Pediatrics in Review 1981 Finberg 113-20-2

EDUCATIONAL OBJECTIVES

66. Appropriate knowledge of theimmediate management of the in-fant with hypertonic dehydration(81/82).67. Appropriate knowledge of theimmediate management of hypo-natremic dehydration (81/82).68. Appropriate familiarity withmanagement of maintenance fluidand electrolyte administration forthe pediatric patient (81/82).

#{149}Montefiore Hospital and Medical Center,Bronx, New York.

pediatrics in review vol. 3 no. 4 october 1981 PIR 113

Treatment of Dehydration in InfancyLaurence Finberg, MD*

NORMAL CHEMICAL ANATOMYAND PHYSIOLOGY

Before discussing dehydration itis worthwhile to review the normalfeatures of an infant with respect tocontent and distribution of water andmineral. Approximately 70% of thelean body mass is water. The distri-bution of this water is shown in Fig1 . The plasma volume owes its integ-rity to its protein content, which is arelatively impermeable species ofmolecule. The extracellular fluidcomposition differs strikingly fromthe intracellular fluid despite themovement of most ions across cellmembranes because of an activetransport system (N&, K, ATPase)in the membrane that extrudes so-dium. The compositional differencesare diagrammed in Fig 2.

The second consideration neces-sary to handle any problem is that ofobligatory water requirements to re-place losses. Table 1 gives the re-lationship between caloric expendi-ture and water loss with the basalstate as the point of reference. Forordinary clinical circumstances re-quirements are about 11/2 timesbasal state. Electrolyte requirementshave a wide range. Practical consid-erations make it necessary to pro-vide solute in an intravenous solu-tion, when one is needed, to preventhemolysis. All conditions may be metby allowing 2 to 3 mEq/kg/day ofboth sodium and potassium. Chlo-ride and bicarbonate (or other base)ions for the healthy infant awaitingsurgery, for example, should be di-vided about 3:1. In disease statesappropriate modification may bemade.

In this brief presentation the treat-ment plans are developed aroundparenteral therapy. In many situa-tions, eg, diarrheal disease, oralfluid will be equally satisfactory if thepatient is able to drink. The readershould be able to adapt the princi-ples to an oral route of administra-tion whenever it is appropriate. Here

we have assumed severe dehydra-tion that requires at least initial par-enteral repair.

CLINICAL EVALUATION OFDEHYDRATION

Dehydration regardless of the eti-ologic factors that produce it is aphysiologic disturbance of clinicalimportance. Proper assessment willlead to appropriate therapy whentreatment is required. In any clinicalevaluation, the tools are the clinicalhistory, the examination of the pa-tient, and a review of laboratorydata. Then should come a sys-tematic analysis of the problem thatresults in a diagnosis of the physio-logic disturbance and suggests thenature of therapeutic intervention, ifany.

In obtaining the history, a numberof points need special stress.Clearly, these are the things thatbear upon the intake of fluid andmineral and on unusual losses ofthese. When it is possible to obtainfrom the history a recent weight ofthe patient, this information mayprove useful as a benchmark. Thepresence of fever, level and durationif possible, is clearly important. Adescription of the patients environ-ment in regard to temperature andhumidity should be at least approxi-mated. Any evidence of infection,local or systemic, is also of impor-tance because of the influence ofinfection on catabolism as well asthe implications of an infection forphysiologic change.

Intensive questioning should becentered on the site of fluid loss andon the type and amount of loss.Since most fluid losses are from thegastrointestinal tract, this is usuallythe focus but it should be pointedout that fluid loss can occur into atissue or through the urine as well.

The symptoms of anorexia andvomiting are of special importancein infancy because a high oral intakeof liquid is essential to life proc-esses, especially during a catabolicstate. Indeed, the advent of vomitingin an infant with diarrhea is whatusually precipitates admission to the

hospital since under most circum-stances this symptom ends the abil-ity of the family to care for the baby.

In examining an infant for dehy-dration, the most important singledetermination is the patients weight.This measurement should always beobtained with great care and preci-sion. If the patient is lethargic, it isimportant also to determine whetherirritability is present both withoutstimulus and when such stimuli assound, light, and touch are applied.Unusual body movements or convul-sive twitchings should be noted, andone should ascertain whether thereare tears.

