eirdrrnn'jT t.s lu{rhu hypokalemia il,:d'irfrnr:grglfraltttrfit6lr

r1,i Ln

6n lfiqtol hypokalemia tl',i tfincrn nr: rn doufitalTvr rno 16ilil rdl rtnd fifluilou'lu{:-huinqn

lf uri nrxdfi insulin g.trsu (ttju hyperalimentation rSoernnr:fnEl hyperglycemia). urfifinr:

nrrr$d r ttfle\tf,lrrqnan hypokalemiac

.1) sole cause
2) "K*srh"i"it"i"n-to" ce^lls"n"Orr"*

a. Hormone administration or excess (insulin, F-adrenergics, aldosterone)

b. Anabolism (recovery trom DKA, marked increase in blood all production)

c. Alkalosis (metabolic. respiratory) -l

d. Other (hypothermia, hypokalemic periodic paralysis)

3) Increased gastrointestinal losses :

a. Upper Gl loss : Vomiting, tube drainage

b. Lower Gl loss : Diarrhea. laxative

4) Increased urinary K losses

a. Associated with ECF volume contraction (high renin, high aldosterone): the most

common

i- Associaled with renal salt loss:diurctics. salt-wasting nephropathy including Bartter's

or Gitelman's syndrome

ii. Associated with non-reabsorbable anions (HCO-S in vomitinq and type 2 RTA,
F-hydroxybytyrate in qEA, hippurale in glue-sniffing)

b. Associaled with hyperlension (hypermineralocorticoid stat€s)

i. High aldosterone, low renin: aldosterone-producing adenoma, adrenal hyperplasia

ii. High aldGterone, high renin : renal artery stenosis. renin-secreting tumor. malignant

nyp€rrensron
iii. Low aldosterone. low renin (non-aldoslerone mediated Cushing syndrome,

exogenous steroid, licorice, Liddle syndrome

c. Other: hypomagnesemia, amphotericin B. dialysis. plasmapheresis

nirrur: clr qfiriurjoulu {r-l'ruinq n

Pot?Lssium Disorder.s ttfivy iauzia 589

n:;du P,-adrenergic receptor ttiu ulr,iuflulufidoon tLny epinephrine nalnta"n tfinqrnfinr:

nry{un1id'r.I'luflo{ Na-K-ATpase n.t.t; alkalosis virlfi x, ornrrodoonrJ. u ECF *onfi'!
lvruyroLfifliltu rcr drprfiourfir cel lau$lu.jr pH figodu o.t osd{ti [K] ann,i 0.2 mmot/L rrn;

0.3 mmol/L 'tu respiratory alkalosis rrfly metabolic alkalosis ntlrirrYlr

n1rfl;1.:lra6!fior6anl,uilitrrulrn niu ra',:nr:inur megatoblastic anemia dru folic
actd fi5o vitamin et2 yio inul neutropenia d?u ev-csr q:lirlfirrnfidcirolnrifinr:td (uptare)

ln uvrarfiururdrlulrndlurJslT rurrn unlrfia hypokatemia ld'

rfttirj upper gastrointestinal loss niu nrryartiu!, nt:gerfiu gastric content itJ.uu
:rln eilru hypokalemia i? n"u metabotic alkatosis lunnjldufi.irnr:4rylfiull uror6ulyr,: ct

c;l tJrn [!0itll'o{e1nfi metabotic atkalosis e-,ltfu lco,- d4.r1ur6onvrh1fifi sooium bicarbonate

aon rflr.rflf,firlcurn un:finr:lriilduro.l di"t"t ttow irlliuffJruiifi hypovotemia 6.rrir1fifi

K iatdosterone turfioogr d{ z flce-flo,tn.irr rirtrfifinr:gryrfiu 1 rJ.}n 1fi ccry tuwrrm:.1

du{:Jrufifi lower Gt toss tor1nuvrariul rtju rio,r lfrunialfrmriru e:uu hypokatemia drlniu

metabotic acidosis nr:dudutu{rlrufildiuln [vrorfiu fiau, fi K stritt rdrrra{ uo:nsilfiaryrfiu
lvtuflolfiu yr'r,r:yl::tr.:r6uotrtt e;finr:nouduo,ito nsiant: hypokalemia rflu:lnfi 60fi

