Chapter 2 Fluid &Elecrolytes

8/13/2019 Chapter 2 Fluid &Elecrolytes

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CHAPTER 2 - Fluid and Electrolyte

Management of the Surgical Patient

G. Tom Shire !!!

Anna"el #ar"er

G. Tom Shire

ANATOMY OF BODY FLUIDS

One of the most critical aspects of patient care is management of the composition of

bod fl!ids and electroltes" Most diseases# man in$!ries# and e%en operati%e tra!ma

ha%e a great impact on the phsiolog of fl!ids and electroltes in the bod" These

changes often e&ceed those bro!ght abo!t b ac!te lac' of alimentation" A thoro!gh

!nderstanding of the metabolism of salt# (ater# and electroltes and of certain

metabolic responses is essential to the care of s!rgical patients"

In the sections that follo(# the anatom of bod fl!ids and the phsiologic principles

that maintain normal fl!id and electroltes are defined# and a classification of

derangements is o!tlined to allo( an organi)ed therape!tic approach"

A prere*!isite to the !nderstanding of fl!id and electrolte management is 'no(ledge

of the e&tent and composition of the %ario!s bod fl!id compartments" +arl attempts

to define these compartments (ere relati%el acc!rate# b!t a more precise definition

has been obtained b man in%estigators thro!gh the !se of isotope tracer techni*!es"

The (ide range of normal %al!es is a f!nction of bod si)e# (eight# and se b!t these

compartments are relati%el constant in the indi%id!al patient in the normal steadstate" The fig!res !sed in this section are appro&imate and presented as a percentage

of bod (eight"

Total Bod ,ater

,ater constit!tes -. to /. percent of total bod (eight" Using de!teri!m o&ide or

tritiated (ater for meas!rement of total bod (ater# the a%erage normal %al!e is 0.

percent of bod (eight for o!ng ad!lt males and -. percent for o!ng ad!lt females"

A normal %ariation of 12- percent applies to both gro!ps" The act!al fig!re for each

health indi%id!al is remar'abl constant and is a f!nction of se%eral %ariables#

incl!ding age and lean bod mass" Beca!se fat contains little (ater# the lean

indi%id!al has a greater proportion of (ater to total bod (eight than the obese

person" The lo(er percentage of total bod (ater in females correlates (ell (ith a

relati%el large amo!nt of s!bc!taneo!s adipose tiss!e and small m!scle mass" Moore

and associates demonstrated that total bod (ater as a percentage of total bod (eight

decreases steadil and significantl (ith age to a lo( of -3 and 4/ percent in males

and females# respecti%el" 5on%ersel# the highest proportion of total bod (ater to

bod (eight is fo!nd in ne(borns# (ith a ma&im!m of /- to 6. percent" D!ring the

first se%eral months after birth# there is a grad!al 7phsiologic8 loss of bod (ater as

infants ad$!st to their en%ironment" At 2 ear of age# the total bod (ater a%erages

appro&imatel 0- percent of the bod (eight and remains relati%el constant

thro!gho!t the remainder of infanc and childhood"


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The (ater of the bod is di%ided into three f!nctional compartments 9Fig" 3:2;" The

fl!id (ithin the bod potassi!m

and magnesi!m are the principal cations# and phosphates and proteins the principal

anions" This is an appro&imation# beca!se fe( data concerning the intracell!lar fl!id

are a%ailable"

+&tracell!lar Fl!id

The total e&tracell!lar fl!id %ol!me represents appro&imatel 3. percent of the bod

(eight" The e&tracell!lar fl!id compartment has t(o ma$or s!bdi%isions" The plasma

%ol!me comprises appro&imatel - percent of the bod (eight in the normal ad!lt"

The interstitial# or e&tra%asc!lar# e&tracell!lar fl!id %ol!me comprises appro&imatel

2- percent of the bod (eight"

The interstitial fl!id is f!rther complicated b ha%ing a rapidl e*!ilibrating

f!nctional component as (ell as se%eral more slo(l e*!ilibrating nonf!nctioning

components" The nonf!nctioning components incl!de connecti%e tiss!e (ater and

(ater that has been termed transcell!lar# (hich incl!des cerebrospinal and $oint

fl!ids" This nonf!nctional component normall represents onl 2. percent of the

interstitial fl!id %ol!me 92 to 3 percent of bod (eight; and sho!ld not be conf!sed

(ith the relati%el nonf!nctional e&tracell!lar fl!id# often called a 7third space#8

fo!nd in b!rns and soft:tiss!e in$!ries"

The normal constit!ents of the e&tracell!lar fl!id are sho(n in Fig" 3:3> sodi!m is the

principal cation# and chloride and bicarbonate the principal anions" ?lasma and

interstitial fl!id differ slightl in ionic composition" Beca!se plasma has a higher

protein content 9organic anions;# its total concentration of cations is higher and itsconcentration of inorganic anions some(hat lo(er than those of interstitial fl!id# as

e&plained b the @ibbs: Donnan e*!ilibri!m e*!ation 9i"e"# the prod!ct of the

concentrations of an pair of diff!sible cations and anions on one side of a

semipermeable membrane is e*!al to the prod!ct of the same pair of ions on the other

side;" For practical considerations# ho(e%er# the ma be considered e*!al" The total

concentration of intracell!lar ions e&ceeds that of the e&tracell!lar compartment and

seems to %iolate the concept of osmolar e*!ilibri!m bet(een the t(o compartments"

This apparent discrepanc is d!e to the fact that the concentration of ions is e&pressed

in millie*!i%alents 9m+*;# (itho!t regard to osmotic acti%it" In addition# some of the

intracell!lar cations probabl e&ist in !ndissociated form"

Osmotic ?ress!re


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alters the effecti%e osmotic press!re in either compartment res!lts in redistrib!tion of

(ater bet(een the compartments" Th!s an increase in effecti%e osmotic press!re in

the e&tracell!lar fl!id# (hich (o!ld occ!r tpicall as a res!lt of increased sodi!m

concentration# (o!ld ca!se a net transfer of (ater from the intracell!lar to the

e&tracell!lar fl!id compartment" This transfer of (ater (o!ld contin!e !ntil the

effecti%e osmotic press!res in the t(o compartments (ere e*!al" 5on%ersel# adecrease in the sodi!m concentration in the e&tracell!lar fl!id (ill ca!se a transfer of

(ater from the e&tracell!lar to the intracell!lar fl!id compartment" Depletion of the

e&tracell!lar fl!id %ol!me (itho!t a change in the concentration of ions (ill not res!lt

in transfer of free (ater from the intracell!lar space"

The intracell!lar fl!id shares in losses that in%ol%e a change in concentration or

composition of the e&tracell!lar fl!id# b!t shares onl slo(l in changes in%ol%ing

loss of isotonic %ol!me alone" For practical considerations# most losses and gains of

bod fl!id are directl from the e&tracell!lar compartment"

NOMAL +G5HAN@+ OF FLUID AND +L+5TOLYT+Sno(ledge of the basic principles go%erning the internal and e&ternal e&changes of

(ater and salt is mandator for care of the patient !ndergoing ma$or operati%e

s!rger" The stable internal fl!id en%ironment# (hich is maintained b the 'idnes#

brain# l!ngs# s'in# and gastrointestinal tract# ma be compromised b s!rgical stress or

b direct damage to an of these organs"

,ater +&change

The normal indi%id!al cons!mes an a%erage of 3... to 3-.. mL (ater per da>

appro&imatel 2-.. mL (ater is ta'en b mo!th# and the rest is e&tracted from solid

food# either from the contents of the food or as the prod!ct of o&idation 9Table 3:2;"

The dail (ater losses incl!de 3-. mL in stools# 6.. to 2-.. mL in !rine# and

appro&imatel 0.. mL as insensible loss" A patient depri%ed of all e&ternal access to

(ater m!st still e&crete a minim!m of -.. to 6.. mL !rine per da in order to e&crete

the prod!cts of catabolism# in addition to the mandator insensible loss thro!gh the

s'in and l!ngs"

Insensible loss of (ater occ!rs thro!gh the s'in 9/- percent; and the l!ngs 93-

percent; and is increased b hpermetabolism# hper%entilation# and fe%er" The

insensible (ater loss thro!gh the s'in is not from e%aporation of (ater from s(eat

glands b!t from (ater %apor formed (ithin the bod and lost thro!gh the s'in" ,ith

e&cessi%e heat prod!ction 9or e&cessi%e en%ironmental heat;# the capacit forinsensible loss thro!gh the s'in is e&ceeded and s(eating occ!rs" These losses ma#

b!t seldom do# e&ceed 3-. mLJda per degree of fe%er" An !nh!midified

tracheostom (ith hper%entilation increases the loss thro!gh the l!ngs and res!lts in

a total insensible loss !p to 2"- LJda"

A fre*!entl o%erloo'ed so!rce of gain is the (ater of sol!tion# (hich is the (ater

that holds carbohdrates and proteins in sol!tion in the cell" Normall# gain of (ater

from this so!rce is )ero# b!t after 4 to - das (itho!t food inta'e# the postoperati%e

patient ma begin to gain significant *!antities of (ater 9!p to -.. mLJda; from

e&cessi%e cell!lar catabolism"

Salt @ain and Losses


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In the normal indi%id!al# dail salt inta'e %aries from -. to E. m+* 9= to - g; as

sodi!m chloride 9Table 3:3;" Balance is maintained primaril b the 'idnes# (hich

e&crete the e&cess salt" Under conditions of red!ced inta'e or e&trarenal losses# the

normal 'idne can red!ce sodi!m e&cretion to less than 2 m+*Jda (ithin 34 h after

restriction" In the patient (ith salt: (asting 'idnes# ho(e%er# the loss ma e&ceed

3.. m+*JL of !rine" S(eat represents a hpotonic loss of fl!ids (ith an a%eragesodi!m concentration of 2- m+*JL in the acclimati)ed person" In the !nacclimati)ed

person# the sodi!m concentration in s(eat ma be 0. m+*JL or more" Insensible fl!id

lost from the s'in and l!ngs# b definition# is p!re (ater" For practical considerations#

normal losses ma be relati%el free of salt in the health indi%id!al (ith normal renal

f!nction"

The %ol!me and composition of %ario!s tpes of gastrointestinal secretions are sho(n

in Table 3:=" @astrointestinal losses !s!all are isotonic or slightl hpotonic#

altho!gh there is considerable %ariation in the composition" These sho!ld be replaced

b an essentiall isotonic salt sol!tion" It is also important to reiterate that

distrib!tional or se*!estration losses of e&tracell!lar fl!id at an point in the operati%eor postoperati%e co!rse also represent isotonic losses of salt and (ater"

5LASSIFI5ATION OF BODY FLUID 5HAN@+S

The disorders in fl!id balance ma be classified in three general categories

dist!rbances of 92; %ol!me# 93; concentration# and 9=; composition" Of primar

importance is the concept that altho!gh these dist!rbances are interrelated# each is a

separate entit"

