Fluidos y Electrolitos- pediatrics

ABBREVIATIONSADH: Antidiuretic hormone or

vasopressinECF: Extracellular fluidICF: Intracellular fluidRTA: Renal tubular acidosisDKA: Diabetic ketoacidosisDI: Diabetes insipidus

Pediatrics in Review Vol. 17 No. 11 November /996 395

BACK TO BASICSA review of

the scientific

foundations

of current

clinical practice

Fluids and Electrolytes-Clinical AspectsNicholas Jospe, MD* and Gilbert Forbes, MDI

Medical practice rests on the foundation of science. Clinicians are constantly making practical decisions and dealing

with immediate situations that demand solutions. Time should be taken to focus on those scientific principles that

underlie our diagnostic and therapuetic maneuvers. This section of Pediatrics in Review presents selected topics that

are relevant to practice from the areas of physiology, pharmacology, biochemistry, and other disciplines; clarification

of these will augment the pediatrician’s understanding of clinical procedures.

Changes in volume and composition

of body fluids due to disorders offluid and electrolyte balance causevarious common clinical illnesses.The rationale for reviewing the diag-nosis and management of fluid and

electrolyte disorders was eloquentlydenoted by Dr Altemeier, when hesuggested that this knowledge

belongs among the core conceptsneeded by the “keepers of the gates,”

that is, primary care pediatricians.’ Inthe body, homeostasis is maintainedby the coordinated action of behav-ioral, hormonal, renal, and vascular

adaptations to volume and osmoticchanges. These core issues have been

outlined in a previous article in thisjournal by Dr Hellerstein, and thecurrent article proceeds from that dis-

cussion.2 Following introductorycomments about body fluid volumeand composition, we provide an

overview of some of the etiologies ofthe disorders of volume, tonicity, andcomposition of body fluids and of thetherapy to correct these disorders.

�Associate Professor of Pediatrics.

‘Professor of Pediatrics, Division of Pediatric

Endocrinology, University of Rochester School

of Medicine and Dentist,y, Rochester, NY.

Sodium, Osmolality, and theVolume of Body Fluids

Total body water, which is 55% to72% of body mass, varies with sex,age, and fat content and is distributed

between the intracellular and extra-cellular spaces. The extracellularfluid (ECF), which comprises aboutone third of total body water,includes the intravascular plasmafluid and the extravascular interstitialfluid. Plasma ions include primarilyNa4, C1, and HCO3, which are

excluded from intracellular environ-ments, and lesser amounts of potassi-um (K�), magnesium, calcium, phos-phates, sulfates, organic acids, and

protein. Interstitial fluid, which sur-rounds the cells, has the same compo-sition as plasma, but with less pro-tein. The principal components ofintracellular fluid (ICF) are K�, pro-teins, magnesium, sulfates, and phos-phates.

In the ECF, Na� and C1 constitute90% or more of the effective solutes.Serum Na� concentration defines therelative amount of sodium and waterin plasma; the maintenance of a nor-mal Na� concentration, thus, con-

tributes to regulation of the volumeof body fluids. The size of the ECFand ICF compartments depends on

the amount of water within each; the

distribution of water depends on theirosmolality. The osmolality of a solu-

tion is a function of the number ofsolute particles or osmoles per unitvolume. In a given patient, the effec-

tive osmolality may be calculated asfollows, using the values of 2.8 and1 8 to convert values of blood ureanitrogen (BUN) and glucose, respec-lively, to mOsni/L:

Osmolality = 2 [Na� in mEq/Ll #{247}[BUN in

mg/dL]/2.8 + [Glucose in mg/dLJ/l8

Normal serum osmolality (265 to285 mOsm/L) is maintained by kid-

ney function, which dilutes or con-centrates urine. This is accomplishedby a variety of mechanisms involvingglomerular filtration, arterial pres-sure, blood flow, physical factors in

at Chulalongkorn University on May 10, 2015http://pedsinreview.aappublications.org/Downloaded from

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TABLE!. Maintenance Requirements for Fluid and Electrolytes, Based on Body Weight

Body Weight 0 to 10 kg 10 to 20 kg >20 kg

Total Water 100 mL/kg 1000 mL +50 mL/kg for 1500 mL #{247}20mL/kg for

Volume each kg >10 kg each kg >20 kg

Sodium 3 mEq/kg 3 mEq/kg 3 mEq/kg

Potassium 2 mEq/kg 2 mEq/kg 2mEq/kg

Chloride 5 mEq/kg 5 mEq/kg 5 mEq/kg

396 Pediatrics in Review Vol. 17 No. /1 November /996

FLUIDS & ELECTROLYTESClInIcal Aspects

the kidneys, the sympathetic nervoussystem, and hormones such as aldos-

terone, atrial natriuretic factor, vaso-pressin, and dopamine. These sys-

tems converge to control water andelectrolyte balance through glomeru-lar ultrafiltration of the plasma fol-

lowed by changes in the electrolytecontent of this ultrafiltrate by tubularreabsorption and secretion. Thesemechanisms, together with thirst,

control both plasma osmolality and

plasma volume.

General Principles of theManagement of DehydrationDisorders affecting the composition

and volume of body fluids requireintervention to maintain or restorenormality. This intervention is

accomplished by: 1) supplying main-tenance requirements, 2) correctingvolume and electrolyte deficits, and

3) replenishing ongoing abnormallosses. The following guidelinesreview how to calculate maintenance

requirements, deficit replacement,

and provisions for ongoing abnormal

losses.

REQUIREMENTS FORMAINTENANCE FLUID ANDELECTROLYTES

As noted previously, homeostasis ismaintained by the coordinated action

of behavioral, hormonal, renal, andvascular adaptations. Outside of these

adaptations, the role of fluid and elec-

trolyte maintenance as a concept is tohelp the physician ensure preserva-tion of this homeostasis by providingall fluid and electrolyte needs whenthese cannot be met by the patient.

