FlUIDS AND ELECTROLITES

FlUIDS AND ELECTROLITES

BY
BY

Dr. Sawsan S.
Dr. Sawsan S.
Shurrab
Shurrab
Maintenance Fluid Therapy

Total body water (TBW) as a

percentage of body weight varies
with age.

During the first year of life, TBW

is about 60 of body weight and
re!ains at this level until puberty.

TBW is divided between two !ain

co!part!ents" intracellular fluid (#$%)
and e&tracellular fluid ('$%).

#n the fetus and newborn, the '$%

volu!e is larger than the #$% volu!e.

By ( year of age, the ratio of the #$%

volu!e to the '$% volu!e approaches
adult levels.

The '$% volu!e is )0of body weight,

and the #$% volu!e is *0 of body
weight .

The '$% is divided further into

plas!a water and interstitial fluid .

+las!a water is about , of body

weight.

The volu!e of plas!a water can be

altered by pathologic conditions,
including dehydration, heart failure,
abnor!al plas!a os!olality, and
hypo-albu!ine!ia.

The interstitial fluid,

nor!ally (, of body
weight, can increase
dra!atically in
diseases associated
with ede!a, such as
heart failure, protein-
losing enteropathy,
liver failure, and
nephrotic syndro!e

The co!position of the solutes in the

#$% and '$% is different.

.odiu! and chloride are the do!inant

cation and anion in the '$%.

+otassiu! is the !ost abundant

cation in the #$%, and its concentration
within the cells is appro&i!ately /0
ti!es higher than in the '$%.

The difference in the distribution of

cations-sodiu! and potassiu!-is due
to the activity of the 0a1,21-3T+ase
pu!p, which uses cellular energy to
actively e&trude sodiu! fro! cells and
!ove potassiu! into cells.
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+roper cell functioning re<uires close

regulation of plas!a os!olality,
intravascular volu!e, and intracellular
and e&tracellular electrolytes.

:aintenance of a nor!al os!olality

depends on control of water balance.

The plas!a os!olality is tightly

regulated to !aintain it between )=, and
)>,!8s!?@g.

:odification of water inta@e and

e&cretion !aintains a nor!al plas!a
os!olality.

Water inta@e and water produced by the

body fro! o&idation balances water
losses fro! the s@in, lungs, urine, and
gastrointestinal tract.

6rinary water losses are regulated

by the secretion of antidiuretic
hor!one (3DA), which sti!ulats
renal tubular reabsorption of water
and decreases urinary water losses.

Thirst is also sti!ulated

hen !olu"e depletion#

Because sodiu! is the principal

e&tracellular cation, and sodiu! is
restricted to the '$%, ade<uate
body sodiu! is necessary for
!aintenance of intravascular
volu!e.

The renin-angiotensin syste! is an

i!portant regulator of renal sodiu!
reabsorption and e&cretion.

The Bu&taglo!erular apparatus

produces renin in response to
decreased effective intravascular
volu!e.

4enin cleaves angiotensinogen,

producing angiotensin #.

3ngiotensin-converting enCy!e
converts angiotensin # into
angiotensin ##.

The actions of angiotensin ## include

direct sti!ulation of the pro&i!al
tubule to increase sodiu!
reabsorption and sti!ulation of the
adrenal gland to increase aldosterone
secretion.

Through its actions in the distal

nephron, aldosterone increases
sodiu! reabsorption.
hen !olu"e e$pan%ion #

.ynthesis of atrial natriuretic peptide

is
increased,and it is produced by the
atria in
response to atrial wall distention.

3long with increasing glo!erular

filtration rate, atrial natriuretic peptide
inhibits sodiu! reabsorption, facilitating
an increase in urinary sodiu! e&cretion.
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:aintenance #9 fluids are used in

children who cannot be fed enterally.

3long with !aintenance fluids,

children !ay re<uire concurrent
replace!ent fluids if they have
e&cessive ongoing losses.

#n addition, if dehydration is present,

the patient also needs to receive
deficit replace!ent.
Maintenance &luid%

3re co!posed of a solution of

water,
glucose, sodiu! potassiu!, and
chloride.

This solution replaces electrolyte

and
water losses fro! the urine and stool,
s@in, and lungs.

The glucose in !aintenance fluids

provides appro&i!ately )0 of the
nor!al caloric needs of the patient.

This percentage is enough to prevent the

develop!ent of starvation @etoacidosis
and di!inishes the protein degradation
that would occur if the patient received
no calories.

:aintenance fluids do not provide

ade<uate calories, protein, fat,
!inerals, or vita!ins.

Because of inade<uate calories, a

child on !aintenance #9 fluids loses
0., to ( of real weight each day.

+arenteral nutrition is especially

i!portant in a patient with underlying
!alnutrition.