If an isotonic salt sol!tion is added to or lost from the bod fl!ids# onl the %ol!me of

the e&tracell!lar fl!id is changed" The ac!te loss of an isotonic e&tracell!lar sol!tion#

s!ch as intestinal $!ice# is follo(ed b a significant decrease in the e&tracell!lar fl!id

%ol!me and little# if an# change in the intracell!lar fl!id %ol!me" Fl!id (ill not be

transferred from the intracell!lar space to refill the depleted e&tracell!lar space as

long as the osmolarit remains the same in the t(o compartments"

If (ater alone is added to or lost from the e&tracell!lar fl!id# the concentration of

osmoticall acti%e particles changes" Sodi!m ions acco!nt for E. percent of the

osmoticall acti%e particles in the e&tracell!lar fl!id and generall reflect the tonicit

of bod fl!id compartments" If the e&tracell!lar fl!id is depleted of sodi!m# (ater (ill

pass into the intracell!lar space !ntil osmolarit is again e*!al in the t(o

compartments"

The concentration of most other ions (ithin the e&tracell!lar fl!id compartment can

be altered (itho!t significant change in the total n!mber of osmoticall acti%e

particles# th!s prod!cing onl a compositional change" For instance# a rise of the

ser!m potassi!m concentration from 4 to 6 m+*JL (o!ld ha%e a significant effect on

the mocardi!m# b!t it (o!ld not significantl change the effecti%e osmotic press!re

of the e&tracell!lar fl!id compartment" Normall f!nctioning 'idnes minimi)e these

changes considerabl# partic!larl if the addition or loss of sol!te or (ater is grad!al"

An internal loss of e&tracell!lar fl!id into a nonf!nctional space# s!ch as the

se*!estration of isotonic fl!id in a b!rn# peritonitis# ascites# or m!scle tra!ma# is

termed a distrib!tional change" This transfer or f!nctional loss of e&tracell!lar fl!idinternall ma be e&tracell!lar 9e"g"# peritonitis;# or intracell!lar 9e"g"# hemorrhagic


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shoc';# or both 9e"g"# ma$or b!rns;" In an e%ent# all distrib!tional shifts or losses

res!lt in a contraction of the f!nctional e&tracell!lar fl!id space"

Kol!me 5hanges

Kol!me deficit or e&cess !s!all is diagnosed b clinical e&amination of the patient"

There are no readil a%ailable# !sef!l laborator tests in the ac!te phase e&ceptmeas!rement of the plasma %ol!me" Direct meas!rement of the e&tracell!lar fl!id

%ol!me !sing radioisotopic tracers is feasible onl in a research setting" There are

se%eral laborator tests# ho(e%er# that indirectl reflect changes in e&tracell!lar fl!id

%ol!me" The blood !rea nitrogen 9BUN; le%el rises (ith an e&tracell!lar fl!id deficit

of s!fficient magnit!de to red!ce glomer!lar filtration" The ser!m creatinine le%el

ma not increase proportionall in o!ng people (ith health 'idnes# and this

discrepanc often is !sed as one test to differentiate prerenal and renal a)otemia" The

concentration of formed elements in the blood# s!ch as the hematocrit# increases (ith

an e&tracell!lar fl!id deficit and decreases (ith an e&tracell!lar fl!id e&cess" The

concentration of ser!m sodi!m is not related to the %ol!me stat!s of e&tracell!lar

fl!id> a se%ere %ol!me deficit ma e&ist (ith a normal# lo(# or high ser!m le%el"

Kol!me Deficit

+&tracell!lar fl!id %ol!me deficit is the most common fl!id disorder in the s!rgical

patient" The lost fl!id is not (ater alone# b!t (ater and electroltes in appro&imatel

the same proportion as the e&ist in normal e&tracell!lar fl!id" The most common

ca!ses of e&tracell!lar fl!id %ol!me deficit are losses of gastrointestinal fl!ids from

%omiting# nasogastric s!ction# diarrhea# and fist!lar drainage" Other common ca!ses

incl!de se*!estration of fl!id in soft:tiss!e in$!ries and infections# intraabdominal and

retroperitoneal inflammator processes# peritonitis# intestinal obstr!ction# and b!rns"

The signs and smptoms of %ol!me deficit are easil recogni)ed and are listed in

Table 3:4" The central ner%o!s sstem and cardio%asc!lar signs occ!r earl (ith ac!te

rapid losses# b!t tiss!e signs ma be absent !ntil the deficit has e&isted for at least 34

h" The central ner%o!s sstem signs are similar to barbit!rate into&ication and ma be

missed if the %ol!me deficit is mild" The cardio%asc!lar signs are secondar to a

decrease in plasma %ol!me and ma be associated (ith %aring degrees of

hpotension in the patient (ith a se%ere e&tracell!lar fl!id %ol!me deficit" S'in t!rgor

ma be diffic!lt to assess in the elderl patient or in the patient (ith recent (eight

loss and is not diagnostic in the absence of other confirmator signs" The bod

temperat!re tends to %ar (ith the en%ironmental temperat!re" In a cool room# the

patient ma be slightl hpothermic and the febrile response to illness ma be

s!ppressed" This occ!rs fre*!entl and can be %er misleading d!ring clinicale%al!ation of the septic patient" After partial correction of the %ol!me deficit# the

temperat!re generall (ill rise to the appropriate le%el" Se%ere %ol!me depletion

depresses all bod sstems and interferes (ith the clinical e%al!ation of a patient" For

e&ample# a %ol!me:depleted patient (ith se%ere sepsis from peritonitis ma ha%e a

normal temperat!re and (hite blood cell co!nt# complain of little pain# and ha%e

!nremar'able findings on abdominal e&amination" The clinical pict!re ma change

dramaticall# ho(e%er# (hen the e&tracell!lar fl!id %ol!me is restored"

Kol!me +&cess

+&tracell!lar fl!id %ol!me e&cess ma be generall iatrogenic or secondar to renal

ins!fficienc# cirrhosis# or congesti%e heart fail!re" ?lasma and interstitial fl!id%ol!mes are increased" In the health o!ng ad!lt the signs are generall those of


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circ!lator o%erload# manifested primaril in the p!lmonar circ!lation# and of

e&cessi%e fl!id in other tiss!e 9see Table 3: 4;" In the elderl patient# congesti%e heart

fail!re (ith p!lmonar edema ma de%elop *!ic'l (ith a moderate %ol!me e&cess"

5oncentration 5hanges

Sodi!m is primaril responsible for the osmolarit of the e&tracell!lar fl!id spacedetermination of the ser!m concentration of sodi!m generall indicates the tonicit of

bod fl!ids" Hponatremia and hpernatremia can be diagnosed on clinical gro!nds

9Table 3:-;# b!t signs and smptoms generall are not present !ntil the changes are

se%ere" 5linical signs of hponatremia or hpernatremia occ!r earl and (ith greater

se%erit (hen the rate of change in e&tracell!lar sodi!m concentration is %er rapid"

5hanges in concentration sho!ld be noted earl b laborator tests and corrected

promptl"

Hponatremia

Ac!te smptomatic hponatremia 9sodi!m less than 2=. m+*JL; clinicall is

characteri)ed b central ner%o!s sstem signs of increased intracranial press!re andtiss!e signs of e&cessi%e intracell!lar (ater" The hpertension probabl is ind!ced b

the rise in intracranial press!re# and the blood press!re !s!all ret!rns to normal (ith

the administration of hpertonic sol!tions of sodi!m salts" Of importance (ith se%ere

hponatremia is the relati%el rapid de%elopment of olig!ric renal fail!re# (hich ma

not be re%ersible if therap is delaed"

Man chronic hponatremic states are asmptomatic !ntil the ser!m sodi!m le%el

falls belo( 23. m+*JL" One important e&ception is the patient (ith increased

intracranial press!re after closed head in$!r# in (hom mild hponatremia ma be

fatal# beca!se of the progressi%e increase in intracell!lar (ater as the e&tracell!lar

fl!id osmolarit falls"

Hpernatremia

5entral ner%o!s sstem and tiss!e signs characteri)e ac!te smptomatic

hpernatremia" This is the onl state in (hich dr# stic' m!co!s membranes are

characteristic" This sign does not occ!r (ith p!re e&tracell!lar fl!id %ol!me deficit

alone and ma be misleading in the patient (ho breathes thro!gh the mo!th" Bod

temperat!re generall is ele%ated and ma approach a lethal le%el# as in the patient

(ith heatstro'e"

,hile %ol!me changes occ!r fre*!entl (itho!t an change in ser!m sodi!mconcentration# the re%erse is not tr!e" The disease states that ca!se a significant ac!te

alteration in the ser!m sodi!m le%el fre*!entl prod!ce a concomitant change in the

e&tracell!lar fl!id %ol!me"

Mi&ed Kol!me and 5oncentration Abnormalities

Mi&ed %ol!me and concentration abnormalities ma de%elop as a conse*!ence of the

disease state or occasionall as a res!lt of inappropriate parenteral fl!id therap"

Moer noted that the clinical pict!re associated (ith a combination of fl!id

abnormalities (ill be an algebraic composite of the signs and smptoms of each state"

Li'e signs prod!ced b both abnormalities (ill be additi%e# and opposing signs (ill

n!llif one another" For e&ample# the tendenc for the bod temperat!re to fall (ith


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an e&tracell!lar %ol!me deficit ma be co!nteracted b the tendenc for it to rise (ith

se%ere hpernatremia"

One of the more common mi&ed abnormalities is an e&tracell!lar fl!id deficit and

hponatremia" This state is readil prod!ced in the patient (ho contin!es to drin'

(ater (hile losing large %ol!mes of gastrointestinal fl!ids" It ma also occ!r in thepostoperati%e period (hen gastrointestinal losses are replaced (ith inade*!ate

%ol!mes of onl - de&trose in (ater or a hpotonic sodi!m sol!tion" An

e&tracell!lar %ol!me deficit accompanied b hpernatremia ma be prod!ced b the

loss of a large amo!nt of hpotonic salt sol!tion# s!ch as s(eat# in the absence of fl!id

inta'e"

The prolonged administration of e&cessi%e *!antities of sodi!m salts (ith restricted

(ater inta'e ma res!lt in an e&tracell!lar %ol!me e&cess and hpernatremia" This

ma also occ!r (hen p!re (ater losses 9s!ch as insensible loss of (ater from the s'in

and l!ngs; are replaced (ith sodi!m: containing sol!tions onl" Similarl# the

e&cessi%e administration of (ater or hpotonic salt sol!tions to the patient (itholig!ric renal fail!re ma rapidl prod!ce an e&tracell!lar %ol!me e&cess and

hponatremia"

Normall f!nctioning 'idnes ma minimi)e these changes to some e&tent and

compensate for man of the imprecise replacements associated (ith parenteral fl!id

administration" In contrast# the patient in an!ric or olig!ric renal fail!re is partic!larl

prone to de%elop these mi&ed %ol!me and osmolar concentration abnormalities" Fl!id

and electrolte management in these patients# therefore# m!st be precise"

Unfort!natel# the fact that a patient (ith normal 'idnes (ho de%elops a significant

%ol!me deficit ma be in a state of 7f!nctional8 renal fail!re often is not appreciated"