Maintenance requirements from sen-

sible and insensible fluid losses are to

be rigorous and depend on energy

expenditure, but they can be calculat-

ed adequately by using body weight.Insensible water losses through the

skin and the respiratory tract, whichusually are electrolyte-free, are high-

er in newborn infants than in adoles-cents. Sensible losses, primarily uri-nary, account for approximately 50%

of daily fluid requirements. Thus, uri-nary fluid losses need not be replacedas long as the total daily urine output

is not more than 50% to 60% of thecalculated water maintenance.

Caloric requirements for growth canbe estimated as equivalent on a kcal-for-mL basis to water requirements.

Factors that increase the requirementsfor calories and for water are fever( 10% for each degree C), physical

activity, ongoing gastrointestinal loss-es, hyperventilation, or hypermeta-

bolic states. Other conditions, such asanuria, oliguria, or congestive heartfailure, may reduce the requirements

for water. Maintenance requirementsfor water vary with weight and can becalculated as outlined in Table 1.Electrolyte requirements, which arerelatively constant throughout child-hood, also are outlined in Table 1. All

abnormal losses, such as those arisingfrom a stoma, nasogastric aspiration,

prolonged diarrhea, or burns, shouldbe analyzed, measured, and replacedvolume for volume.

ESTIMATION OF DEFICIT

Water and electrolyte deficits resultfrom either normal or increased lossesin the face of decreased or normalintake. Findings on history, physicalexamination, and laboratory studiesprovide the tools to gauge volumedepletion. One must inquire aboutfever, vomiting and/or diarrhea, andurine output to establish the site(s) of

fluid loss and the type and amount of

loss. Careful attention should be paidto recent feeding, including type andvolume of food and drink, and to

assessing weight change. The physicalexamination provides clues for esti-mating the extent of dehydration, asoutlined in Table 2. This informationis used to gauge the percent dehydra-

tion, which then is expressed as milli-liters of body water deficit per kilo-gram of body weight. For example, adehydration of 10% corresponds to awater deficit of 100 mL/kg bodyweight.

Measurement of electrolytes is notrequired if the patient appears to have

lost less than 5% of body weight andhas an obvious cause for the fluid loss.When the body weight loss is greater

than 5% or when the cause of thedehydration is uncertain, laboratory

studies should be obtained to look forabnormalities of electrolyte and acid-base balance. Laboratory findings mayinclude, in addition to serum elec-

trolyte abnormalities, elevations ofBUN, hematocrit, or albumin due tohemoconcentration. The plasma creati-nine concentration is a more reliableindex of renal function than is theBUN concentration because creatinineconcentration is influenced less by

dietary protein load and tissue break-down, although it does vary with ageand muscle mass. Most children do

not require pH, calcium, phosphorus,magnesium, glucose, or albumin con-centration determinations.

Isonatremic DehydrationThe most common cause of dehydra-tion in infants is diarrhea, which is anet fluid secretion greater than thecapacity of the intestine to absorbfluid, or failure to absorb normalsecretions. The fluid content of the



- FLUIDS & ELECTROLYTESClinical Aspects

TABLE 2. Estimation of Dehydration

Extent of Dehydration Mild Moderate Severe

Weight Loss-Infants 5% 10% 15%

Weight Loss-Children 3%-4% 6%-8% 10%

Pulse Normal Slightly increased Very increased

Blood Pressure Normal Normal to orthostatic, Orthostatic to shock

>l0mmHgchange

Behavior Normal Irritable, more thirsty Hyperirritable to lethargic

Thirst Slight Moderate Intense

Mucous Membranes* Normal Dry Parched

Tears Present Decreased Absent, sunken eyes

Anterior Fontanelle Normal Normal to sunken Sunken

External Jugular Vein Visible when Not visible except Not visible even withsupine with supraclavicular supraclavicular pressure

pressure

Skin* (Less Useful in Capillary refill Slowed capillary Very delayed capillaryChildren >2 Y) >2 sec refill, 2-4 sec refill (>4 sec) and

(decreased turgor) tenting; skin cool,acrocyanotic, or mottled*

Urine Specific Gravity (SG) >1.020 >1.020; oliguria Oliguna or anuria

* These signs are less prominent in patients who have hypernatremia.

Pediatrics in Review Vol. 17 No. 11 November 1996 397

intestinal tract is a mixture of diet and

secretions from the stomach, the pan-creas, the bile ducts, and the intestine.The secretory process of diarrhea

causes Na�, Cl, and water losses. Indiarrhea from rotavirus infection, lossof HCO3 and K� in the small intes-tine leads to metabolic acidosis and

K� depletion. In general, childrenwho have a brief illness and anorexiapresent with proportional water and

electrolyte losses, that is, isotonicdehydration. Dehydration compro-mises the function of many organsystems so that body fluid homeosta-sis cannot be maintained. An impor-

tant treatment objective is to restorerenal function so that the kidney canassist in correcting the acid-base and

electrolyte imbalance. Moderate vol-ume depletion may be treated withoral fluids, even though parenteralfluid administration is the norm inNorth America and western Europe.

Indeed, rehydration therapy usingoral fluids is effective, cost-efficient,and adaptable and lowers hospital uti-lization. Parenteral fluids should begiven to children who have severevolume depletion, with altered states

of consciousness, intractable vomit-ing, and abdominal distention or

ileus. For infants weighing less than4.5 kg or who are younger than3 months, it is more prudent to pro-vide parenteral than oral therapy. The

following sections address parenteral

and oral rehydration, but monitoringof the patient’s status using clinicaland laboratory data is crucial toensure the proper implementation ofeither form of rehydration.