K excretion < 15 mmouday. UK/Uc.*r < 1.5 mmol/mmol creatinine. Eo TTKG < g

n{lfi fi nrrqryrdu K mr,,:fl aarr; urj,,r rfl un{ltn{1 ldrf u

t I nri frfi votume deptetion rirtfifi nyperatoosteronism drilrYufirle{udd{fifi oistar

flow d.t l,rv.iqln u'r6ontrdlora.:. nr:ldurn-lilRorr: y?afi non+eabsorbabte anion rnluflaoms

(nr:r.rd t do +y a.;

Z1 nojt.tfifi hypermineralocorticoid state otnarruqdrrl 1n'r:t.0fi t .fia q) O.) r3.:lrnfifi

nr:r4ni,: aldosterone qtfl adrenal gland rLrnfio n6, nr:fiar:d,lfiqvrdnntg aldosterone ni du
luirrnru (niu Cushing syndrome) un:ldiuornnruuanir,Jnru (niu steroid abuse, ticorice)

a"nr*ru;rfrdqto.rfl:Jransjld6o'hjvrlnlxy EcF votume contraction un:fiaruo'u1nfinar

s1 n{filrifi hypertension Lrotadtunl?y normovotemia idrn'rlun:tl ol'lurrt:-irrio

inqn 6o hypomagnesemia [!fl; magnesium depletion

nr:duf,uddrfi'o-lun{lrifinr:gqrfiu1vr *noriurrndn (renat K toss) 6B uu K- excretion

> 30 mmol/L ria > t5 mmol/day U*/uc.* > 1.5 mmol/mmal creatinine, y5o .l-ffc > g

Slnlludnrt (symptoms)s

{ilrudfi mitc hypokatemia (K g-3.S mmot/L} d.lu rnq:l fio1nr:lo1 rdo 1r1lunarnrr
fi:;niun'ra.: lvfiarnr:roiud:;uurdu ::dlun;nfilrrda niu daunrdu lrifiu:r n:nirfirr fia.,:
gn il{:hud 1r1 tunnrorrni:.nn y?on"rarjr.:morir arce;?l! rhabdomyotysis fi1ule6iMn

cyu r'r,nu'ruB?nqm !g'ru

oufi{nrr:vru'lqrru (respiratory lailure) ornlrrfi6jrde::uu:,1tfiutto duorifiion:rnr:nnarta,r
lK'.1 d1flfuflnlrrr$ide e: rfiorjofllil{rJrufifiT:nri':loo$ 16r mju cardiac ischemia, heart failure

14ia left ventricular hypertrophy tJlriou

ECG abnormalities

e:rrrr.rirfiorlnfirfia Kl sirnirfiSorvirriu 2.5-3 mmoUl loucyl'rll U wave, T wave flattening

uia ST segment changes (grJfr 4)

Iltlii uaor U wave'lufiitrtfrfi bypokalemia

Arrhythmias associated with hypokalemia
Hypokatemia rflunrrtqto.r rtrlo rdufio{'rnrc tiaii'rleuqnrfiu (cardiac arrest)Ioaronrt

odr.,rij.: firiruf.ildilLar digitatis oejriau e:finrr rda,ra.:lunr:rfinfirlo rfiufinr-.:rr: q'rn hypo-

Ventricular tachycardia I Ventricular fibri ation W, VF)
riJufir:rl'jrnrr: hypokatemia e:n::{ulfirfinr w Lray vF lfi louronr;adrliirtu{rhliifi

W/vr nunarndr! rdarirtonru riuuvrc'u (acute myocardial infarction) fidorruydljrnr:fnur
hi 1r1 turnrnrtrlnnir 3.9 mmot/Lc 0lqeynacrrrrldu,r'lunr:ufio vr 16

rirter6!ftFr{,lyryd.r 2 u :ldalaer'l nolnuo,:sio cardioversion uny defibri ation fi'r
R'rlc hypokalemia hi'l6fljnmurft 1l

Long QT syndrcme and Torsade de pointes

riJunrr;firfioorn ion channel ftvriyfirdlfifi ventricutar repotarization dr,:rufinlnfi

nr:rro1lturo16ur rrn:l?160r'roLrrJnfi16ur.r lflun'r lrqdr6"qro.,rnrrrirmufin:lnfilo,r ion channel
e"tnailr fithflarqeyrutdruotnr:lflun (syncope) yio cardiac anest rdnrirdo,'lun1:inu1n1x:
ddaufib hypokatemia ir:rflu'iri MgSo, uri{ilru