As the %ol!me deficit progresses# the glomer!lar filtration rate falls precipito!sl# and

the 'idnes< !ni*!e f!nctions for maintaining fl!id homeostasis are lost" These

changes ma occ!r (ith onl a mild %ol!me deficit in the elderl patient (ith

borderline renal f!nction" In these elderl patients# the blood !rea nitrogen le%el ma

rise higher than 2.. mgJdL in response to the fl!id deficit (ith a concomitant rise in

the ser!m creatinine le%el" Fort!natel# these changes !s!all are re%ersible (ith earl

and ade*!ate correction of the e&tracell!lar fl!id %ol!me deficit"

5omposition 5hanges

5ompositional abnormalities of importance incl!de changes in acid:base balance and

changes in the concentration of potassi!m# calci!m# and magnesi!m"

Acid:Base Balance

The pH of the bod fl!ids is normall maintained (ithin narro( limits in spite of the

large load of acid prod!ced endogeno!sl as a b:prod!ct of bod metabolism" The

acids are ne!trali)ed efficientl b se%eral b!ffer sstems and s!bse*!entl e&creted

b the l!ngs and 'idnes"

The important b!ffers incl!de proteins and phosphates# (hich pla a primar role in

maintaining intracell!lar pH# and the bicarbonatecarbonic acid sstem# (hich

operates principall in the e&tracell!lar fl!id space" The proteins and hemoglobin

ha%e onl minor infl!ence in the e&tracell!lar fl!id space# b!t the latter is of primesignificance as an intracell!lar b!ffer in the red blood cell"


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A b!ffer sstem consists of a (ea' acid or base and the salt of that acid or base" The

b!ffering effect is the res!lt of the formation of an amo!nt of (ea' acid or base

e*!i%alent to the amo!nt of strong acid or base added to the sstem" The res!ltant

change in pH is considerabl less than if the s!bstance (ere added to (ater alone"

Th!s inorganic acids 9e"g"# hdrochloric# s!lf!ric# phosphoric; and organic acids 9e"g"#lactic# pr!%ic# 'eto acids; combine (ith base bicarbonate# prod!cing the sodi!m salt

of the acid and carbonic acid

H5l NaH5O= Na5l H35O=

The carbonic acid formed is then e&creted %ia the l!ngs as 5O3" The inorganic acid

anions are e&creted b the 'idnes (ith hdrogen or as ammoni!m salts" The organic

acid anions generall are metaboli)ed as the !nderling disorder is corrected#

altho!gh some renal e&cretion ma occ!r (ith high le%els"

The f!nctions of the b!ffer sstems are e&pressed in the Henderson: Hasselbalch

e*!ation# (hich defines the pH in terms of the ratio of the salt and acid" The pH of thee&tracell!lar fl!id is defined primaril b the ratio of the amo!nt of base bicarbonate

9the ma$orit as sodi!m bicarbonate; to the amo!nt of carbonic acid 9related to the

5O3content of al%eolar air; present in the blood

pH p log BH5O= J H35O= 3/ m+*JL J 2"== m+*JL 3. J 2 /"4

The term p represents the dissociation constant of carbonic acid in the presence of

base bicarbonate# (hich b meas!rement is 0"2" At a bod pH of /"4# the ratio m!st be

3.2# as depicted" From a chemical standpoint# this is an inefficient b!ffer sstem# b!t

the !n!s!al propert of 5O3 of beha%ing as an acid or changing to a ne!tral gas

s!bse*!entl e&creted b the l!ngs ma'es it *!ite efficient biologicall"

As long as the 3.2 ratio is maintained# regardless of the absol!te %al!es# the pH (ill

remain at /"4" ,hen an acid is added to the sstem# the concentration of bicarbonate

9the n!merator in the Henderson:Hasselbalch e*!ation; decreases" Kentilation

immediatel increases to eliminate larger *!antities of 5O3# (ith a s!bse*!ent

decrease in the carbonic acid 9the denominator in the Henderson:Hasselbalch

e*!ation; !ntil the 3.2 ratio is reestablished" Slo(er# more complete compensation is

effected b the 'idnes (ith increased e&cretion of acid salts and retention of

bicarbonate" The re%erse occ!rs if an al'ali is added to the sstem" espirator

acidosis and al'alosis are prod!ced b dist!rbances of %entilation# (ith an increase ordecrease in the denominator and hence a change from the 3.2 ratio" 5ompensation is

primaril renal# (ith retention of bicarbonate and increased e&cretion of acid salts in

respirator acidosis and the re%erse process in respirator al'alosis"

The fo!r tpes of acid:base dist!rbances are listed in Table 3:0" Use of the 5O3

combining po(er 9appro&imates the plasma bicarbonate; or 5O3 content 9incl!des

bicarbonate# carbonic acid# and dissol%ed 5O3; and 'no(ledge of the patient


10/36

e&ist (itho!t an change in the ser!m 5O3content> determinations of the pH and

?5O 3 from a freshl dra(n arterial blood sample are necessar for diagnosis"

More comple& acid:base dist!rbances are enco!ntered fre*!entl" 5ombinations of

respirator and metabolic changes ma represent compensation for the initial acid:

base dist!rbance or ma indicate t(o or more coe&isting primar disorders 9Table 3:/;"

A 'no(ledge of the pH# bicarbonate concentration# and ?a5O 3allo(s an acc!rate

diagnosis of most acid:base dist!rbances" Ho(e%er# the clinical interpretation of these

meas!rements is associated (ith some inherent problems" Altho!gh the ?a5O 3 is

considered an acc!rate inde& of primar respirator dist!rbances# changes in the le%el

ma represent compensation for a primar metabolic alteration" Th!s a depressed

?a5O 3 9belo( 4. mmHg; is characteristic of respirator al'alosis b!t also represents

the normal compensator response to a metabolic acidosis" Similarl# the le%el of

plasma bicarbonate cannot be regarded e&cl!si%el as an inde& of metabolic

dist!rbances" An ele%ated plasma bicarbonate le%el ma indicate a primar metabolical'alosis or a compensator response to chronic respirator acidosis" Astr!p and

colleag!es proposed the !se of the standard bicarbonate and base e&cess %al!es" Base

e&cess 9or deficit; directl e&presses# in m+*JL# the amo!nt of fi&ed base 9or acid;

added to each liter of blood" This defines the metabolic component of acid:base

disorders"

One !sef!l approach to defining p!re# combined# or compensated dist!rbances relates

meas!red changes in ?a5O 3 and pH to calc!lated changes that (o!ld be e&pected

from p!re etiologies" ,ithin reasonable phsiologic ranges# a 2.:mmHg change in

?a5O 3ields a .".6 change in pH from the normal %al!es of ?a5O 3 94. mmHg; and

pH 9/"4;"

espirator Acidosis

This condition is associated (ith retention of 5O3secondar to decreased al%eolar

%entilation" The more common ca!ses are listed in Table 3:0" Initiall the ?a5O 3 is

ele%ated 9!s!all abo%e -. mmHg;# and the ser!m bicarbonate concentration

9meas!red as 5O3content; is normal" In the chronic form# the ?a5O 3 remains

ele%ated# and the bicarbonate concentration rises as renal compensation occ!rs"

This problem ma be partic!larl serio!s in the patient (ith chronic p!lmonar

disease# in (hom pree&isting respirator acidosis ma be accent!ated in thepostoperati%e period" A n!mber of conditions res!lting in inade*!ate %entilation 9e"g"#

air(a obstr!ction# atelectasis# pne!monia# ple!ral eff!sion# pain from an !pper

abdominal incision# or abdominal distention limiting diaphragmatic e&c!rsion; ma

e&ist singl or in combination to prod!ce respirator acidosis" Altho!gh restlessness#

hpertension# and tachcardia in the immediate postoperati%e period ma be ca!sed

b pain# similar signs indicate inade*!ate %entilation (ith hpercapnia" The !se of

narcotics in this sit!ation compo!nds the problem b depressing respiration"

Management in%ol%es prompt correction of the p!lmonar defect# (hen feasible# and

meas!res to ens!re ade*!ate %entilation" +ndotracheal int!bation and mechanical

%entilation occasionall are necessar" Strict attention to tracheobronchial hgiened!ring the postoperati%e period is an important pre%enti%e meas!re in all patients# and


11/36

partic!larl in those (ith chronic p!lmonar disease" +nco!raging deep breathing and

co!ghing# !sing h!midified air to pre%ent inspissation of secretions# and a%oiding

o%ersedation are all indicated"

espirator Al'alosis

espirator al'alosis is a more common problem in the s!rgical patient thanpre%io!sl recogni)ed" Hper%entilation beca!se of apprehension# pain# hpo&ia#

central ner%o!s sstem in$!r# and assisted %entilation are all common ca!ses" An of

these conditions ma ca!se a rapid decrease in the ?a5O 3 and increase in ser!m pH"

The ser!m bicarbonate concentration is normal in the ac!te phase b!t falls (ith

compensation if the condition persists"

The ma$orit of patients (ho re*!ire %entilator s!pport in the postoperati%e period

de%elop %aring degrees of respirator al'alosis" This ma be the inad%ertent res!lt of

improper !se of the mechanical respirator# or it ma occ!r d!ring attempts to raise the

?O 3 in a hpo&ic patient" ?roper management of the patient on a mechanical

%entilator re*!ires fre*!ent meas!rements of blood gases and appropriate correctionsof the %entilator pattern (hen indicated" The ?a5O 3sho!ld not be allo(ed to fall

belo( =. mmHg# as serio!s complications ma occ!r# partic!larl in the presence of a

complicating hpo'alemia or metabolic al'alosis" @enerall the ?a5O 3 can be

maintained at an acceptable le%el b proper ad$!stments of the %entilator rate and

%ol!me"

The dangers of a se%ere respirator al'alosis are those related to potassi!m depletion

and incl!de the de%elopment of %entric!lar arrhthmias and fibrillation# partic!larl in

patients (ho are digitali)ed or ha%e pree&isting hpo'alemia" Other complications

incl!de a shift of the o&hemoglobin dissociation c!r%e to the left# (hich limits the

abilit of hemoglobin to !nload o&gen at the tiss!e le%el e&cept at lo( tiss!e o&gen

tensions# and the de%elopment of tetan and con%!lsions if the le%el of ioni)ed

calci!m is significantl depressed" The de%elopment of hpo'alemia ma be *!ite

s!dden and is related to entr of potassi!m ions into the cells in e&change for

hdrogen and an e&cessi%e !rinar potassi!m loss in e&change for sodi!m" Se%ere and

persistent respirator al'alosis often is diffic!lt to correct and ma be associated (ith

a poor prognosis beca!se of the !nderling ca!se of hper%entilation" The treatment

of al'alosis is directed primaril to(ard pre%enting the condition b the proper !se of

mechanical %entilation and correcting pree&isting potassi!m deficits"

Metabolic AcidosisMetabolic acidosis res!lts from the retention or gain of fi&ed acids 9diabetic