PARENTERAL REHYDRATION

The first phase of treatment is to

expand the vascular volume rapidly,with the goals of preventing shock

when a circulatory deficit is severeand improving renal function.Intravenous normal saline or Ringerlactate (10 to 20 mL/kg) should begiven over 1 hour. This infusionshould be subtracted from the pro-

posed total volume for the day. Fivepercent albumin, 10 mLlkg, is needed

only in neonates, malnourishedinfants, and hypernatremic patients inshock. The benefit of normal saline or

Ringer lactate is a transient expansionof the intravascular space, but thisbenefit dissipates as the crystalloid

solution equilibrates with the remain-der of the extravascular interstitial

fluid. Compared with normal saline,Ringer lactate has a more physiologicNa� to Cl ratio (1.17:1); has a slight-ly lower Na concentration ( I 30 mEq/L); and contains calcium, potassium,and lactate.

The next phase of treatment isaimed at correcting the deficit, pro-viding maintenance, and, if needed,replacing ongoing abnormal losses.In severe depletion, it may be appro-

priate to give one half of the calculat-ed deficit over the first 8 hours and

the second half over the next16 hours; maintenance needs are pro-vided at a steady rate. During this

phase, 5% glucose should be used asthe stock solution; NaCI is added

according to the estimated need.Children who have isonatremic dehy-dration require 8 to 10 mEq of Na�per kg of body weight for repletion of

deficit and 3 mEq/kg per day formaintenance. This Na� is given in avolume consisting of the calculatedmaintenance for water (Table I) andthe estimated water deficit (Table 2).

Once urine flow is verified, KC1 isadded at a concentration of 20 mmol/L to prevent the clinical effects of K’�

depletion. Intravenous K� administra-tion should not be greater than



398 Pediatrics in Review Vol. 17 No. 11 November 1996

FLUIDS & ELECTROLYTESClinical Aspects

4 mEqlkg per day to avoid exceeding

the capacity for cellular uptake of K�,

thereby inducing hyperkalemia. Inmost infants who have diarrheal dehy-dration, diarrhea subsides rapidly withtherapy, presumably from “bowel

rest.” However, for patients who havecontinued heavy diarrhea, stool vol-umes should be measured to maintainan appropriate intake relative to out-put; such losses should be replaced

volume for volume. Normal saline ortwo-thirds normal saline with 20mmolIL of KC1 may be used safely toreplace most fluid losses from gastricor intestinal drainage. Metabolic aci-

dosis may occur from diarrhea, but itis usually mild and resolves oncerenal function is restored. In severe

metabolic acidosis, bicarbonateadministration may be required.

ORAL REHYDRATION

As noted previously, therapy usingoral fluids is effective, even withongoing diarrhea or vomiting. For themajority of patients who have gastro-enteritis and either no dehydration or,

at most, moderate dehydration, oralrehydration therapy is all that is nec-essary. This distinction is importantbecause there are two categories oforal hydration solutions available. Thefirst includes the oral maintenancesolutions used either after parenteralrehydration or early in diarrheal ill-

ness to prevent dehydration. These are

used to replace losses in infants whohave gastroenteritis from commoninfections. The second categoryincludes the oral rehydration solu-

tions, which have a higher Na� con-

centration. As a guideline for oralrehydration, small aliquots are given

as tolerated to provide approximately50 mL/kg over 4 hours in mild dehy-dration and up to 100 mL/kg over6 hours in moderate dehydration.Once rehydration is accomplished,maintenance fluid is given at100 mLlkg per day. The electrolyte

composition (in mEqfL) and carbohy-

drate composition (in percent) of thecommercially available oral solutionsare indicated in Table 3. Of note,

household clear-liquid beverages,

such as broths, juices, sodas, and tea,are inappropriate for the treatment ofdiarrheal dehydration.

Hyponatremia andHyponatremic Dehydration

The differential diagnosis of hypona-tremia will be reviewed in the context

of hypovolemia, euvolemia, andhypervolemia to underscore the fact

that a low serum Na� concentrationdoes not necessarily imply decreasedtotal body Na’ content. The signs andsymptoms of hyponatremia correlatewith the rapidity and extent of the fallin serum Na� concentration. Centralnervous system (CNS) symptoms

include apathy, nausea and vomiting,headache, seizures, or coma; the mus-culoskeletal symptoms include

cramps and weakness. Thus, infantswho have hyponatremic dehydration

may appear quite ill, because fluidloss in combination with hyponatrem-ia leading to circulatory insufficiency

causes a disproportionate reduction inECF volume. As serum osmolalityfalls, water moves into cells, causingmusculoskeletal dysfunction andputting the brain at risk for swelling.The brain adapts to hyponatremia bypushing interstitial fluid into the cere-brospinal fluid and by extruding cellu-

lar solutes, primarily K� and aminoacids. The relevance of this point is tostress that rehydration puts the brainat risk for dehydration, or even injury,

if the correction of fluid and elec-

trolyte losses is much more rapid thanthe rate at which the brain can recoversolute. In severe hyponatremia, it is

advisable to effect a correction inplasma Na’� concentration of no more

than 10 to 12 mEq/L per day to avoidundue fluid shifts.

DIFFERENTIAL DIAGNOSIS

Hypovolemia

In pediatrics, by far the most frequent

cause of hypovolemic hyponatremiais viral gastroenteritis, with vomiting,

diarrhea, or both. Other causes ofhypovolemic hyponatremia include

TABLE 3. Composition of Commercial Oral Hydration Solutions

Na’ (mEqlL) K’ (mEqIL) cr (mEq/L) BASE (mEqlL) CARBOHYDRATE(% WEIGHT FORVOLUME)

MAINTENANCESOLUTIONS:

Resol (Wyeth)* 50 20 50 Citrate, 34 2% Glucose

Ricelyte (Mead Johnson) 50 25 45 Citrate, 34 3% Rice syrup solids

Pedialyte (Ross) 45 20 35 Citrate, 30 2.5% Glucose

REHYDRATION

SOLUTIONS:

Rehydralite (Ross) 75 20 65 Citrate, 30 2.5% Glucose

World Health Organization

formulation(for use in cholera)