.odiu! and potassiu! are given in

!aintenance fluids to replace losses
fro! urine and stool.

:aintenance re<uire!ents are ) to /

!'<?@g?day for sodiu! and ( to )
!'<?@g?day for potassiu!.
'ody ei(ht )*(+ ,olu"e -er Day
0-(0 (00!lD@g
((-)0 (000 !l1,0 !lD@g for
each ( @g !ore than (0
@g
:ore than )0 (,00 1)0 !l D@g !ore
than )0 @g

:aintenance fluids usually contain D,

in <uarter nor!al saline (0.) plus )0
!'<?7 of potassiu! chloride.

8r D, in half 0. plus )0 !'<?7 of

potassiu! chloride.

0. is isotonic to plas!aE <uarter or

half 0. is not isotonic.

$hildren weighing less than about )0

do best with the solution containing
<uarter 0. because of their high
water needs per @ilogra!.

#n contrast, larger children and adults

!ay receive the solution with half 0. .
Dehydration and 4eplace!ent
Dehydration and 4eplace!ent
Therapy
Therapy

E!aporati!e %*in water lo%%e% can be

especially significant in neonates,
especially pre!ature infants who are
under radiant war!ers or who are
receiving phototherapy .

'urn% can result in !assive losses of

water and electrolytes

Fe!er leads to a predictable increase

in insensible losses, causing a (0 to
(, increase in !aintenance water
needs for each (F$ increase in
te!perature greater than /=F$.

Tachypnea or a tracheo%to"y
increases evaporative losses fro! the
lungs

The (a%trointe%tinal tract is potentially a

source of considerable water and
electrolyte losses.
The losses should be replaced after they
occur,
using a solution with the sa!e electrolyte
concentration as the gastrointestinal fluid.

An increa%e in urine !olu"e li@e the

polyuric phase of acute tubular
necrosis, diabetes !ellitus, and
diabetes insipidus .
The patient !ust receive !ore than
standard !aintenance fluids when the
urine output is e&cessive to prevent
dehydration.

Third %pace lo%%e% !anifest with

ede!a and ascites and are due to a
shift of fluid fro! the intravascular
space into the intersitial space.
4eplace!ent of third space fluid is
e!pirical but should be anticipated.

DE./DRATION

Dehydration, !ost often due to

gastroenteritis, is co!!on in children.

The first step in caring for a child with

dehydration is to assess the degree of
dehydration.

The degree of dehydration dictates

the urgency of the situation and the
volu!e of fluid needed for
rehydration.

The degree of dehydration is

underesti!ated in hypernatre!ic
dehydration because the os!otically
driven shift of water fro! the
intracellular space to the e&tracellular
space helps to preserve the
intravascular volu!e.

The opposite occurs with

hyponatre!ic dehydration.

3n infant with "ild dehydration (/

to , of body weight dehydrated) has
few clinical signs or sy!pto!s.

3n infant with "oderate dehydration

has intravascular space depletion
which is evident by an increased heart
rate and reduced urine output. The
patient is (0 dehydrated and needs
fairly pro!pt intervention.

3n infant with %e!ere dehydration is

gravely ill. The decrease in blood
pressure indicates shoc@.

The infant is appro&i!ately (,

dehydrated and should receive
i!!ediate and aggressive #9 therapy.

:ild, !oderate, and severe

dehydration represent /, 6, and
> of body weight lost in older
children and adults.
Laboratory E!aluation

.eru! B60 and creatinine

concentrations are useful in assessing a
child with dehydration.

9olu!e depletion without renal

insufficiency !ay cause a disproportionate
increase in the B60, with little or no
change in the creatinine concentration.

3 significant elevation of the creatinine

concentration suggests renal insufficiency.
Calculation o& De&icit%

3 child with dehydration has lost

waterE there is usually a concurrent loss
of sodiu! and potassiu!.

The water deficit is the percentage of

dehydration !ultiplied by the patientGs
weight (for a (0-@g child, (0 of (0 @g
H ( 7 deficit).
Approach to Dehydration

The child with severe dehydration

re<uires acute intervention to ensure that
there is ade<uate tissue perfusion.

The child is given a fluid bolus, usually )0

!7?@g of the isotonic solution or ringer
lactate, over about )0 !inutes and it could
be repeated .

Typically the child has so!e

general clinical i!prove!ent,
including a lower heart rate,
nor!aliCation of the blood
pressure, i!proved perfusion, and
a !ore alert affect.

3fter shoc@ therapy,the child receives

nor!al !aintenance fluids and the
re!aining fluid deficit.

%or a patient with isotonic

dehydration, D, half 0. with )0 !'<?7
of potassiu! chloride is usually an
appropriate fluid.

+otassiu! usually is not included in the #9

fluids until the patient voids, unless
significant hypo@ale!ia is present.