'etoacidosis# lactic acidosis# a)otemia; or the loss of base bicarbonate 9diarrhea#

small:bo(el fist!la# renal ins!fficienc (ith inabilit to resorb bicarbonate;" The

e&cess of hdrogen ions res!lts in lo(er pH and ser!m bicarbonate concentration" The

initial compensation is p!lmonar# (ith an increase in the rate and depth of breathing

and depression of the ?a5O 3"

enal damage ma interfere (ith the important role of the 'idnes in the reg!lation of

acid:base balance" The 'idnes ser%e a %ital f!nction in this regard thro!gh the

e&cretion of nitrogeno!s (aste prod!cts and acid metabolites and the resorption of

bicarbonates" If renal damage occ!rs and these f!nctions are lost# metabolic acidosisde%elops rapidl and ma be diffic!lt to control"


12/36

,ith normal 'idnes# metabolic acidosis ma de%elop (hen the capacit of the

'idnes for handling a large chloride load is e&ceeded" This is partic!larl common in

patients (ho ha%e e&cessi%e losses of al'aline gastrointestinal fl!ids 9biliar#

pancreatic# small:bo(el secretions; and are maintained on parenteral fl!ids for an

e&tended period" 5ontin!ed replacement of these losses (ith fl!ids that ha%e aninappropriate chloride: bicarbonate ratio# s!ch as isotonic sodi!m chloride sol!tion#

(ill not correct the pH change> the !se of a balanced salt sol!tion# s!ch as lactated

inger


13/36

transf!sions and the administration of lactated inger the initial dose sho!ld not e&ceed -. mL of

/"- sol!tion 94- m+* NaH5O= containing E. mOsm;# and the decision for

additional doses sho!ld be based on meas!rements of pH and ?a5O 3 (hen possible"

Similarl# pH correction of more protracted states of metabolic acidosis ma be

indicated# b!t it sho!ld be accomplished slo(l" Since no satisfactor form!la for

estimating the amo!nt of al'ali needed has been de%ised# fre*!ent meas!rements of

ser!m electrolte le%els and blood pH are the best g!ide to therap"

Metabolic Al'alosis

Metabolic al'alosis res!lts from the loss of fi&ed acids or the gain of bicarbonate and

is aggra%ated b an pree&isting potassi!m depletion" The pH and plasma bicarbonate

concentration are ele%ated" 5ompensation for metabolic al'alosis is primaril b renal

mechanisms> respirator compensation generall is small and cannot be detected inmost patients" arel# hpercapnia ma represent a compensator response to

metabolic al'alosis in patients (itho!t chronic p!lmonar disease" ,hen this is

s!spected# rapid red!ction in ?a5O 3 b mechanical %entilation sho!ld be a%oided"

ather# the ?a5O 3 (ill fall as the metabolic al'alosis is corrected"

The ma$orit of patients (ith metabolic al'alosis ha%e some degree of hpo'alemia# a

res!lt in part of the infl!& of potassi!m ions into the cells as hdrogen ions effl!& into

the ser!m" The dangers of metabolic al'alosis are the same as those disc!ssed for

respirator al'alosis"

A problem commonl enco!ntered in the s!rgical patient is hpochloremic#hpo'alemic metabolic al'alosis res!lting from persistent %omiting or gastric s!ction


14/36

in the patient (ith ploric obstr!ction" Unli'e %omiting (ith an open plor!s# (hich

in%ol%es a combined loss of gastric# pancreatic# biliar# and intestinal secretions#

%omiting (ith an obstr!cted plor!s res!lts in loss of fl!id (ith high chloride and

hdrogen ion concentrations in relation to sodi!m" Initiall the !rinar e&cretion of

bicarbonate increases to compensate for the al'alosis" This increase in !rinar

bicarbonate e&cretion res!lts from net hdrogen ion resorption b the renal t!b!larcells# (ith accompaning potassi!m ion e&cretion" As the %ol!me deficit progresses#

aldosterone:mediated sodi!m resorption is accompanied b potassi!m e&cretion" The

res!lting hpo'alemia leads to e&cretion of hdrogen ions in place of potassi!m ions

b this mechanism# prod!cing parado&ic acid!ria" The net res!lt is a self:perpet!ating

al'alosis (ith hpo'alemia" ?roper management incl!des replacement of the

e&tracell!lar fl!id %ol!me deficit (ith isotonic sodi!m chloride sol!tion in addition to

replacement of potassi!m" Kol!me repletion sho!ld be started and a good !rine o!tp!t

obtained before potassi!m is administered"

arel# se%ere hpo'alemic metabolic al'alosis in a patient (ith ploric o!tlet

obstr!ction ma be refractor to standard therap" This occ!rs most often in patients(ho also ha%e se%ere hpochloremia and se%eral liters of nasogastric drainage dail"

In the past# the inf!sion of ammoni!m chloride or arginine hdrochloride (as the

!s!al method for increasing the le%el of non%olatile acids" Ho(e%er# inf!sion of

ammoni!m chloride ma prod!ce ammonia to&icit# and arginine hdrochloride is no

longer a%ailable commerciall" The !se of ."2 N to ."3 N hdrochloric acid is a safe

and effecti%e therap for correction of se%ere# resistant metabolic al'alosis" The

inf!sion sho!ld be administered o%er a period of 0 to 34 h# (ith meas!rements of pH#

?a5O 3# and ser!m electroltes e%er 4 h" @enerall# 2 or 3 L of sol!tion o%er a

period of 34 h is s!fficient# b!t additional hdrochloric acid sho!ld be inf!sed (hen

indicated b appropriate clinical and laborator e%idence" Temporar control of the

al'alosis (ith this method !s!all is s!ccessf!l# b!t the !nderling ca!se sho!ld be

controlled as soon as possible"

?otassi!m Abnormalities

The normal dietar inta'e of potassi!m is appro&imatel -. to 2.. m+* dail# and in

the absence of hpo'alemia# the ma$orit of this is e&creted in the !rine" Ninet:eight

percent of the potassi!m in the bod is located (ithin the intracell!lar compartment at

a concentration of appro&imatel 2-. m+*JL# and it is the ma$or cation of intracell!lar

(ater" Altho!gh the total e&tracell!lar potassi!m in a /.:'g male (o!ld amo!nt

appro&imatel to onl 0= m+* 94"- m+*JL P 24 L;# this small amo!nt is critical to

cardiac and ne!rom!sc!lar f!nction" In addition# the t!rno%er rate in the e&tracell!larfl!id compartment ma be e&tremel rapid"

The intracell!lar and e&tracell!lar distrib!tion of potassi!m is infl!enced b man

factors" Significant *!antities of intracell!lar potassi!m are released into the

e&tracell!lar space in response to se%ere in$!r or s!rgical stress# acidosis# and the

catabolic state" A significant rise in ser!m potassi!m concentration ma occ!r in these

states in the presence of olig!ric or an!ric renal fail!re# b!t dangero!s hper'alemia

9greater than 0m+*JL; rarel is enco!ntered (hen renal f!nction is normal" After

se%ere tra!ma normal or e&cessi%e !rinar %ol!mes ma not reflect the 'idne


15/36


16/36

Hpo'alemia also ma be a serio!s problem in the patient (ho is maintained on

intra%eno!s n!trition" Large *!antities of s!pplemental potassi!m generall are

necessar to restore depleted intracell!lar stores and to meet the re*!irements for

tiss!e snthesis d!ring the anabolic phase"

Most of the factors that infl!ence potassi!m metabolism res!lt in e&cess e&cretion#and a tendenc to(ard hpo'alemia occ!rs fre*!entl in the s!rgical patient# e&cept

(hen shoc' or acidosis interferes (ith the normal renal handling of potassi!m"

The signs of potassi!m deficit are related to fail!re of normal contractilit of s'eletal#

smooth# and cardiac m!scle and incl!de (ea'ness that ma progress to flaccid

paralsis# diminished to absent tendon refle&es# and paraltic ile!s" Sensiti%it to

digitalis# (ith cardiac arrhthmias and +5@ signs of lo( %oltage# flattening of T

(a%es# and depression of ST segments# are characteristic" Signs of potassi!m deficit

ma be mas'ed b those of a se%ere e&tracell!lar fl!id %ol!me deficit" epletion of

the %ol!me deficit ma f!rther aggra%ate the sit!ation b lo(ering the ser!m

potassi!m le%el thro!gh dil!tion"

Hpo'alemia is best dealt (ith thro!gh pre%ention" In the replacement of

gastrointestinal fl!ids# it is safe to replace the !pper limits of loss# beca!se an e&cess

is readil handled b the patient (ith normal renal f!nction" No more than 4. m+*

sho!ld be added to a liter of intra%eno!s fl!id# and the rate of administration sho!ld

not e&ceed 4. m+*Jh !nless the +5@ is being monitored" In the absence of specific

indications# potassi!m sho!ld not be gi%en to the olig!ric patient or to patients d!ring

the first 34 h after se%ere s!rgical stress or tra!ma"

5alci!m Abnormalities

The ma$orit of the 2... to 23.. g of bod calci!m in the a%erage:si)ed ad!lt is

fo!nd in the bone in the form of phosphate and carbonate" Normal dail inta'e of

calci!m is 2 to = g" Most of this is e&creted %ia the gastrointestinal tract# and 3.. mg

or less is e&creted in the !rine dail" The normal ser!m le%el is 6"- to 2."- mgJdL#

abo!t half of (hich is non:ioni)ed and bo!nd to plasma protein" An additional non:

ioni)ed fraction 9- percent; is bo!nd to other s!bstances in the plasma and interstitial

fl!id# and the remaining 4- percent is the ioni)ed portion that is responsible for

ne!rom!sc!lar stabilit" Determination of the plasma protein le%el# therefore# is

essential for proper analsis of the ser!m calci!m le%el" The ratio of ioni)ed to non:

ioni)ed calci!m is also related to the pH> acidosis ca!ses an increase in the ioni)ed

fraction# and al'alosis ca!ses a decrease"

Dist!rbances of calci!m metabolism generall are not a problem in the postoperati%e

patient (itho!t complications# (ith the e&ception of s'eletal loss d!ring prolonged

immobili)ation" o!tine administration of calci!m to the s!rgical patient# therefore# is

not needed in the absence of specific indications"

Hpocalcemia

The smptoms of hpocalcemia# (hich ma be seen (hen ser!m le%els are belo( 6

mgJdL# incl!de n!mbness and tingling of the circ!moral region and the tips of the

fingers and toes" The signs are of ne!rom!sc!lar origin and incl!de hperacti%e

tendon refle&es# positi%e 5h%oste'


17/36

carpopedal spasm# con%!lsions 9(ith se%ere deficit;# and prolongation of the Q:T

inter%al on the +5@"

The common ca!ses incl!de ac!te pancreatitis# massi%e soft:tiss!e infections

9necroti)ing fasciitis;# ac!te and chronic renal fail!re# pancreatic and small:bo(el

fist!las# and hpoparathroidism" Transient hpocalcemia is a fre*!ent occ!rrence inthe hperparathroid patient after remo%al of a parathroid adenoma# o(ing to

atroph of the remaining glands and a%id bone !pta'e" Asmptomatic hpocalcemia

ma occ!r (ith hpoproteinemia 9normal ioni)ed fraction;# b!t smptoms ma appear

(ith a normal ser!m calci!m le%el in a patient (ith se%ere al'alosis" In this case there

is a decrease in the phsiologicall acti%e or ioni)ed fraction of total ser!m calci!m"