90 20 80 HCO#{231},30 2% Glucose

* Includes cakium, 4 mEqIL; magnesium, 4 mEqIL; phosphate,5 mEqIL



Pediatrics in Review Vol. /7 No. /1 November /996 399


percutaneous losses or third space

sequestration of fluid, as in ascites,burns, or peritonitis. Patients whohave cystic fibrosis are prone to

develop hyponatremic dehydration,

particularly in hot weather, becausetheir sweat has an abnormally high

concentration of Na� and Cl. In all ofthese cases, urinary Na� concentration

is expected to be <20 mEq/L as thebody seeks to conserve Nat On the

other hand, renal loss (urinary Na�>20 mEqfL) also can cause hypov-

olemic hyponatremia. This may fol-low the use of diuretic medications oroccur in salt-wasting nephropathy,proximal renal tubular acidosis

(RTA), and lack of or resistance to

mineralocorticoid.

Euvolemia

The most common cause of eu-volemic hyponatremia is the syn-

drome of inappropriate antidiuretichormone (ADH) secretion, which is a

problem of water retention, not Na�depletion (urinary Na� usually>20 mEqIL). The causes of inappro-priate ADH secretion include tumors,pulmonary disorders, CNS infection,and a host of drugs. In addition,euvolemic hyponatremia may occur ininfants fed excessively diluted infant

formula.

Hypervolemia

Hypervolemic hyponatremia may

result from conditions associated with

edema in which water is retained in

excess Na�, such as nephrosis, con-gestive heart failure, cirrhosis, orrenal failure.

MANAGEMENT

The general principles for managing

dehydration have been outlined previ-ously, and additional guidelines areincluded in this section.

Hypovolemic patients who havehyponatremia require volume expan-sion, using a solution containing saltto correct the Na� deficit (10 to12 mEqlkg of body weight or even

15 mEq/kg in severe hyponatremia)and to include the Na� maintenanceneeds (3 mEq/kg per day in 5% dex-trose solution). For a serum Na� con-centration of 120 to 130 mEq/L, thisamount should be given over a24-hour period. For a serum Na� con-

centration <120 mEqIL, the rehydra-

tion should be spread out over thenumber of days it takes to raise theNa� concentration to 130 mEq/L by

10 mEq/day (eg, 2 days for a Na� of1 10 mEq/L) and provide that fractionof the deficit along with the daily

maintenance requirement. On theother hand, symptomatic hyponatrem-

Ia (headache, lethargy, disorientation)requires urgent therapy to prevent the

potential complications of hypona-tremia, such as seizure or coma,which result from the movement ofwater into brain cells. In the presence

of these symptoms or complications,Na’� administration is urgent, regard-

less of the absolute level of serumNa’�. Hypertonic saline (3% salinesolution), either with or without loop

diuretic agents and water restriction,should be used to raise the serum Na�by I to 2 mEqfL per hour or halfwaytoward normal during the first 8

hours. A correction using 3% salineover 4 hours can be calculated accord-ing to the following formula:

Sodium deficit in mEq = (125 - observed[Na�]) X body weight in kg x 0.6

Finally, the presence of high urinaryNa� and low urinary K� excretion,when these reflect the kidney’s lack ofmineralocorticoid action, indicates the

need for mineralocorticoid medicationin addition to fluids to ensure correc-

tion of the volume deficit.

Euvolemic patients who have

hyponatremia require restriction ofwater intake. Asymptomatic individu-als require only water restriction; ede-

matous patients require restriction ofboth water and Na� (greater restric-tion of water than of Nat), using

diuresis with intravenous furosemide.Na� administration in this setting is

inappropriate.

Hypervolemic patients who havehyponatremia require water and sodi-

um restriction. The hypervolemicstate may be accompanied by edemaand cardiopulmonary evidence of

fluid overload and implies retention of

water and Na4 with an inappropriatelyhigh proportion of water relative to

Na4. In patients whose renal failure ismild, water restriction is effective, butdialysis is required in those who haveoliguria or anuria.

Hypernatremia andHypernatremic Dehydration

As a rule, the hypernatremic patient

also is dehydrated, with a greater lossof water relative to solute; eventhough total body Na4 may be

increased or normal, it most com-monly is decreased. Thus, as in

hyponatremia, the serum Na4 concen-tration does not reflect the total bodyNa4 content. As hypernatremia leads

to hypertonicity of the plasma, thebody protects itself by secreting ADH

and by increasing thirst. Thus, mdi-viduals who are unable to secrete orrespond to ADH and those who have

no access to water are particularlyprone to hypernatremia. Affected

patients, especially infants, frequentlyexhibit disturbances of conscious-ness, such as lethargy or confusion,

and other signs of neuromuscular irri-tability, such as muscle twitching,hyperreflexia, or even convulsions.Finally, fever is not uncommon, andthe skin may feel thickened ordoughy or velvet-soft in texture.

Extracellular hypertonicity drawswater from cells, thus decreasing cell

size. In the brain, this may lead to

tearing of arachnoid tissue and tosubarachnoid, intradural, or subduralhemorrhages. When the hypertonicity

develops insidiously, brain cells adapt

by generating intracellular osmoles, aprocess called “idiogenic osmole pro-

duction.” This process decreases theextracellular-to-intracellular osmoticgradient, thereby protecting against

cell shrinkage. To avoid inducingcerebral edema once correction ofplasma hypertonicity is initiated, it is

important to know that dissipation ofthe intracellular osmoles is not rapid.Hence, correction of the hyperna-

tremia should be relatively slow.Severe hypernatremia (serum Na4

concentration >160 mEqfL) can resultin permanent CNS sequelae and isassociated with a mortality that

reaches 10%.