Aalf of the total fluid is given over the first =

hoursE previous boluses are subtracted
fro! this volu!e.

The re!ainder is given over the ne&t (6

hours. $hildren with significant ongoing
losses need to receive an appropriate
replace!ent solution
.yponatre"ic dehydration

#t produces a !ore substantial

intravascular volu!e depletion owing to
the shift of water fro! the e&tracellular
space into the intracellular space.

.o!e patients develop neurologic

sy!pto!s.

:ost patients with hyponatre!ic

dehydration do well with the sa!e
general approach .

4apid correction of hyponatre!ia (I()

!'<?7?)* hr) should be avoided because
of the ris@ of central pontine
"yelinoly%i%
.ypernatre"ic dehydration

The !ove!ent of water fro! the

intracellular space to the e&tracellular
space during hypernatre!ic
dehydration partially protects the
intravascular volu!e.

6rine output !ay be preserved

longer, and there !ay be less
tachycardia.

$hildren with hypernatre!ic

dehydration are often lethargic and
irritable when touched.

Aypernatre!ia !ay cause fever,

hypertonicity, and hyperrefle&ia.

:ore severe neurologic sy!pto!s

!ay develop if cerebral bleedin( or
thro!bosis occurs.

#diogenic os!oles are generated

within the brain during the develop!ent
of hypernatre!ia.

These idiogenic os!oles increase the

os!olality within the cells of the brain,
providing protection against brain cell
shrin@age .

These idiogenic os!oles dissipate

slowly during correction of
hypernatre!ia.

With rapid lowering of the e&tracellular

os!olality during correction of
hypernatre!ia, water !oves fro! the
e&tra-cellular space into the cells of the
brain, producing cerebral ede"a which
produces seiCures, brain herniation,
and death.

To !ini!iCe the ris@ of cerebral

ede!a, the seru! sodiu!
concentration should not decrease
!ore than () !'<?7 every )* hours.

The deficits in severe hypernatre!ic

dehydration !ay need to be corrected
over ) to * days

:onitoring of the seru! sodiu!

concentration and adBust!ent of the
therapy is based on the result.

0onetheless, the initial resuscitation-

rehydration phase of therapy re!ains
the sa!e as for other types of
dehydration.
8ral 4ehydration
8ral 4ehydration

:ild to !oderate dehydration due to

diarrhea can be treated effectively using
oral rehydration solution (84.) .

The 84. relies on the coupled transport

of sodiu! and glucose in the intestine.

8ral rehydration therapy has significantly

reduced the !orbidity and !ortality fro!
acute diarrhea.
ORS contain%
ORS contain%
#
#

0a " >0 !!o?l

2 " )0 !!ol?l

$hloride" =0 !!ol?l

Bicarb." /0 !!ol?l

5lucose "((( !!ol?l

,0 !7?@g of the 84. should be given

within * hours to patients with !ild
dehydration.

(00 !7?@g should be given over * hours

to patients with !oderate dehydration.

3n additional (0 !7?@g of 84. is given

for each stool.

Breastfeeding and for!ula !il@ should

be allowed after rehydration and not
delayed !ore than )* hours.
./-ONATREMIA
./-ONATREMIA
Etiolo(y

-%eudohyponatre"ia is a laboratory
artifact that is present when the plas!a
contains high concentrations of protein or
lipid.

.ypero%"olality, resulting fro!

!annitol infusion or hyperglyce!ia so
water !oves down its os!otic gradient
fro! the intracellular space into the
e&tracellular space, diluting the sodiu!
concentration.

.ypo!ole"ic .yponatre"ia
There has been a higher net
sodiu!
loss than water lossE this is due to
either renal or e&trarenal.

#f the sodiu! loss is due to a nonrenal

disease, the urine sodiu!
concentration is very low, as the
@idneys atte!pt to preserve the
intravascular volu!e by conserving
sodiu!.

#n renal salt-wasting diseases, the

urine sodiu! is inappropriately
elevated.

Eu!ole"ic .yponatre"ia
o
These patients typically have an
e&cess of total body water and a slight
decrease in total body sodiu!.
o
They usually appear nor!al or have
subtle signs of fluid overload.
o
#n SIAD., there is secretion of 3DA .
o
.#3DA is associated with pneu!onia,
!echanical ventilation, !eningitis,
and other $0. disorders (trau!a).
o
#nfants also can develop euvole!ic
hyponatre!ia as a result of
consu!ption of large a!ounts of
water or inappropriately diluted
for!ula in the absence of dehydration.

.yper!ole"ic .yponatre"ia
There is an e&cess of total body water
and sodiu!, although the increase in
water is greater than the increase in
sodiu! li@e
#n renal failure and heart failure.

Clinical Mani&e%tation%

Ayponatre!ia causes a fall in the

os!olality of the e&tracellular space.