5alci!m le%els also ma fall (ith a se%ere depletion of magnesi!m"

Treatment is directed to(ard correction of the !nderling ca!se and repletion of the

deficit" Ac!te smptoms ma be relie%ed b the intra%eno!s administration of calci!m

gl!conate or calci!m chloride" 5alci!m lactate ma be gi%en orall# (ith or (itho!t

s!pplemental %itamin D# in the patient re*!iring prolonged replacement" The ro!tineadministration of calci!m d!ring massi%e transf!sions of blood is contro%ersial and

reflects the pa!cit of st!dies in (hich calci!m ion le%els ha%e been meas!red" In the

ma$orit of st!dies# calci!m ion concentrations ha%e been estimated from meas!red

total ser!m calci!m le%els" A%ailable data indicate that the ma$orit of patients

recei%ing blood transf!sions do not re*!ire calci!m s!pplementation" The binding of

ioni)ed calci!m b citrate generall is compensated for b the mobili)ation of

calci!m from bod stores" For patients recei%ing blood as rapidl as -.. mL e%er -

to 2. min# calci!m administration is recommended" An appropriate dose# according to

Moore


18/36

A ser!m calci!m concentration of 2- mgJdL or higher re*!ires emergenc treatment"

Most patients ha%e an e&tracell!lar fl!id %ol!me deficit beca!se of the effects of

hpercalcemia 9%omiting# pol!ria;# and %igoro!s %ol!me repletion (ith salt sol!tions

lo(ers the calci!m le%el b dil!tion and increased !rinar calci!m e&cretion" apid

correction of the associated e&tracell!lar fl!id %ol!me deficit immediatel lo(ers the

ser!m calci!m le%el b dil!tion and b increased renal clearance# (hich ma bea!gmented b f!rosemide administration"

Oral or intra%eno!s inorganic phosphates effecti%el lo(er ser!m calci!m b

inhibiting bone resorption and forming calci!m:phosphate comple&es that are

deposited in soft tiss!es and bone" Intra%eno!s !se ma ca!se an abr!pt fall in

calci!m# and tetan# hpotension# and ac!te renal fail!re ha%e been reported (ith this

form of therap" If intra%eno!s phosphor!s is !sed# it sho!ld be gi%en slo(l o%er a

period of appro&imatel 23 h once dail for no more than 3 or = das" Inorganic

phosphates are contraindicated in patients (ith hperphosphatemia or renal fail!re"

Intra%eno!s sodi!m s!lfate also lo(ers ser!m calci!m b increasing !rinar e&cretion

of calci!m" It is less effecti%e than phosphate salts# ho(e%er# and probabl is no moreeffecti%e than normal saline"

5orticosteroids decrease resorption of calci!m from bone and red!ce the intestinal

absorption of %itamin D" The ha%e been !sef!l in treating hpercalcemic patients

(ith sarcoidosis# melomas# lmphomas# and le!'emias# altho!gh the red!ction in

ser!m calci!m ma not be apparent for 2 or 3 (ee's" Mithramcin# a ctoto&ic dr!g#

effecti%el lo(ers ser!m calci!m in 34 to 46 h b direct action on the bones" The dr!g

is relati%el safe in the small doses !sed# and the calci!m le%el ma remain normal for

se%eral das to (ee's after a single dose" 5alcitonin ind!ces a moderate decrease in

ser!m calci!m# b!t the effect is diminished (ith repeated administration" The

definiti%e treatment of ac!te hpercalcemic crisis in patients (ith

hperparathroidism is immediate s!rger"

In the patient (ith metastatic cancer# a pre%enti%e approach to hpercalcemia sho!ld

be ta'en" The ser!m calci!m le%el is chec'ed fre*!entl> if it is ele%ated# the patient is

placed on a lo(:calci!m diet and meas!res to ens!re ade*!ate hdration are

instit!ted"

Magnesi!m Abnormalities

The total bod content of magnesi!m in the a%erage ad!lt is appro&imatel 3...

m+*# abo!t half of (hich is incorporated in bone and onl slo(l e&changeable" Thedistrib!tion of magnesi!m is similar to that of potassi!m# the ma$or portion being

intracell!lar" Ser!m magnesi!m concentration normall ranges from 2"- to 3"-

m+*JL" The normal dietar inta'e of magnesi!m is appro&imatel 3. m+* 934. mg;

dail" The larger part is e&creted in the feces and the remainder in the !rine" The

'idnes sho( a remar'able abilit to conser%e magnesi!m> on a magnesi!m:free diet#

renal e&cretion of this ion ma be less than 2m+*Jda"

Magnesi!m Deficienc

Magnesi!m deficienc is 'no(n to occ!r (ith star%ation# malabsorption sndromes#

protracted losses of gastrointestinal fl!id# prolonged intra%eno!s fl!id therap (ith

magnesi!m:free sol!tions# and d!ring total parenteral n!trition (hen inade*!ate*!antities of magnesi!m ha%e been added to the sol!tions" Other ca!ses incl!de ac!te


19/36

pancreatitis# treatment of diabetic 'etoacidosis# primar aldosteronism# chronic

alcoholism# amphotericin B therap# and a protracted co!rse after thermal in$!r"

The magnesi!m ion is essential for proper f!nction of most en)me sstems# and

depletion is characteri)ed b ne!rom!sc!lar and central ner%o!s sstem hperacti%it"

The signs and smptoms are similar to those of calci!m deficienc# incl!dinghperacti%e tendon refle&es# m!scle tremors# and tetan (ith a positi%e 5h%oste'


20/36

parenteral hperalimentation %aries b!t 23 to 34 m+* dail is effecti%e for the a%erage

patient"

Magnesi!m sho!ld not be gi%en to the olig!ric patient or in the presence of a se%ere

%ol!me deficit !nless act!al magnesi!m depletion has been demonstrated" If gi%en to

a patient (ith renal ins!fficienc# considerabl smaller doses are !sed and the patientis caref!ll obser%ed for signs or smptoms of to&icit"

Magnesi!m +&cess

Smptomatic hpermagnesemia# altho!gh rare# is most commonl seen (ith se%ere

renal ins!fficienc" etention and acc!m!lation of magnesi!m ma occ!r in an

patient (ith impaired glomer!lar or renal t!b!lar f!nction# and the presence of

acidosis ma rapidl compo!nd the problem" Ser!m magnesi!m le%els tend to parallel

changes in potassi!m concentration in these cases" In patients on ordinar dietar

inta'es of magnesi!m# increased ser!m concentrations do not occ!r !ntil the

glomer!lar filtration rate falls belo( =. mLJmin" Magnesi!m:containing antacids and

la&ati%es 9mil' of magnesia# epsom salts# @el!sil# Maalo&; are commonladministered in *!antities that are s!fficient to prod!ce to&ic ser!m le%els of

magnesi!m in patients (ith impaired renal f!nction" Other conditions that ma be

associated (ith smptomatic hpermagnesemia incl!de earl thermal in$!r# massi%e

tra!ma or s!rgical stress# se%ere e&tracell!lar %ol!me deficit# and se%ere acidosis"

The earl signs and smptoms of magnesi!m e&cess incl!de letharg and (ea'ness

(ith progressi%e loss of deep tendon refle&es" Interference (ith cardiac cond!ction

occ!rs (ith increasing le%els of magnesi!m# and changes in the +5@ 9increased ?:

inter%al# (idened QS comple and ele%ated T (a%es; resemble those seen in

hper'alemia" Somnolence leading to coma and m!sc!lar paralsis occ!r in the later

stages# and death is !s!all ca!sed b respirator or cardiac arrest"

Treatment consists of immediate meas!res to lo(er the ser!m magnesi!m le%el b

correcting coe&isting acidosis# replenishing pree&isting e&tracell!lar %ol!me deficit#

and (ithholding e&ogeno!s magnesi!m" Ac!te smptoms ma be temporaril

controlled b the slo( intra%eno!s administration of - to 2. m+* of calci!m chloride

or calci!m gl!conate" If ele%ated le%els or smptoms persist# peritoneal dialsis or

hemodialsis is indicated"

FLUID AND +L+5TOLYT+ TH+A?Y

?arenteral Sol!tionsMan different electrolte sol!tions# (ith %ario!s compositions# are a%ailable for

parenteral administration 9Table 3:E;" Se%eral of the more commonl !sed sol!tions

are disc!ssed belo(" The choice of a partic!lar fl!id depends on the patient


21/36

metaboli)e lactate is !n(arranted e%en (hen inf!sing large *!antities of lactated

inger


22/36

!s!all in%ol%es a combination of the t(o# b!t the internal redistrib!tion fre*!entl is

o%erloo'ed"

The phenomenon of internal redistrib!tion or translocation of e&tracell!lar fl!id is

pec!liar to man s!rgical diseases> in the indi%id!al patient# the loss ma be *!ite

large" Altho!gh the concept of a 7third space8 is not ne(# it !s!all is considered onlin relation to patients (ith massi%e ascites# b!rns# or cr!sh in$!ries" Of more

importance is the third:space loss into the peritone!m# the bo(el (all# and other

tiss!es (ith inflammator lesions of the intraabdominal organs" The magnit!de of

these losses ma not be f!ll appreciated (itho!t reali)ation that the peritone!m alone

has appro&imatel 2"6 m3 of s!rface area" A slight increase in thic'ness from

se*!estration of fl!id# (hich (o!ld not be appreciated on cas!al obser%ation# ma

res!lt in a f!nctional loss of se%eral liters of fl!id" S(elling of the bo(el (all and

mesenter and secretion of fl!id into the l!men of the bo(el ca!se e%en larger losses"

Similar deficits ma occ!r (ith massi%e infection of the s!bc!taneo!s tiss!es

9necroti)ing fasciitis; or (ith se%ere cr!sh in$!r"

These 7parasitic8 losses remain a part of the e&tracell!lar fl!id space and ma be

meas!red as a slo(l e*!ilibrating %ol!me" The term nonf!nctional is !sed beca!se

the fl!id is no longer able to participate in the normal f!nctions of the e&tracell!lar

compartment and ma $!st as (ell ha%e been lost e&ternall" An transfer of

intracell!lar fl!id to the e&tracell!lar compartment for replenishment of the loss is

insignificant in the ac!te phase" The patient (ith ascites ma ha%e an enormo!s total

e&tracell!lar fl!id %ol!me# b!t the f!nctional component is se%erel depleted" The

same is tr!e of e&tensi%e inflammator or obstr!cti%e lesions of the gastrointestinal

tract# altho!gh the loss is not as ob%io!s" These losses e%o'e the signs and smptoms

of an e&tracell!lar fl!id %ol!me deficit (ith or (itho!t the concomitant e&ternal loss

of fl!ids"