Patients taking antiarrhythmic drug

Hypokalemia e;aaqmf, antianhythmic ?o,,ru1nqiild ot".lriutufiftafi\{trinulnrr:frtq
rfiufioe-rvr: rirulirornr:ri'rnoirrfirrnd'udliudo,,rfitfiuirfi:lrtfi hypokalemia uio'tri uoncrn
dnrr:do:rairqrf,lrjfi.r r:otdtrotur antianhythmic class lll uiu sotalol drlfifiilrarfin anhythmia

1n?u

Potassium Disorders ztftvg,t inwin 597

Approach to hypokal€mia

rirli 2 !ru! rrud 1 (uilu{fid t1 'ldarnrrnr.n6finir'fuaranr:n:?oyt.',,1io\:rjtf6nr

yzrut't! (acid-base status)

?s€ulgrypqka lemia _ --

-Emergency ?:EK6, PaCO, llove t0 therapy

- 6itelman, BarHer - Periodic paralysis sporadic, - chronic diarrhea
- Mg++ deficiency famillial thyrotoxic - Renal tubular acidosis
- lvlineralocorticold like - Toluene abuse
- H0rmonesiB-adrenergics, - Acetazolamide
excess $ate insulin

twuPid uantuuznxluntt approach n12t hypoklemia (uuud t)

Renal K conserve Renal K loss

TTKG<3 TTKG >3
K exc.rate <15-20 rrmoYday E erc.rate >15-Po mmol/day

uk/!creat < 1.5 UULJcreat > 1.5

Extra renal loss Metabolic [,,leta bol:c
- Decreased inbke ACr00srs Alkalosis
-Formef renal K loss

'Hormones: Insulin, Periodic poralysls
p-aCrenergics .Sporddic

. l,letabolic a1 ka losis . Familal
.Anabolrc status
. Thyrotoxic

wuq0i z uda,tttulnxllntz apprach nlxJ hypokatemja luuai Z)

592 rrtdlininqndugru

ldrniuuuufi z (unu4fi d 2) uan?1nia{nfl 1,tn6fi n ravnl?ln:odrtufir u"tlddoXarfi

rfiru6u1 niu nlild'uInfiq ttn; volume status ttfl3n15ff??oq'lrfin'r:grurfiu K vrr.:ioorr:vio

\', o ftfru'-J!flu60119-,{Su-n-,,
[rJ 5',]r|o',rU

1. {ilxu hypokalemia .ir rfludo.,rldirnrrinurSr-rriruvioLj njufi cardiac arrhythmia

(VT /F, cardiac anest) v5aa{'lun'r?tiifin1?:x1u'tedltuat (impending respiratory failure) niu

vru'lodr r.r?o eaco, rfr rl:u drfi nm:o'tnrirrfi ot'htnr:inuroeir''tSlrdru

re. fi{rjfinrr:gnriu :J:v rfiuutrn'ir{:lrufi renal toss niolrilnrfll?ga'rn K* excretion

rate. TTKG ia Uk/Ucreatinine ratio (rrnu{fifi 2)

3. dn?udlilfi renal K- loss 6o K- excretion < 15-20 mmoyday. TTKG < s tfirrunarrlq
latridri:ci6, rvd'u ltq tunarnrr un:nr:sr:rcdt,tntu 1unu4fifi z1

- fir t{ tuunra rsrir'rn :J:;i6rfiori'l ta''rldarvrrnrflilaro:nrJirrrulrn {:Jra
i paralysis unl fiqnn:ndr.rtflurJna tfiaofi,J hypokalemic periodic paralysis (HPP)

rud':qornr:rrrn6finnfl{R1xv hyperthyroidism unvfn:J::i6n:ounirttiouunortvn
O-gnUS\t

- nr:dfi K. shift a'rnfi'rrfiqdu"l viofinr:ld'irf,'uo1n1r x. riou rflubilfiurnrrnd

ovrir'Ififi seuere hypokalemia lutrnroYudu vSorflulrnlun::ri'.lrir1fifi paralysis

- dT nirnojudfin'rrqsy!fru K r1n6u.i (extra-renat K- toss) dd, r{'rudonsjrdfi oiarrtrea

cv ]ldrtJfi! normal anion gap metabolic acidosis

+. n{#fi renal K loss (K excretion > 15-20 mmol/day, TTKG > 3 t5o U*/Uo*, > 1.5
mmol/mmol creatinine) urioldrflu z n{dnd