The skin provides many clues tothe state of hydration. This is partic-ularly true in infancy up to the ages1 to 2 years. In older children, ex-amination of the skin is less usefulin determining the state of hydration.Two signs of special importance arechanges in elasticity and in turgor.When the abdominal skin in normalinfants is pinched, it will snap backpromptly on release. When dehydra-tion has progressed to a seriouspoint, pinched skin will remainstanding in folds because elasticityhas been lost. This sign may also beseen, however, in serious under-nu-trition without dehydration. The na-ture of the subcutaneous tissue isdifferent in older children and adults,and this loss of elasticity will not beelicited when they are dehydrated.The presence of turgor is a sign ofcirculatory adequacy. One exam-

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INTERSTITIALFLUID19%LBM SKI

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ICE45% LBM

TRANSCELLULAR*ATER I%LBM

NON-AQUEOUSTISSUE 28% LBM :

LEANBODYMASS(FATFREE)OFINFANT

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INTERSTITIALFLUID

Fig 2. Ionic profiles of body fluids. Composition of the three physiologically importantcompartments is shown with separating barrier indicated. Concentrations (mEq/liter) areshown and left hand scale (mOsm/kg) emphasizes nonidentity of these measures except forunivalent unbound ions. Shaded areas indicate low or absent osmotic activity because of largemolecule size or because of binding of ion to large molecule. Protein and amino acids haveimportant osmolal contribution, even in low concentration because of relative impermeability.ECF, Extracellular fluid; ICF, intracellular fluid.

TABLE 1 . Basal Caloric Expenditure for Infants and Children

A geWeight

(kg)Surface Area

(sq m)Calories

(/kg)Newborn 2.5-4 0.2-0.23 501 wk to 6 mo 3-8 0.2-0.35 65-706tol2mo 8-12 0.35-0.45 50-6012 to 24 mo 10-15 0.45-0.55 45-502 to 5 yr 1 5-20 0.6-0.7 456toloyr 20-35 0.7-1.1 40-4511 to 15 yr 35-60 1.5-1.7 25-40Adult 70 1 .75 15-20

* Water expenditure equals 1 mI/calorie.

Fluids and Electrolytes

PIR 1 1 4 pediatrics in review #{149} vol. 3 no. 4 october 1981

-ALIMENTARYTRACTTC*#{149}l%LBM

I

Fig 1. Diagram of normal distribution ofbody water in lean body mass (LBM). Adiposetissue is not associated with significant water.Arrows indicate flows of water and ions.Transcellular water (TCW) includes waterwithin intestines (out of scale on diagram, butpotentially much greater than normal). OtherTcw is water sequestered tightly in tissuesand not rapidly involved in acute bodychanges. ECF, Extracellular fluid; ICF, intra-cellular fluid.

ines for it by pinching the skin andsqueezing out the blood from thepinched area and thereby causing acolor change. In the healthy patient,the color returns almost instantane-ously upon release. Slowness in thereturn of color denotes a loss ofturgor. Very slow return in the ab-sence of a local skin problem (oredema) indicates shock.

Pulse rate and pressure are mostimportant determinations sincetachycardia is the first manifestation

of dehydration. The examination ofthe muscle tone including checkingfor nuchal rigidity and testing thedeep tendon reflexes is a helpfulassessment as will be discussed be-low. Auscultation of the heart andlungs gives information on the qual-ity of the heart sounds and confirmsobservations with respect to the rateand depth of breathing.

Routine laboratory studies in de-hydration should include a hemato-crit and a urinalysis. In addition to

these routine studies, in a dehy-drated patient blood should bedrawn for analysis (as a minimum) ofthe urea nitrogen level and the elec-trolytes (sodium, potassium, chlo-ride, and bicarbonate). If a more ex-tensive analysis is desired, bloodgases plus calcium, phosphorus,magnesium, glucose, and albuminshould be measured. Most patientsdo not require such an extensivework-up. For complicated or unusualcases, however, such studies canbe quite valuable.

Having obtained the data basefrom history, examination, and pre-liminary laboratory data, the nextstep is a systematic analysis of fivecardinal clinical points. Each shouldbe reviewed in assessing the pa-tients status although in the mostseverely ill patients, one may initiallyhave to forgo laboratory informationaltogether because of the urgencyof the patients condition. The fiveclinical points are: (1) volume, (2)osmolality, (3) hydrogen ion status,(4) intracellular ions, and (5) skeletal


DEHYDRATION

pediatrics in review vol. 3 no. 4 october 1981 PLR 115

ions. Each of these will be discussedin detail enabling the physician todefine the degree of dehydration,the distortion of body water distri-bution, and the metabolic disturb-ances arising from effects upon hy-drogen, potassium, and calciumions. The first two points of assess-ment are more important than thelast three if the patient has poten-tially adequate renal and pulmonaryfunction. The homeostatic mecha-nisms of kidneys and lungs will cor-rect the metabolic disturbances ifthe volume and space disturbancesare quickly and appropriately cor-rected. Patients with impaired renalor pulmonary function will requirecareful attention to all five points ofassessment.

When going through these as-sessments, one should determinewhether an emergency state exists.The dehydration may be classifiedinto hypernatremic, isonatremic, orhyponatremic states. Finally, themetabolic disturbances includingthose of hydrogen ion should beevaluated.