+&act *!antification of these deficits is impossible and probabl !nnecessar" The

defect can be estimated on the basis of the se%erit of the clinical signs" A mild deficit

represents a loss of appro&imatel 4 percent of bod (eight> a moderate loss is 0 to 6

percent of bod (eight> and a se%ere deficit is appro&imatel 2. percent of bod

(eight" 5ardio%asc!lar signs predominate (hen there is ac!te rapid loss of fl!id from

the e&tracell!lar fl!id compartment (ith fe( or no tiss!e signs" In addition to the

estimated deficit# fl!ids lost d!ring treatment m!st be replaced"

Immediatel after diagnosis of a %ol!me deficit# prompt fl!id replacement (ith abalanced salt sol!tion sho!ld be started" 5ontin!ing therap is tailored to the response

of the patient# based on fre*!ent clinical e&amination" eliance on a form!la or a

single clinical sign to determine the ade*!ac of res!scitation is perilo!s" ather#

re%ersal of the signs of the %ol!me deficit# combined (ith stabili)ation of the blood

press!re and p!lse and an ho!rl !rine %ol!me of =. to -. mL are !sed as general

g!idelines" An ade*!ate ho!rl !rine o!tp!t# altho!gh !s!all a reliable inde& of

%ol!me replacement# ma be totall misleading" The e&cessi%e administration of

gl!cose 9o%er -. g in a 3: to =:h period; ma res!lt in osmotic di!resis# (hile an

osmotic agent s!ch as mannitol tends to prod!ce !rine at the e&pense of the %asc!lar

%ol!me" ?atients (ith chronic renal disease or incipient ac!te renal damage from

shoc' and in$!r also ma ha%e inappropriatel high !rinar %ol!mes" In addition# therapid administration of salt sol!tions ma transientl e&pand the intra%asc!lar


23/36

%ol!me# increase the glomer!lar filtration rate# and res!lt in an immediate o!tpo!ring

of !rine# altho!gh the total e&tracell!lar fl!id space remains *!ite depleted"

The choice of the proper fl!id for replacement depends on concomitant concentration

or compositional abnormalities" ,ith p!re e&tracell!lar fl!id %ol!me loss or (hen

onl minimal concentration or compositional abnormalities are present# the !se of abalanced salt sol!tion# s!ch as lactated inger


24/36

the presence of metabolic al'alosis# and MJ0 sodi!m lactate 920/ m+*JL each of

sodi!m and lactate; is !sed to correct an associated acidosis" 5orrection of the ser!m

sodi!m concentration ma re*!ire onl a fe( liters of these sol!tions> the remainder

of the %ol!me deficit ma be replaced (ith lactated inger


25/36

deficit is re%ealed onl (hen the compensator mechanisms are abolished (ith

anesthesia" This problem is pre%ented b maintaining baseline re*!irements and

replacing abnormal losses of fl!ids and electroltes b intra%eno!s inf!sions in the

preoperati%e period"

In addition to blood losses d!ring operation# there appear to be e&tracell!lar fl!idlosses d!ring ma$or operati%e proced!res" Some of these# incl!ding edema from

e&tensi%e dissection# collections (ithin the l!men and (all of the small bo(el# and

acc!m!lations of fl!id in the peritoneal ca%it# are clinicall discernible and (ell

recogni)ed" The are belie%ed to represent distrib!tional shifts# in that the f!nctional

%ol!me of e&tracell!lar fl!id is red!ced# b!t not e&ternall lost from the bod" These

f!nctional losses often are referred to as 7parasitic losses#8 7third space edema#8 or

7se*!estration8 of e&tracell!lar fl!id" Another so!rce of e&tracell!lar fl!id loss d!ring

ma$or operati%e tra!ma is the (o!nd# tho!gh this is a smaller loss and diffic!lt to

*!antif e&cept in e&tensi%e and ma$or operati%e proced!res"

At the beginning of the t(entieth cent!r s!rgeons became a(are that man changesocc!rred in !rinar o!tp!t# blood %ol!me# and fl!id and electrolte composition

d!ring and after s!rger" Assessment of these changes a(aited the de%elopment of

analtic techni*!es and their application to patient st!dies" In the follo(ing 3- ears#

saline sol!tions in %aring combinations (ere gi%en to patients !ndergoing operation#

often in e&cessi%e amo!nts" ,or' in the late 2E=.s and earl 2E4.s b Moer and

others indicated that d!ring and after operati%e proced!res# saline and (ater sol!tions

sho!ld be (ithheld entirel beca!se most of the fl!id administered is retained"

The possibilit (as recogni)ed that the operati%e and postoperati%e retention of salt

and (ater administered in relati%el small amo!nts might be phsiologic retention to

replace a deficit of salt and (ater inc!rred b the operati%e proced!re" S!bse*!ent

st!dies re%ealed that f!nctional e&tracell!lar fl!id decreases (ith ma$or abdominal

operations# largel as se*!estered loss into the operati%e site" This e&tracell!lar fl!id

%ol!me deficit can be replaced d!ring the operati%e proced!re" These data led to the

concl!sion that the need for an e&tracell!lar 7mimic8 in the form of balanced salt

sol!tion can be clinicall estimated" Intraoperati%e correction of the %ol!me deficit

(ith salt sol!tion mar'edl red!ces postoperati%e olig!ria b!t is not intended to

s!bstit!te for blood replacement" It is belie%ed to be a phsiologic s!pplement# or an

ad$!nct# to replace se*!estered losses"

The pend!l!m th!s s(!ng from the indiscriminate !se of salt sol!tions in the first*!arter of the t(entieth cent!r to almost total (ithholding of fl!id and electroltes

from s!rgical patients in the second *!arter of the cent!r> toda indications are that

proper management lies bet(een these t(o e&tremes" Some g!idelines are necessar

for the intraoperati%e administration of saline sol!tions as a 7mimic8 for the

se*!estered e&tracell!lar fl!id" Beca!se this %aries from an almost imperceptible

minim!m to a high of appro&imatel = L d!ring an !ncomplicated proced!re#

*!antification is e&tremel diffic!lt (ith a%ailable means of meas!ring f!nctional

e&tracell!lar fl!id" 5onse*!entl# no acc!rate form!la for intraoperati%e fl!id

administration can be deri%ed" Some arbitrar b!t clinicall !sef!l g!idelines are as

follo(s 92; Blood sho!ld be replaced to maintain an acceptable red blood cell mass

irrespecti%e of an additional fl!id and electrolte therap" 93; The replacement ofe&tracell!lar fl!id sho!ld begin d!ring the operati%e proced!re" 9=; Balanced salt


26/36

sol!tion needed d!ring operation is appro&imatel ."- to 2 LJh# b!t onl to a

ma&im!m of 3 to = L d!ring a 4:h ma$or abdominal proced!re# !nless there are other

meas!rable losses"

Using a similar fl!id regimen# Thompson and associates reported e&periences in a

series of 0/. patients !ndergoing ma$or aortoiliac reconstr!cti%e proced!res" In thisgro!p of patients# the a%erage amo!nt of lactated inger


27/36

of E.J0. mmHg and a p!lse of less than 23. in postoperati%e patients ma not be

s!fficient to pre%ent renal ischemia !nless# in addition to lac' of signs of shoc'# !rine

flo( is ade*!ate 9=. to -. mLJho!r;" +%al!ation of the le%el of conscio!sness#

p!pillar si)e# air(a patenc# breathing patterns# p!lse rate and %ol!me# s'in (armth

and color# bod temperat!re# !rine o!tp!t# and a critical re%ie( of the operati%e

proced!re and the operati%e fl!id management# are recommended" Beca!se operati%etra!ma fre*!entl in%ol%es loss or transfer of significant *!antities of (hole blood#

plasma# or e&tracell!lar fl!id that can be onl grossl estimated# circ!lator instabilit

is most commonl ca!sed b !nderestimated initial losses or insidio!s# concealed

contin!ed losses" Operati%e blood loss !s!all is estimated b the operating s!rgeon

to be 2- to 4. percent less than the isotopicall meas!red blood loss from that patient"

For a patient (ith circ!lator instabilit# f!rther %ol!me replacement of an additional

2... mL isotonic salt sol!tion# (hile determining (hether contin!ing losses or other

ca!ses are present# often resol%es the problem"

It is !nnecessar and probabl !n(ise to administer potassi!m d!ring the first 34 h

after operation !nless a definite potassi!m deficit e&ists" This is partic!larl importantfor the patient s!b$ected to prolonged operati%e tra!ma in%ol%ing one or more

episodes of hpotension and for the posttra!matic patient (ith hemorrhagic

hpotension" Olig!ric renal fail!re or the more insidio!s high:o!tp!t renal fail!re ma

de%elop# and the administration of e%en a small *!antit of potassi!m ma be

detrimental"

$ater Poto%erati&e Period

The problem of %ol!me management d!ring the postoperati%e con%alescent phase is

one of acc!rate meas!rement and replacement of all losses" In the other(ise health

indi%id!al# this in%ol%es the replacement of meas!red sensible losses# (hich !s!all

are of gastrointestinal origin# and the estimation and replacement of insensible losses"

The insensible loss !s!all is relati%el constant and a%erages 0.. mLJda" This ma

be increased b hpermetabolism# hper%entilation# and fe%er to a ma&im!m of

appro&imatel 2-.. mLJda" The estimated insensible loss is replaced (ith -

de&trose in (ater" This loss ma be partiall offset b an insensible gain of (ater

from e&cessi%e tiss!e catabolism in the postoperati%e patient (ith complications#partic!larl if associated (ith olig!ric renal fail!re"

Appro&imatel 2 L of fl!id sho!ld be gi%en to replace that %ol!me of !rine re*!ired

to e&crete the catabolic end prod!cts of metabolism 96.. to 2... mLJda;" In the

indi%id!al (ith normal renal f!nction# this ma be gi%en as - de&trose in (ater

beca!se the 'idnes are able to conser%e sodi!m (ith e&cretion of less than 2 m+*

dail" It is probabl !nnecessar to stress the 'idnes to this degree# ho(e%er# and a

small amo!nt of salt sol!tion ma be gi%en in addition to (ater to co%er !rinar loss"

In elderl patients (ith salt:losing 'idnes or in patients (ith head in$!ries# an

insidio!s hponatremia ma de%elop if !rinar losses are replaced (ith (ater" Urinar

sodi!m in these circ!mstances ma e&ceed 2.. m+*JL and res!lt in a dail loss of


28/36

significant amo!nts of sodi!m" Meas!rement of !rinar sodi!m facilitates acc!rate

replacement"

Urine %ol!me is not replaced on a milliliter:for:milliliter basis" A !rinar o!tp!t of

3... to =... mL on a gi%en da ma represent di!resis of fl!ids gi%en d!ring s!rger

or ma represent e&cessi%e fl!id administration" If these large losses are completelreplaced# the !rine o!tp!t progressi%el increases# and this ma proceed to a sit!ation

resembling diabetes insipid!s# (ith !rinar o!tp!ts in e&cess of 2. LJda"