Diarrhea, which usually results inisonatremic or hyponatremic dehy-

dration, may cause hypernatremia inthe presence of persistent fever,anorexia, vomiting, and decreasedfluid intake. Beyond gastrointestinaldisease, other causes of hyperna-



tremia include water and Na4 deficit


400 Pediatrics in Review Vol. 17 No. 11 November 1996

from percutaneous losses or renallosses and water losses from central

or nephrogenic diabetes insipidus(DI) or pharmacologic agents, such as

lithium, cyclophosphamide, or cis-platin. These entities are characterizedby a relatively greater water than Na�

loss and usually induce a hypo-volemic state. Na� excess from saltpoisoning causes hypernatremia butnot dehydration. Finally, prematurity,

inability to regulate water intake, lackof renal regulation, hyperpnea,

diaphoresis, high solute intake, andenteric infection with organisms caus-ing inflammation and malabsorptioncan cause hypernatemia. The modern

tendency is to offer milk (cow or soy)or infant formula feedings to infantswho have diarrhea as a means ofimproving nutrition. Such feedings

should have a low content of proteinand electrolytes that require renalexcretion. Half-strength formula orhuman milk are obvious choices.

MANAGEMENT

Hypovolemic patients who have

hypernatremia have a relativelygreater water than Na� loss. Initial

therapy requires administration of nor-mal saline or Ringer lactate to restorean effective circulating plasma vol-ume. Five percent albumin solution orplasma also can be used. Hypovolemic

patients who have hypernatremiarequire a hypotonic solution contain-ing salt to restore the Na4 deficit (2 to5 mEqlkg of body weight) and tobegin the Na4 maintenance (3 mEq/kgof Na4) in solution containing 20 to40 mmollL of KC1 and 5% glucose.For a serum Na� concentration of 150to 160 mEq/L, this volume should begiven over a 24-hour period. Because

ECF osmolarity may fall more rapidly

than the brain can dissipate the idio-genic osmoles generated to protectintracellular osmolarity, an elevated

serum Na� concentration should becorrected by no more than 10 mEq/Lper day. For a serum Na4 concentra-

tion >160 mEq/L, the rehydration

should be spread out over the numberof days necessary to lower the Na4

concentration to 150 mEq/L by10 mEq/day (eg, 2 days for a Na4 of170 mEq/L). Both the daily fraction ofthe deficit and the daily maintenance

requirement should be provided. The

degree of hypotonicity of the fluidadministered is less important than tothe rate of correction.

Euvolemic patients who havehypernatremia resulting from excessinsensible water losses or from DI(solute-free water losses) requirewater replacement and, where appro-

priate, therapy for the management ofthe DI. Rehydration should be

accomplished by using hypotonicsaline, aiming to correct the serumNa4 concentration by no more than

10 mEq/L/day. The “water deficit” inDI, assuming that total body Na4 hasremained unchanged, may be estimat-

ed by using the following formula

(adapted from Avner3):

Water deficit = (normal body

water) - (current body water)

Current body water = 0.6 x body

weight in kg x normal [Na� 1/

observed [Na�]

Normal body water = 0.6 x body

weight in kg

Hypervolemic patients who have

hypernatremia resulting from excesssalt administration or hyperaldostero-nism require diuresis with concomi-

tant water administration.

PotassiumPotassium is the most abundant intra-

cellular cation; thus, acute serumchanges do not reflect total body K4stores. Chronic changes, especially in

hypokalemia, do reflect body stores.The serum K4 concentration is adjust-ed in the terminal nephron of the kid-ney, and a small loss occurs throughthe stool. The ratio of intracellular toextracellular K4 is the major determi-nant of the resting electrical potential

across cell membranes and, thus, con-tributes to the action potential ofneural and muscular tissue. Abnor-malities of serum K4 are potentiallylife-threatening, due to effects on car-diac function, because of the role of

K4 in neuromuscular irritability. Also,K4 plays an important role in cellmetabolism. In acidemia, the concen-tration of K4 in the ECF is increasedby cellular secretion of K4; the con-centration of serum K4 usually rises

by approximately 1 mEq/L when the

pH drops by 0.1 unit; in alkalosis, theconverse occurs.

Hypokalemia

DIAGNOSIS

Hypokalemia (serum K4 concentra-

tion <3 mEqfL) has a lengthy differ-ential diagnosis. The most frequentcauses of net loss of K4 are gastroin-

testinal losses or renal losses. Giventhat the K4 concentration of gastricfluids is fairly high, nasogastric suc-tion or protracted vomiting may

induce hypokalemia. Renal losses canresult from either administration ofdiuretics or mineralocorticoids orfrom intrinsic renal tubular disease,

such as Bartter syndrome. Barttersyndrome is characterized by hyper-reninemia and hyperaldosteronism,which results in hypokalemia,

hypochloremia, and alkalosis.

Because nearly all K4 is intracellular,hypokalemia also may result fromtranscellular shifts of K� from serumto cells, as in acute alkalosis. Themost severe manifestations ofhypokalemia are arrhythmias, neuro-

muscular excitability (hyporeflexia orparalysis, decreased peristalsis orileus), and rhabdomyolosis. A goodestimate of intracellular K4 can bemade from the electrocardiogram,where flattened T waves, a shortened

P-R interval and QRS complex, and

finally, the appearance of U waves

are observed.

MANAGEMENT

In the presence of cardiac arrhyth-mias, extreme muscle weakness, orrespiratory distress, patients shouldreceive KCI intravenously and closecardiac monitoring. Once the serumK4 is stabilized, the oral route ofadministration is preferable. Thechoice of potassium salt depends onthe etiology. If the patient is likely tobe hypophosphatemic, a phosphatesalt should be used. In metabolic

alkalosis, KC1 should be used; inrenal tubular acidosis (RTA), eitherthe citrate or bicarbonate salt should

be used. When hypokalemia is associ-ated with depleted body stores orchronic K4 wasting states, K4 supple-mentation may be needed for weeks




even pulmonary edema.

Pediatrics in Review Vol. /7 No. /1 November /996 401

at doses of 3 to 5 mEq/kg per day.