Water !oves fro! the e&tracellular

space to the intracellular space to !aintain
os!otic e<uilibriu!.

Brain cell swelling is responsible for

!ost of the sy!pto!s of hyponatre!ia.

0eurologic sy!pto!s of
hyponatre!ia include anore&ia,
nausea, e!esis, !alaise, lethargy,
confusion, agitation, headache,
seiCures, co!a, and decreased
refle&es.

+atients !ay develop hypother!ia

and $heyne-.to@es respirations.

Ayponatre!ia can cause !uscle

cra!ps and wea@ness.
Treat"ent

4apid correction of hyponatre!ia can

produce central pontine !yelinolysis.
3voiding !ore than a () !'<?7
increase in the seru! sodiu! every )*
hours is prudent, especially if the
hyponatre!ia developed gradually.

Treat!ent of hypovole!ic
hyponatre!ia re<uires ad!inistration
of #9 fluids with sodiu! to provide
!aintenance re<uire!ents and deficit
correction and to replace ongoing
losses.

%or children with .#3DA, water

restriction is the cornerstone of the
therapy.

Treat!ent of hypervole!ic
hyponatre!ia centers on restriction of
water and sodiu! inta@e, but disease-
specific !easures, such as dialysis in
renal failure, also !ay be necessary.

'!ergency treat!ent of sy!pto!atic

hyponatre!ia, such as seiCures, uses
#9 hypertonic saline to increase the
seru! sodiu! concentration rapidly,
which leads to a decrease in brain
ede!a.

3 child often i!proves after receiving

* to 6 !7?@g of / sodiu! chloride.
./-ERNATREMIA
./-ERNATREMIA
Etiolo(y

.odiu! into&ication is fre<uently

iatrogenic in a hospital setting resulting
fro! correction of !etabolic acidosis
with sodiu! bicarbonate.

#n hyperaldosteronis!, there is renal

retention of sodiu! and resultant
hypertensionE the hypernatre!ia is !ild.

Aypernatre!ia resulting fro! water

losses develops only if the patient
cannot drin@ ade<uately because of
neurologic i!pair!ent, e!esis, or
anore&ia.

Aereditary nephrogenic diabetes

insipidus which is &- lin@ed causes
!assive urinary water losses and
dilute urine.

3c<uired nephrogenic diabetes

insipidus !ay be secondary to
interstitial nephritis, sic@le cell
disease, hypercalce!ia, hypo@ale!ia,
or !edications (lithiu! or
a!photericin).

$hildren with diabetes insipidus have

inappropriately dilute urine.

#f the defect is due to central diabetes

insipidus, the urine output decreases,
and the urine os!olality increases in
response to ad!inistration of an 3DA
analogue (central causes of 3DA
deficiency include tu!or, infarction, or
trau!a).

There is no response to an 3DA

analogue in a child with nephrogenic
diabetes insipidus
Clinical Mani&e%tation%

:ost children with hypernatre!ia are

dehydrated and have the typical signs
and sy!pto!s of dehydration .

$hildren with hypernatre!ic

dehydration tend to have better
preservation of intravascular volu!e .

Blood pressure and urine output are

!aintained.

+robably because of intracellular

water loss, the pinched abdo!inal
s@in of a dehydrated, hypernatre!ic
infant has a doughy feel.
3s the e&tracellular os!olality
increases, water !oves out of brain
cells, resulting in a decrease in brain
volu!e which result in tearing of
intracerebral veins and bridging blood
vessels as the brain !oves away fro!
the s@ull and the !eninges.
+atients !ay have subarachnoid,
subdural, and parenchy!al
he!orrhage.
.eiCures and co!a are possible
se<uelae of the he!orrhage.
Treat!ent

#f the seru! sodiu! concentration is

lowered rapidly, brain swelling results
and !anifests as seiCures .

The goal is to decrease the seru!

sodiu! by less than () !'<?7 every )*
hours, a rate of 0., !'<?7?hr.

#f a child develops seiCures fro! brain

ede!a secondary to rapid correction,
ad!inistration of hypotonic fluid
should be stopped, and an infusion of
/ saline can increase the seru!
sodiu! acutely, reversing the cerebral
ede!a or co!a.

#n a child with hypernatre!ic

dehydration, as in any child with
dehydration, the first priority is
restoration of intravascular volu!e
with isotonic fluid.

3 child with central diabetes insipidus

should receive an 3DA analogue to
prevent further e&cessive water loss.

3 child with nephrogenic diabetes

insipidus re<uires a urine replace!ent
solution to offset ongoing water
losses.

$hronically, reduced sodiu! inta@e,

thiaCide diuretics, and nonsteroidal
anti-infla!!atory drugs can decrease
water losses in nephrogenic diabetes
insipidus.