Sensible losses# b definition# can be meas!red or# as in the case of s(eating#

estimated" @astrointestinal losses !s!all are isotonic or slightl hpotonic# and the

are replaced (ith an essentiall isotonic salt sol!tion" ,hen the estimated loss is

slightl abo%e or belo( isotonicit# appropriate corrections can be made in the dail

(ater administration# (hile isotonic salt sol!tions are !sed to replace these losses

%ol!me for %ol!me" S(eating !s!all is not a problem e&cept (ith the febrile patient#

in (hom losses ma# b!t seldom do# e&ceed 3-. mLJda per degree of fe%er"

+&cessi%e s(eating ma represent a considerable loss of sodi!m in the !nacclimati)edindi%id!al"

Determination of ser!m electrolte le%els !s!all is !nnecessar in the patient (ith an

!ncomplicated postoperati%e co!rse maintained on parenteral fl!ids for 3 to = das" A

more prolonged period of parenteral replacement or one complicated b e&cessi%e

fl!id losses re*!ires fre*!ent determinations of the ser!m sodi!m# potassi!m# and

chloride le%els and of carbon dio&ide combining po(er" Ad$!stments then can be

made (ith intra%eno!s fl!ids of appropriate composition"

Dail maintenance fl!id sho!ld be administered at a stead rate (hile the losses are

inc!rred" If gi%en o%er a shorter period# renal e&cretion of the e&cess salt and (ater

ma occ!r (hile the normal losses contin!e o%er the f!ll 34:h period" For the same

reason# fl!ids of different composition are alternated# and additi%es to intra%eno!s

fl!ids 9e"g"# potassi!m chloride and antibiotics; are e%enl distrib!ted in the total

%ol!me of fl!id gi%en"

Dail fl!id orders sho!ld begin (ith an assessment of the patient


29/36

(ell" +&cesses administered o%er se%eral das# ho(e%er# (ill soon e&ceed the

'idnes< abilit to e&crete sodi!m" It is important to determine acc!ratel# from inta'e

and o!tp!t records and ser!m sodi!m concentrations# the act!al needs of the patient

managed o%er se%eral postoperati%e das" Attention to the signs and smptoms of

o%erload !s!all pre%ents %ol!me e&cess" It occ!rs most fre*!entl (ith attempts to

meet e&cessi%e %ol!me losses that are not meas!rable# s!ch as those res!lting fromincompletel controlled fist!la drainage"

The earliest sign of %ol!me o%erload is (eight gain d!ring the catabolic period# (hen

the patient sho!ld be losing R to lbJda" Hea% eelids# hoarseness# or dspnea on

e&ertion ma appear rapidl" 5irc!lator and p!lmonar signs of o%erload appear late

and represent a massi%e o%erload" ?eripheral edema ma be a sign# b!t it does not

necessaril indicate %ol!me e&cess" In the absence of additional e%idence for %ol!me

o%erload# other ca!ses for peripheral edema sho!ld be considered" O%ere&pansion of

the total e&tracell!lar fl!id ma coe&ist (ith depletion of the f!nctional e&tracell!lar

fl!id compartment# along (ith decreased effecti%e circ!lating plasma %ol!me"

Hponatremia

Significant postoperati%e alterations in ser!m sodi!m concentration are infre*!ent

(hen the fl!id res!scitation d!ring operation has incl!ded ade*!ate %ol!mes of

isotonic salt sol!tions" The 'idnes retain the abilit to e&crete moderate e&cesses of

salt (ater administered in the earl postoperati%e period if f!nctional e&tracell!lar

fl!id has been ade*!atel replaced d!ring the operati%e or immediate postoperati%e

period" ?re%io!s st!dies of sodi!m balance re%ealed that patients do e&crete sodi!m

after the f!nctional deficit inc!rred b the shift of e&tracell!lar fl!id has been

replaced" ,right and @ann demonstrated normal capacit to e&crete (ater

postoperati%el (hen isotonic salt sol!tions are administered before a challenge (ith

a (ater load" The commonl described hponatremia associated (ith s!rgical

proced!res and tra!matic in$!r is pre%ented b the replacement of e&tracell!lar fl!id

deficits" The dail maintenance of normal osmolarit is simplified b the replacement

of obser%able losses of sodi!m content"

Hponatremia ma occ!r easil (hen (ater is gi%en to replace losses of sodi!m:

containing fl!ids or (hen (ater administration consistentl e&ceeds (ater losses" The

latter ma occ!r (ith olig!ria or in association (ith decreased (ater loss thro!gh the

s'in and l!ngs# intracell!lar shifts of sodi!m# or the cell!lar release of e&cessi%e

amo!nts of endogeno!s (ater" Se%ere or refractor hponatremia is !nli'el to occ!r

(hen renal f!nction remains normal"

In the presence of hperglcemia# determination of the gl!cose concentration is

necessar to e%al!ate the significance of a depressed ser!m sodi!m le%el" Beca!se

gl!cose does not enter cells b passi%e diff!sion# it e&erts an osmotic force in the

e&tracell!lar compartment" This contrib!tion to osmotic press!re is normall small#

b!t (ith an ele%ated gl!cose concentration the increased osmotic press!re ca!ses the

transfer of cell!lar (ater into the e&tracell!lar compartment# res!lting in a dil!tional

hponatremia" Hence hponatremia ma be obser%ed (hen the total effecti%e osmotic

press!re in the e&tracell!lar compartment is normal or e%en abo%e normal" +ach 2..:

mgJdL rise abo%e normal in the blood gl!cose le%el res!lts in a decrease in the ser!m

sodi!m concentration of 2"0 to = m+*JL"


30/36

+ndogeno!s ,ater elease

The patient maintained on intra%eno!s fl!ids (itho!t ade*!ate caloric inta'e (ill#

bet(een the fifth and tenth das# gain significant *!antities of (ater 9ma&im!m -..

mLJda; from e&cessi%e cell!lar catabolism# thereb decreasing the *!antit of

e&ogeno!s (ater re*!ired per da"

Intracell!lar Shifts

Sstemic bacterial sepsis often is accompanied b a precipito!s drop in ser!m sodi!m

concentration" This s!dden change is poorl !nderstood# b!t it !s!all accompanies

loss of e&tracell!lar fl!id as interstitial or intracell!lar se*!estrations" The condition

can be treated b (ithholding free (ater# restoring e&tracell!lar fl!id %ol!me# and

initiating treatment of the sepsis"

Hpernatremia

Hpernatremia 9ser!m sodi!m concentration abo%e 2-. m+*JL;# altho!gh

!ncommon# is a dangero!s abnormalit" Unli'e decreased ser!m sodi!m

concentration# hpernatremia is prod!ced easil (hen renal f!nction is normal" Thee&tracell!lar fl!id hperosmolarit res!lts in a shift of intracell!lar (ater from (ithin

the cell to the e&tracell!lar fl!id compartment> in this sit!ation# a high ser!m sodi!m

le%el ma indicate a significant deficit of total bod (ater" In s!rgical patients

hpernatremia is most often the res!lt of e&cessi%e or !ne&pected (ater losses# b!t it

ma res!lt from !se of salt:containing sol!tions to replace (ater losses" 5lassification

of (ater losses ma be helpf!l in pre%enting and treating this abnormalit"

+&cessi%e +&trarenal ,ater Losses

,ith increased metabolism from an ca!se# b!t partic!larl (hen it is associated (ith

fe%er# the (ater loss thro!gh e%aporation of s(eat ma reach a le%el of se%eral liters

dail" ?atients (ith a tracheostom in a dr en%ironment can 9(ith high min!te

%ol!mes; lose as m!ch as 2 to 2"- L of (aterJda b this ro!te" Increased (ater

e%aporation from a gran!lating s!rface is of significant magnit!de in the thermall

in$!red patient# (ith losses as great as = to - LJda"

Increased enal ,ater Losses

+&tremel large %ol!mes of sol!te:poor !rine ma res!lt from hpo&ic damage to the

distal t!b!les and collecting d!cts or loss of antidi!retic hormone stim!lation from

damage to the central ner%o!s sstem" In both instances# fac!ltati%e (ater resorption

is impaired" The former occ!rs in high:o!tp!t renal fail!re> this is the most common

tpe of renal fail!re after se%ere in$!r or operati%e tra!ma" The latter occ!rs (ithe&tensi%e head in$!ries accompanied b temporar diabetes insipid!s"

Sol!te Loading

High protein inta'e ma prod!ce an increased osmotic load of !rea that necessitates

the e&cretion of large %ol!mes of (ater" Hpernatremia# a)otemia# and e&tracell!lar

fl!id %ol!me deficits follo(" These can be pre%ented b an inta'e of / mL of (ater

per gram of dietar protein"

+&cessi%e gl!cose administration res!lts in the need for a large %ol!me of (ater for

e&cretion" Osmotic di!retics# s!ch as mannitol and !rea# also res!lt in the obligator

e&cretion of a large %ol!me of (ater and increased !rinar sodi!m losses" In addition#


31/36

isotonic salt sol!tions# if !sed to replace p!re (ater losses# rapidl prod!ce

hpernatremia"

Ac!te enal Fail!re

Ac!te renal ins!fficienc after tra!ma or s!rgical stress is a lethal complication" The

diagnosis is based on persistent olig!ria and chemical e%idence of !remia afterstabili)ation of the circ!lation" The clinical co!rse is characteri)ed b olig!ria lasting

from se%eral das to se%eral (ee's follo(ed b a progressi%e rise in dail !rine

%ol!me !ntil the e&cretor and concentrating f!nctions of the 'idne are grad!all

restored"

Ac!te renal fail!re is classified according to its ca!se as prerenal# renal# or postrenal

9Table 3:2.;" The most common ca!se is se*!estered or third: space loss in the area

of the s!rgical proced!re" Shoc' from blood loss and occl!sion of small arteries 9e"g"#

renal arter emboli; also ma ca!se prerenal fail!re" enal arter occl!sions are less

common ca!ses than %ol!me depletion or hpotensi%e shoc'" The common intrarenal

ca!ses of renal fail!re in the postoperati%e patient incl!de endoto&emia# tra!ma# dr!gs9s!ch as aminoglcosides;# or the generation of pigment deli%er to the 'idnes 9as

(ith moglobin;# or destabili)ed hemoglobin 9as (ith a cardiac bpass machine;"

?ostrenal ca!ses are almost al(as beca!se of obstr!ction of the !reter# the bladder#

or the !rethra"

Therap of ac!te renal fail!re after s!rger begins (ith remo%al of the ca!se" ,ith

prerenal a)otemia# for e&ample# correction of the e&tracell!lar fl!id %ol!me deficit

(ith an e&tracell!lar fl!id %ol!me mimic# s!ch as lactated inger


32/36

94; Hperphosphatemia and hpocalcemia !s!all e%ol%e in patients (ith

posttra!matic ac!te renal fail!re beca!se of inade*!ate e&cretion and e&cessi%e

release from in$!red tiss!e"

9-; Hpermagnesemia occ!rs reg!larl beca!se the 'idne is the ma$or organ for

reg!lating magnesi!m balance" Magnesi!m le%els can rise rapidl in patients (ithac!te renal fail!re# partic!larl if magnesi!m:containing preparations s!ch as antacids

are administered"