Therapy for Bartter syndromeincludes prostaglandin synthetase

inhibitors, KC1, and a potassium-

sparing diuretic.

Hyperkalemia


The most common cause of hyper-

kalemia (serum K4 concentration>5.5 mEq/L) in infants and children

is “pseudohyperkalemia” from

hemolysis of the blood sample, which

warrants repeating the determination

in a free-flowing venous samplewhen this is suspected. Children may

display hyperkalemia in disordersresulting from or accompanied by

transcellular shifts, as occur in meta-bolic acidosis or tissue catabolism, or

in disorders of decreased urinary

excretion, such as acute or chronic

renal failure, volume depletion, orhypoaldosteronism. In salt-losing

congenital adrenal hyperplasia due to

complete deficiency of the enzyme21-hydroxylase, the symptoms in

affected male infants appear in thefirst weeks of life and include dehy-dration and failure to thrive togetherwith low serum Na4 and high K4 con-

centrations. Affected female infants

usually are diagnosed at birth beforeelectrolyte abnormalities develop

because of ambiguity of the externalgenitalia. Finally, certain diuretic

medications, such as angiotensin-

converting enzyme inhibitors and

non-steroidal anti-inflammatory

agents may induce hyperkalemia.

DIAGNOSIS

Manifestations of hyperkalemia

include cardiac arrhythmias, pares-thesias, muscle weakness, or paraly-

sis. As with hypokalemia, the electro-cardiogram is helpful in diagnosis;narrow, peaked T waves and short-

ened QT intervals are observed at K4concentrations >6 mEq/L and

depressed ST segment and widenedQRS complex at K4 concentrations

>8 mEq/L.

MANAGEMENT

Patients should have close cardiac

monitoring. The fastest way to antag-

onize potentially life-threateninghyperkalemia is to administer intra-

venous calcium. The onset of actionis rapid and the duration is less than

30 minutes. Emergent measures tocause K4 to redistribute to the intra-

cellular space include the administra-tion of NaHCO3 or glucose andinsulin. Thereafter, ion exchange

resins, such as sodium polystyrene

sulfonate (Kayexalate#{174}), are used

either orally or as a retention enema.

Finally, severe hyperkalemia may betreated with hemodialysis, which is the

most effective way to remove K4,yielding quicker results than peritonealdialysis.

Acid-Base DisordersThe pH of the body fluids normally is

between 7.35 and 7.45. When the pH is

brought outside this range by a primary

disturbance, it is restored toward nor-mal by one of the two major homeosta-

tic mechanisms that buffer pH changes.

These two buffering mechanisms usethe lung and the kidney, which modify

the ratio of the partial pressure of CO2(Pco2) to the concentration of HCO3.In plasma, the carbonic acid-bicarbon-

ate system governs both Pco2 and

HCO3:

H20 + C0244 H,C03 +-* H� + HC03

This relationship is described by the

Henderson-Hasselback equation:

pH = 6. 1 4 log [HCO3i/[H2C03]

where 6.1 is the negative logarithm of

the dissociation constant of carbonic

acid; the concentration of H2C03 fre-quently is expressed as the partial pres-

sure of CO2 (normal, 35 to 45 mm Hg).Acid-base homeostasis uses buffers

that absorb excess H� ions. The firstmechanism by which the pH is main-tained includes both extracellular

buffers, such as the bicarbonate/carbon-ic acid system and the serum proteins,

and intracellular buffers, such as pro-teins, phosphates, and hemoglobin. The

second mechanism for maintaining pHis alveolar regulation of the Pco2.Having a normal Pco2 or a normal con-

centration of HCO3 does not imply a

normal pH; thus, to evaluate acid-base

disorders, a concomitant arterial (orvenous) blood gas and electrolyte

chemistry panel are required. It isimportant to remember that infants nor-mally maintain a slightly lower HCO1concentration (21 .5 to 23.5 mEq/L)than adults (23 to 25 mEqfL). Acid-base disturbances can result from alter-

ations in either Pco2 or HCO3 due tochanges in acid production, acid buffer-

ing, and acid excretion. A deviation inHCO3 causes a metabolic alkalosis oracidosis; a deviation in Pco, causes a

respiratory alkalosis or acidosis.

Metabolic AcidosisAcidosis results from the addition ofacid or the removal of alkali frombody fluids, and it evokes a compen-

satory response consisting of in-creased alveolar ventilation (respira-tory alkalosis) and a fall in Pco2. Thisadaptation, hyperpnea (defined as

deep, pauseless respirations), doesnot lead to complete normalization ofpH, but it occurs rapidly, beginningwithin minutes. The clinical manifes-

tations of acidosis include depressedmyocardial contractility, arrhythmias,

arteriolar dilatation, hypotension, and

DIAGNOSIS

A fixed acid (HA) added to the extra-cellular fluid will be buffered in large

part by HCO3:

HA + NaHCO3 �-* NaA + H,CO3#�H,O + CO2

The formation of the sodium salt

implies loss of HCO3 and formationof anions unmeasured in the routinelaboratory determination that include

proteins, phosphates, sulfates, and

organic anions. These unmeasuredanions are referred to as the anion

gap, which can be estimated indirect-

ly as:

Anion gap = Na� - (C� + HC01)

= lO-l2mEq/L

The anion gap is kept steady by renalexcretion of the constantly producedunmeasured anions, but this steadystate is disturbed if large amounts ofacid are added exogenously or pro-duced endogenously. Thus, for everymole of titratable acid, the concentra-



402 Pediatrics in Review Vol. 17 No. 1/ November /9%


tion of HCO3 falls by 1 mole. Theanion gap can be either increased or

normal in acidosis. Acidoses with a

normal anion gap (hyperchloremia)result from either renal or gastroin-testinal loss of HC03. The acidoseswith an increased anion gap include

diabetic ketoacidosis (DKA), lactic

acidosis, toxin ingestions (salicylates,

ethylene glycol), and uremia. Of note,

a decreased anion gap may occurwithout the presence of acidosis inconditions accompanied by hypoalbu-minemia, hyperkalemia, hypercal-

cemia, or laboratory errors.