+.t ndufifiare: metabolic acidosis ovfidnrru:tflu normal anion gap metabolic

acidcsis dt:fi'r hyperkalemia cvttil.,tTaflld urine net charge (NHa secretion) 'lrrflu distal renal

tubular acidosis 1nfn1 nia hippuric acidosis clnn'lTo|]n'l'l (glue sniffing)

+.e n{liifi hypokalemia irrri:.t metabolic atkalosis sunTnu'ld yolume status $n;
blood pressure rrunrflun{ldfi EcF votume contraction 1nr:rrd t {o +1 a1 un:nnjrdfi ecr
volume nfi drrnr hypertension (mineralocorticoid-like excessl itttnrjldo;rrri.: ttannr lv4ld
Tnu'lt:coi! renin un;t:ri'r atdesterone 'lurnrf, r dlnr:r'rfi 1 do 4) b)

n'rtinvrRms hypokalemias

n,lli-fl:J1ly2$- fl1ln?1 ?uttl\nB{nl?Y hypokalemia un:o1n'lludonsl'r{'l t? r"t-!n't:tlF?'uJ

fiqilnfiilr.rndu!{fitir'lcv5o cardiac arrhythmia

flrtru#lriiorrnqru:,r
am?!fi01n1:€iauu:,,r r6nriauniafiurinrrrfin:ln6rarnfiu'lvtflrrirlc lnalriur arrhvthmia

Poussiurlr Di-sordcrs nivy inuvfa 593

ruaylrifi digitatis intoxication 1 d.rriu6o.rir ufill nr: ir4'nurfimrrurtdiEnr:fiuriou lorr:rrfi

z) tirfiunia'hivrrr NG iube lrild 6{rior:rurlfirnrr peripherat vein nrurt:rduron K- lrjLnu 40

mmot/L 'lunr:a:nrufi'lrifinglao nr:ufibnr:rfirtfi 1xl rroqjtu::n"rdhjrfluoiun:rr niu [x']
tfil3-3.5 mmol/L un-rernu"urioul
u ar6u rtouyrufrl1 {i,i0141{rxn1yn1u'lu

zqrtrofi LLflFhr oral form oJ potassium replacement

Type Form Amount of |f Rout6 lndieatiofl Pr$cription I

KCI Elixir 15 ml = 20 mEq Oral Shift lf weakness. 30 ml oral stal then

r the observe weakness, can repeat
dose after 4-6 hrs

Oral K dei lf serum K 3.0-3.5. 15 ml qid pc.

Alkalosis lf serum K 2.0 3.0. 30 ml qid

Follow up serum K next 12-24 h.

lV NPO 40 mEq in NS92 or NSS
form
KCI Tablet 1 tab = 10 mEq Oral 1000 ml in 8-12 hrs

K Citrate Mix. '15 ml = 9 mEq Oral Gl irritate 1-2 tabs oral tid pc.

?Taste Dose equivalent

Acidosis 30 ml oral qid pc

fiileufii tite-ttrreatening arhylfi mia ltio cardiac arrest

frugrunrufddrn"rplufidlun4ildAa hypokatemiaori'r{t6fl'res'lxjlfuflltvqtann']:fi cardiac
arrhythmia fiquu:.: 1w, vF) x60 cardiac arrest e:fifllrvqdu1 drndrulana arrtqiidrd"rplu

firhuinqfiFo n1x;1l1ou nfi[6u (magnesium depletion), nr:'ldil oigitatis ttn; myocardial
ischemia o.rriu .iliudo.rvldr rfi nd1 tLfl :inurl druriu rolo

n'r:lfiTvrurarfiur.rvrnurulu{rJrunnjrd:rln'.:lu{:Jrufifiarnr:dautt:-rrrnua:ad'lu
nrr:fiarce:finrrvru'lofir.r lvnr (impending respiratory {ailure) et'hi x-'luaot:r 10-20 mmol/hr
vn{ centrat vein ddra'rpfio fio.:flnr:lhr:sr't EKG monitoring odr,:siotfio,J :rlfr,t6onrr::nil

1rl 'luunrolrnn t -e rirTr'r rx ri,r6nar itlrru:loomvun:trfirfilsl

fir arrhythmia lriddu drrfludo.rfier:rut'lti magnesium rorurududrs rrnu4fifi e npJ
rrurrrrnr:inurn'r1v hypokalemia

ia6ouorn ue:ffsfi.rtviirlunrtinsr hypokalemia
11 nr:no:-rauotoianrrlfiTnuncrdullu{ilrufifi severe hypokalemia o:rfim:n"l [rl 1d

fi'r'lutir.ru:n lfin rdo,rqrnturtadti,rrro K- n'.niu x' iitriq: rdr}lvrouvuturtndriou rirtfi:vnir