?redisposing Factors

A n!mber of specific factors ma contrib!te to the de%elopment of postoperati%e renal

fail!re# incl!ding the follo(ing

Tra!ma

Tra!ma generall contrib!tes to ac!te renal fail!re in the s!rgical patient as a res!lt of

the hpo%olemic shoc' ca!sed b blood loss" In addition# moglobin!ria ma

accompan se%ere tra!ma if there has been significant cr!sh in$!r (ithrhabdomolsis" Similarl# if the patient has recei%ed blood transf!sions after tra!ma#

small amo!nts of incompatible blood (ill prod!ce intra%asc!lar hemolsis and

hemoglobin!ria# leading to ac!te renal fail!re" +&tracell!lar fl!id %ol!me depletion is

a common complicating factor in the tra!ma patient beca!se of the de%elopment of

prolonged ile!s# peritonitis# or se*!estration of fl!id at a site of in$!r prod!cing

hpo%olemia" The de%elopment of sepsis is a f!rther contrib!ting factor in these

patients"

Sepsis

The onset of sepsis from an ca!se# incl!ding specific infections# s!ch as !rinar#

biliar# or intraperitoneal sepsis and contamination from colon proced!res or from

se%ere tra!ma# ca!ses ac!te renal fail!re" +ndoto&in from an so!rce is the priming

agent for the release of endogeno!sl prod!ced cto'ines# s!ch as t!mor necrosis

factor 9TNF;# that ha%e been sho(n clearl to prod!ce ac!te renal fail!re" It m!st be

remembered that nephroto&ic antibiotics that are !sed to treat sepsis ma themsel%es

ca!se or (orsen ac!te renal fail!re"

5ardiop!lmonar bpass

As man as - to 3- percent of patients (ho ha%e had prolonged cardiop!lmonar

bpass ha%e olig!ric renal fail!re or the less fre*!entl lethal nonolig!ric renal

fail!re" This is most li'el from hpoperf!sion of the 'idnes"

enal transplantation

Fail!re of a transplanted 'idne to f!nction in the earl postoperati%e period sho!ld

raise *!estions concerning technical problems (ith the renal arter# obstr!ction of

!rinar flo(# or intra%asc!lar %ol!me problems beca!se of contin!ed bleeding in the

patient" Hperac!te re$ection# (hich is !ncommon# also sho!ld be considered"

Urologic s!rger

Urologic proced!res pose additional and specific problems for de%elopment of ac!te

renal fail!re after s!rger" These problems !s!all are ca!sed b obstr!ction in one

form or another" Obstr!ction ma occ!r at the le%el of the 'idne# !reter# bladder# or!rethra as a res!lt of !rologic proced!res" emo%al of the obstr!ction or ca!se of


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obstr!ction sho!ld relie%e the ac!te renal fail!re" The presence of obstr!ction can be

determined b radiographic# tomographic# and comp!ted tomograph st!dies"

Kasc!lar disease

If the blood flo( to the 'idne is interr!pted for a prolonged period# as in operations

on the abdominal aorta or the renal arter# ac!te renal fail!re ma res!lt" Ac!te renalfail!re ma be delaed beca!se of an obstr!ction from an organi)ing hematoma

aro!nd a %asc!lar anastomosis or !reteral strict!res at the site of the !reteral

de%asc!lari)ation" Similarl# immediate postoperati%e hemorrhage ma ca!se

hpo%olemia and ac!te renal fail!re"

?ree&isting renal disease

This can contrib!te to postoperati%e renal fail!re" ,hen the 'idne is diseased

beca!se of nephrosclerosis# diabetes# chronic glomer!lonephritis# or chronic t!b!lar

interstitial nephritis# the organ is predisposed to the de%elopment of ac!te renal

fail!re"

adiographic contrast agents

,hen !sed preoperati%el# contrast agents can be a predisposing factor> a transient

red!ction in renal f!nction might ha%e occ!rred preoperati%el"

Dr!gs

A n!mber of dr!gs can lead to postoperati%e renal to&icit and ac!te renal fail!re" The

most prominent are the aminoglcosides# for (hich renal to&icit has been reported#

e%en (ith caref!l monitoring and maintenance of recommended dr!g le%els"

5closporine# amphotericin B# and nonsteroidal anti:inflammator dr!gs also ma

contrib!te to postoperati%e ac!te renal fail!re" The commonl !sed chlorinated

inhalation anesthetic agents ha%e been responsible for primar ac!te renal fail!re after

operation as (ell"

Laborator St!dies

Urinalsis

+&amination of the !rine is an essential diagnostic test in patients (ith postoperati%e

renal fail!re" The presence of blood or moglobin is a positi%e diagnostic test# and red

cell casts ma be present in the !rine of patients (ith !rinar obstr!ction" Sodi!m#

creatinine# !rea# and osmolalit le%els sho!ld be meas!red in the !rine"

Urine Osmolalit

?atients (ith ac!te renal fail!re are isosthen!ric> that is# the !rine osmolalit is close

to that of plasma# tpicall near =.. mOsmJL" ?atients (ith prerenal a)otemia ha%e

osmolalities of -.. mOsmJL or more 9Table 3: 22;" The ratio of !rine:to:plasma

osmolalit has been sho(n to be more discriminating than !rinar %al!es alone"

Urine:to:plasma osmolalit ratios of less than 22. are consistent (ith ac!te renal

fail!re# b!t prerenal a)otemia !s!all prod!ces ratios of 23- or higher"

Urine Urea and 5reatinine

The !rine:to:plasma !rea and !rine:to:plasma creatinine ratios are the most !sef!l in

diagnosing ac!te renal fail!re postoperati%el" A !rine:to: plasma creatinine ratiobelo( 3. is indicati%e of ac!te renal fail!re# and a ratio abo%e 4. indicates prerenal


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a)otemia" A !rine:to:plasma !rea ratio of less than = indicates t!b!lar in$!r# and a

ratio abo%e 6 !s!all indicates prerenal a)otemia"

Urine Sodi!m

The !nderperf!sed 'idne is sodi!m retaining# and a lo( !rine sodi!m concentration

is characteristic of prerenal a)otemia" Ho(e%er# (hen ac!te renal fail!re has occ!rred#there is diminished sodi!m reabsorption b the 'idne" ?atients (ith ac!te renal

fail!re !s!all ha%e a higher !rine sodi!m le%el 9abo%e 4. m+*JL;" Kal!es of !rine

sodi!m concentration bet(een 3. and 4. m+*JL are nondiscriminator"

5onse*!entl# !rine sodi!m concentration is not as sensiti%e in pro%iding diagnostic

acc!rac as is the !rine:to:plasma !rea ratio"

Management of the ?atient (ith +stablished Ac!te enal Fail!re

,hen the diagnosis of ac!te renal fail!re is made (ith rising le%els of blood !rea

nitrogen and creatinine and lo( !rine %ol!me# initial efforts sho!ld be directed to(ard

correcting re%ersible ca!ses" Attention then is t!rned to fl!id and electrolte balance

problems occ!rring beca!se of ac!te renal fail!re and ad$!sting the dosage of anadministered dr!g to compensate for impaired elimination"

Fl!id and +lectrolte Management

Hper'alemia

Of all the electrolte abnormalities that are enco!ntered in ac!te renal fail!re#

hper'alemia is the most serio!s# and it m!st be treated earl" Untreated hper'alemia

leads to cardiac arrest" The se%erit of the hper'alemia can be estimated b the +5@

changes# incl!ding pea'ed T (a%es# prolonged ? inter%als# loss of ? (a%es# and

(idening of the QS comple&"

,hen significant +5@ changes are apparent# calci!m inf!sion (ith 2 to 3 g 2.

calci!m gl!conate sho!ld be administered o%er 2. to 2- min to stabili)e the cardiac

membranes and ne!trali)e the to&ic effects of hper'alemia" This therap fre*!entl

is lifesa%ing# b!t the ser!m potassi!m le%el m!st be lo(ered *!ic'l" This ma

incl!de the administration of ins!lin# concentrated gl!cose# and intra%eno!s sodi!m

bicarbonate" +nteric cation: e&change resins or dialsis therap m!st be !sed fairl

soon to remo%e the potassi!m from the bod"

Fl!id Kol!me

In a patient (ith renal fail!re and little or no !rine o!tp!t# e&cessi%e inta'e of salt and

(ater (ill be retained# e%ent!all ca!sing p!lmonar edema and congesti%e heartfail!re" Fl!id inta'e sho!ld be restricted to replacing meas!red fl!id losses pl!s -.. to

0.. mL per da of insensible loss" 5aref!l balance st!dies of inta'e and o!tp!t are

mandator" Once an e&tracell!lar fl!id %ol!me deficits ha%e been corrected# the

*!antit of maintenance fl!ids amo!nt onl to meas!rable losses and insensible loss"

Hponatremia

Hponatremia e%ol%es earl# !s!all beca!se of e&cessi%e free (ater a%ailabilit from

brea'do(n of protein# carbohdrate# and fat as (ell as administered free (ater" If

ser!m sodi!m concentration falls belo( 23. m+*JL# dialsis is the onl therape!tic

endea%or that corrects hponatremia"


35/36

Metabolic Acidosis

Metabolic acidosis is almost ine%itable (hen the 'idne fails to remo%e acid b:

prod!cts from the bod" Treatment in%ol%es the !se of sodi!m bicarbonate# b!t

dialsis is often re*!ired as (ell" +&cessi%e restriction of protein in the catabolic

in$!red patient in order to dela the need for dialsis is not ad%isable"

Other +lectrolte Abnormalities

Hpocalcemia and hperphosphatemia ma occ!r in the patient (ho has e&perienced

a cr!sh in$!r or a b!rn co%ering a significant proportion of bod s!rface area" Se%ere

hperphosphatemia ma re*!ire dialsis" Hpocalcemia can be managed (ith caref!l

replacement of calci!m"

Use of Dialsis in Ac!te enal Fail!re

The indications for dialsis are listed in Table 3:23" Dialsis is best initiated before

the occ!rrence of the life:threatening complications of ac!te renal fail!re s!ch as

hper'alemia# se%ere acidosis# !remic encephalopath# or !remic pericarditis" There

are fo!r forms of dialsis for ac!te renal fail!re hemodialsis# peritoneal dialsis#contin!o!s arterial:%eno!s dialsis# and contin!o!s %eno%eno!s !ltrafiltration"

Hemodialsis is the most effecti%e and is the treatment of choice in the %er

hpercatabolic patient" Hemodialsis ma re*!ire 4 to - h of dail dialsis to

co!nteract the effects of the hpercatabolism" In others# dialsis ma be done three to

fo!r times per (ee'# depending on the rate of hpercatabolism" A ma$or ad%antage of

hemodialsis is that remo%al of fl!id b !ltrafiltration is easil controlled"

?eritoneal dialsis fre*!entl is !sed for the patient (ith se%ere heart disease#

incl!ding coronar arter disease and mocardial infarction"

Chapter 2 Fluid &Elecrolytes

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