DIFFERENTIAL DIAGNOSISNormal Anion Gap (Hyperchloremic)Acidosis

When HC03 is lost from the body,

either through the gastrointestinaltract or the kidney, Cl is the only

other anion readily available to helpmaintain fluid volume. Dispropor-

tionately increased Cl absorption,along with Na4, compensates for theloss of HCO3, causing hyper-

chloremia and leaving the anion gapunchanged. Diarrheal fluid, which in

infants and children commonly is

high in HC03, is high in K4 and lowin Cl. In addition, ECF contraction

from diarrhea results in hyper-

chloremia because the remaining C1is confined to a smaller volume of

distribution. Thus, diarrhea causeshypokalemia and hyperchloremicacidosis. Failure to excrete acid

occurs in mild chronic renal insuffi-ciency and RTA. RTA is a group oftubular transport disorders thatincludes three primary types summa-

rized below.

In type I or distal RTA, which is

caused by impaired distal H4 secre-tion, urine pH is greater than 6. The

defective H4 secretion causes renalHCO3 wasting, especially during

periods of rapid growth when largeamounts of HCO3 are required tobuffer endogenously generated acid.

In type 2 or proximal RTA, urinepH also is greater than 6 because

there is a failure to reabsorb HC03.K4 loss also is common, leading tohypokalemia. Type 2 RTA may be an

isolated finding but more frequentlyoccurs as part of the Fanconi syn-

drome, which also includes urinaryproximal tubule loss of glucose, cal-cium, phosphate, amino acids, sodi-

um, potassium, uric acid, and otherorganic acids. Failure to thrive is aprominent clinical feature of type 2RTA.

Type 4 RTA in pediatrics com-

monly results from a variety of con-ditions with a lack of or resistance toaldosterone causing impaired K4 and

H4 secretion. Findings includeincreased plasma renin activity,hyponatremia and hyperkalemia, andvolume depletion.

Increased Anion Gap Acidosis

Common causes include DKA, lacticacidosis, ingestion of toxins, and

renal failure. In DKA, the overpro-duction and underutilization of beta-hydroxybutyric acid and acetoaceticacid cause a metabolic acidosis,

which is characterized by a low plas-ma HCO3 concentration andincreased concentration of the anions

of these acids. Lactic acidosis mayoccur in the setting of sepsis andhypovolemic or hypotensive shock.In addition, lactic acidosis may result

from certain inborn errors of carbo-

hydrate or amino acid metabolism.Within the category of toxin inges-

tion in children, salicylate overdoseis not infrequent. The initial responseis a respiratory alkalosis followed by

ketosis, lactic acidosis, and loss of

HCO3, which is used to buffer thesalicylic acid. Vomiting may compli-cate the situation further. Younger

children more likely will presentwith metabolic acidosis than respira-

tory alkalosis. Ethylene glycol inges-tion (found in antifreeze or cleaning

solutions) may be dangerous or fatal.In acute or severe chronic renal fail-

ure, metabolic acidosis is commonbecause anions such as phosphate

and sulfate are not excreted, con-tributing to the unmeasured anionconcentration.

TREATMENT

Sodium bicarbonate is the agent of

choice in acute acidosis requiringintervention. No matter what the

cause, bicarbonate should be givenwhen plasma HCO3 is <5 mmol/L.

Bicarbonate should be added to a

hypotonic solution and given as acontinuous infusion over 1 hour. Theamount to infuse may be calculatedby using the following formula:

Amount to infuse in mEq = body weight

in kg (15 - observed [HCO31) x 0.5

In diarrhea, the severity of the aci-dosis varies according to the etiology.

With severe watery diarrhea, the stoolHC03 concentration may reach40 mEq/L, resulting in moderate-to-

severe metabolic acidosis. In additionto volume replacement, which is theprincipal arm of therapy, it may be

necessary to add HC03 to the intra-

venous fluid. Before giving HCO3,

the serum K4 concentration must bedetermined. If it is normal or low,

treatment with HCO3 may induce orworsen hypokalemia and lead to neu-

romuscular complications. It shouldbe emphasized, however, that forpatients who have moderate-to-mildacidosis (HC03 >10 to 15 mEq/L or

pH >7.2), all that is required is to cor-rect the dehydration and electrolyte

losses so the kidney can excrete theexcess H4 ions effectively.

Children who have type 1 RTAneed 5 to 15 mEqfkg per day of sup-plemental alkali. Oral sodium citrateis more palatable than bicarbonatesalt. The maintenance dose is highly

variable and is titrated to normalize

the patient’s plasma HC03 concen-tration. A fixed HC03 loss persists,

even when the serum HC03 concen-

tration is low, so these infants are atrisk for severe acidosis when they

cannot maintain oral alkali supple-mentation. After age 6 years, affected

children exhibit a reduction in urinaryHC03 loss, allowing a reduction inthe dose of alkali. Prior to appropriate

treatment, renal K4 and Ca4 lossesmay occur. Children who have type 2

RTA may require up to 20 mEqlkg ofsupplemental alkali as well as oral

potassium supplements. Childrenwho have type 4 RTA require admin-istration of NaCI and possibly miner-

alocorticoid replacement. Hyperkale-mia responds to restriction of oralintake of K4; low doses (I to 2 mEq/kg per day) of HCO3 may berequired for correction of acidosis.