594 ntfrriainqmdlSru

1x1 tuunrolrlvdudrluril:u:n (;rJd e1 uo:rfluoio'tfiurnnn6r$jlilivrrunr:1fi'Tr,rrflorfurJ fifl'.o

rrnriufirft'tfi K rnnnu'luo-n:rriruirrdr ::d:.r trl evrfiuduorirmmrir lgrJd a1 arccvrir}i

rfiqn'r'rs hyperkalemia d,l!r,'rni,'rarrrfluff qlfi udadieilfi
2) lilauduuos ufihcr ruq ddra'rytu4rJrriinqn fi a hypomagnesemia r?o magnesium

deptetion rirlfinr:ufib hyperkatemia rirlddrunclridtSc

SerumK<3,0mmol/l

Seek expert help:

No Symtomg Ufs thr€dtoning lrypokslaomla

ECG may shoM Assoclabd wlth any fftythmia
U wa\re€ W most common
T wave tlattening
ST segment changes Assoclatod wllh $vcra dlgoxin toxldty

with unstabls cardiac rhythm

Potasssium chloride Potassium chloride lV
10 mmol/trr 20 mmol/hr
Increase dietary K
(Max rats: 20 mmd ove|10
min follow€d by 10 mmd
over 10 min)

magnesium Sulphate Magn€eium Sulphate lV
not n€oessary unless
Mg level low 5ml

ov6r 30 min

Fe-check K
(recommended after every 40 mmd if normal renal function

or atter every 20 mmol if severe rsnal impairmenl)

Consider cause ol hypokalaemia and address all precipitating factors

wugfri a uf,nn emergency treatment algorithm for hypokalemic patient"

Potassium Dis<rrders tiiug't inutin 595

3) flrfinrrranrdu do'rerfiooun:rflfi,rf,inmn hypokaremia d'ortrinr:inurvriufiloulrir{a.r

iunr:n:reifi ed'urrarrrqfi aurni
+1 hinr:ifi potassium rnuyulunr:ncnrflnaTno rfro.terno:n::dunr:rdr insutin L!flr

rfirnr:ra6oura,:Tn*yrRriur r{r rrnd

S; firfirJ'lafi metabotic acidosis iudru'l*inr:ufih acidosis riauufib hypokatemia

rrflvo;rirtri 1r1lulrorau'rii.rsr\n.1n'j16ru un riulun:rfl.ir lflu ldufi acidosis :uu:',:ouorrrfiu6igl

ld nr:ud}rnrr:ri,,:oo.,r1ildruriu ua;dr:ri.,,: cardiac arrhythmia [o:nl.ly respiratory faiture

adr-r1nfifio

Hyperkalemia

fi urr 6on.n:fi fi nrr ru rdlfi ulo,rl,r uvrorfr tL l'lunarolr [K,l rJt n nil s m mot/L

Normal physiologic response to hyperkalemia5

tiafi hyperkatemia a:n::fiunt:ya'r atdosterone ?1n adrenal gland ttinijtnl:fliu

1rr unc16errvrrr'ln rfl us{adrtfi

'1) K. excretion > 100-150 mmot/day ldalrfrlflaarr: z+ ri.:Irr)

2) TTKG > I

3) Urine K / urine creatinine ratio > 1O-1S mmol/mmol creatinine

3qrrr,tfi lLf,oiflltfi nso$ hyperkalemia6

1) High K'intake (an unlikely sote cause)

2) Shift of K from ICF ro the ECF

a. Cell necrosis : rhabdomyolysis, intravascular hemolysis
b- Hormone deficiency or blockade of insulins, l3-adrenergics, aldosterone
c. Metabolic acidosis: inorganic acid
d. Increased tissue catabolism
e. Other: digitalis overdose. hyperkalemic periodic paralysis. succinylcholine
3) Decreased renal K.excretion

a. Hypoaldosteronism (at:i,rfi 4)

b. Renal Jailure
c. Low distal delivery of urine (effective circulating volume depletion)
d. Hyperkalemic type 1 FITA.
e- Selective impairment o'f potassium excretion

f. U reterojejunosto my

irmn: nrr:fr lurjoaluftJruinq n