In DKA, therapy with fluids andinsulin allows for the ketoacids to bemetabolized and for acid to be excret-

ed by the kidneys, thus regeneratingHCO3. Therefore, administration of

bicarbonate is not required for mostpatients who have DKA. Moreover,the potential complications of bicar-bonate therapy include rebound



Pediatrics in Review Vol. 17 No. 11 November 1996 403

hypokalemia, “overshoot” metabolic

alkalosis, hypernatremia, and para-doxic CNS acidosis. However, manyrecommend administering bicarbonate

if the pH is below 7.0.In severe lactic acidosis, the main-

stay of treatment is correction of theunderlying process. However, admin-istration of bicarbonate offsets thenegative inotropic and arrhythmo-

genic effects of acidemia and offers

time to address the principal cause.For patients who have ingested ethyl-ene glycol, therapy includes gastriclavage, charcoal administration, andintravenous ethanol or even immedi-ate dialysis in severe cases.

Metabolic AlkalosisAlkalosis results from a gain of base

or a loss of acid. It leads to tissuehypoxia, CNS changes, and muscularirritability and may cause seizuresand arrhythmias. The common clini-cal manifestations, thus, are lethargy,confusion, and ultimately, neuromus-cular irritability and seizures. Somepatients exhibit diminished respira-tory excursion as the body attempts to

retain CO2.


The causes of metabolic alkalosis fall

into four categories. The first catego-ry includes alkalosis due to alkaliadministration. The second comprisesthe chloride-responsive alkaloses,usually from gastrointestinal acid and

chloride loss; this category includesthe most common cause of hypo-

kalemia in pediatrics, namely, vomit-

ing and/or nasogastric aspiration. Inthese patients, urinary Cl concentra-tion usually is below 20 mEqfL. Thethird group includes chloride-resis-tant alkaloses, such as Cushing syn-

drome, Bartter syndrome, or primaryaldosteronism. The last categoryincludes secondary aldosteronism orother causes of mineralocorticoid

excess and, finally, refeeding follow-ing fasting and in persons who haveanorexia nervosa or bulimia.

TREATMENT

Therapy is centered on identifyingand treating the underlying pathology.In mild-to-moderate alkalosis, provi-sion of Cr will allow the kidney to

excrete the excess base. In severe

alkalosis, hydrochloric acid adminis-tration may be necessary. Alternative

choices for therapy are ammoniumchloride or arginine monohydrochlo-ride, although these are contraindi-

cated in hepatic and renal disease,respectively. In obstructive vomitingor nasogastric aspiration, the loss ofacid may be offset by providing an

adequate supply of chloride salt, 1 to2 mEq/kg per day. Such patients often

have a deficit of potassium, whichshould be corrected. In hyperaldos-

teronism, an antagonist such asspironolactone will correct the hyper-

tension and the hypokalemia andrestore a normal acid-base status.

Amiloride may be equally effective.

Hypokalemia and alkalosis areobserved in Bartter syndrome, which

is characterized by hyperreninemichyperaldosteronism and hypersecre-tion of renal prostaglandins. These

may respond to indomethacin, butadditional KC1 may be needed. InCushing syndrome, therapy is direct-ed at the underlying process.

Respiratory Acidosis

Respiratory acidosis is induced by an

increase in Pco2, which lowers plas-ma pH rapidly. Causes include airwayobstruction, anatomic abnormalitiesthat compromise the movement of thethoracic cage, CNS depression orimmaturity, and neuromuscular

defects. Hypercapnea per se is notnearly as detrimental as the hypox-

emia that usually accompanies thesedisorders. However, patients whohave the Pickwickian syndrome(massive obesity, ineffectual respira-tory exchange) may exhibit somno-lence, hypertension, and even retinal

edema as a consequence of hypercap-nea. Intervention is required to cor-rect or compensate for the underlyingcausal process; alkali administrationis not indicated in the setting of purerespiratory acidosis.

Respiratory AlkalosisRespiratory alkalosis is caused by adecrease in PCO2, the result of hyper-ventilation. Acute respiratory alkalo-

sis from hyperventilation inducesdizziness, confusion, and rarely,seizures. These signs and symptoms


result from acutely decreased cerebral

blood flow, which is less prominentin chronic respiratory alkalosis. Thecauses of respiratory alkalosis include

those that can lead to hyperventila-tion, various CNS disorders, and psy-

chobehavioral disturbances . Inter-vention is directed toward correcting

the underlying causal process. Inacute hyperventilation, rebreathinginto a bag will decrease the severityof symptoms.

ConclusionIn our experience, as many mistakesare made by improper monitoring ofthe patient as in the initial diagnosis.

Patients differ widely both in symp-

toms and signs and in their responsesto treatment. Hence, the physician,

after making a presumptive diagnosisand deciding on a course of therapy,must monitor the patient’s responsecarefully. In this way, mistakes injudgment can be recognized promptlyand appropriate corrections made in

the treatment regime.

REFERENCESI . Altemeier WA. A pediatrician’s view: any-

one for a game of bridge. Pediatr Ann.

1995;24:10-11

2. Hellerstein S. fluids and electrolytes: physi-

ology. Pediatrics in Review l993;14:70-79

3. Avner ED. Clinical disorders of water

metabolism: hyponatremia and hyperna-

tremia. Pediatr Ann. 1995;24:23-30

SUGGESTED READINGCasteels HB, Fiedorek SC. Oral rehydration

therapy. Pediatr CliiiNorth Am. l990;37:

295-3 11

Finberg L, Kravath RE, Fleischman S. Water

and Electrolytes in Pediatrics: Physiology,

Pathophysiology, and Treatment. 2nd ed.

Philadelphia, Penn: WB Saunders Company;

1993

Haber Ri. A practical approach to acid-base dis-

orders. West JMed. l991;155:l46-151

Hellerstein S. Fluids and electrolytes: physiolo-gy. Pediatrics in Review. l993;14:70-79

Zelikovic I. Renal tubular acidosis. PediatrAnn.

1995;24:48-54



DOI: 10.1542/pir.17-11-3951996;17;395Pediatrics in Review

Nicholas Jospe and Gilbert ForbesClinical Aspects−−BACK TO BASICS: Fluids and Electrolytes

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