1. Volume

The therapist has three consider-ations with respect to volume. Thefirst of these is to assess the degreeof deficit. This, of course, is achange in composition and can beexpressed as in milliliters per kilo-gram of body weight or as a per-centage of weight loss. In jargon,this is often designated as 5% or10% dehydration, by which ismeant 5% or 10% body weight loss.The least objectively detectable def-icit is approximately 50 mI/kg (5%acute weight loss). Elevated pulserate and diminished pulse pressure,diminution of output of tears andurine, may be the only manifesta-tions. When a deficit of approxi-mately 100 mI/kg exists, a constel-lation of clinical signs is usually pres-ent. These include depressed fon-tanelle in infants and sunken eye-balls in patients at any age, loss ofelasticity and of turgor of the skin,and other evidences of circulatorydeficit which include coolness andacrocyanosis or mottling of the skinof the extremities, feeble hearttones, and a weak, rapid pulse. The

brachial blood pressure is usuallymaintained. At this point the patientis in medical shock from the loss ofextracellular fluid. Between theabove two landmarks, one can inter-polate-but not with precision-in-termediate degrees of deficit. Whenthe deficit over a short period of timeapproaches 1 5% of the body weight,blood pressure drops and a mori-bund state ensues.

The basis for estimating the vol-ume of deficit has been the dehy-drated weight rather than calculatingthe hydrated weight and using it.This error is compensated for inthe clinical calculations by also ig-noring the water of oxidation pro-duced by the patient in each timeperiod, an error in the opposite di-rection. The net result of these twoomissions is that they cancel oneanother for most patients when ther-apy is for a short time period-a dayor two.

The volume of fluid estimated asthe deficit should be thought of asprimarily deficit from extracellularfluid. Therefore, it is a fluid with asodium concentration of about 150mEq/liter, chloride 1 1 5-1 20 mEq/liter, and bicarbonate or other baseof 25 to 30 mEq/liter. After consid-ering the next several analysispoints, these estimates may be mod-ified.

While assessing the deficit it isalso appropriate to consider the vol-ume needs of the patient to replaceongoing obligatory losses. This fluidvolume assessment is sometimes re-ferred to as maintenance fluid. Oneassesses the metabolic state of thepatient to estimate these ongoinglosses. At basal conditions there isan age- or size-dependent caloricexpenditure which in turn deter-mines water expenditure. Deviationsfrom the basal state include bodytemperature changes, ventilationchanges, and changes from muscu-lar movement. At average clinicalconditions of normal body tempera-ture ( 1 C) a slight increase in ven-tilation and with normal movement inbed, the caloric and water expendi-ture are about 1#{189}times the basalamount. On an experimental basisrather precise increments for any ofthe abnormalities described can bedefined, but this is not practical din-

ically nor does it prove to be evenadvisable to attempt such detailedcalculation. A margin of safety of10% has proven clinically safe;this makes meticulous precision un-necessary. A marked increase inany one of the three important van-ables will move the ongoing obliga-tony losses to approximately doublebasal state. Should all three be in-creased, that is, high fever, hypen-ventilation , and continued convul-sive movements, the effect would beto triple the basal expenditure. Fromthese guideposts, reasonable esti-mates may be readily made by theclinician. The water estimates hereare free of electrolyte. Table 1 givesbasal energy expenditure data forinfants.

A final concern with respect tovolume is related to continued ab-normal losses. In a few diseases,such as Asiatic cholera, these canbe estimated from empirical data,but for most of the etiologies causingdiannheal disease on other problems,the abnormal losses will have to beascertained by continuing direct ob-servation of the patient.

2. Osmolality

The term as used here is a one-word shorthand way of saying thatwhats being assessed is a disturb-ance of the distribution of water inthe body spaces. The principal em-phasis at this point in the analysis isto determine whether the patient is:hyponatnemic, with a relative pre-pondenance of water in the cells atthe expense of extracellular fluid;isonatnemic with a proportionateconstriction of body fluids; on hypen-natremic, with relative cellular des-sication, the displaced water beingfound in the extracellular space.

The history is helpful in makingthese distinctions. If purging hasprogressed for a number of days,sodium losses will be high, particu-larly if no sodium intake has oc-curred during this period. In fact, ifrelatively mineral-free water hasbeen offered by any route, a hypo-natnemic state will result. If the pa-tient has maifltained regular food in-take followed by an abrupt cessationof intake with on without vomiting,then water losses will tend to pre-


* Associated history and signs encountered with differing physiologic disturbances when 100 mI/kg rapid weight losthas occurred secondary to diarrheal disease. These cumulative descriptions are clinically probable stereotypes;exceptions may be seen though usually a cluster of these findings will prove an accurate predictor. No one attribute orsign is specific; moreover, the disease process may change the disturbance from one part of the illness to another asmay partial therapy. The manifestations listed may be either the cause of or the result of the physiologic disturbance.


PIR 1 1 6 pediatrics in review #{149} vol. 3 no. 4 october 1981

TABLE 2. Clinical P rofiles of Physiologic Distu rbances in Dehydration*

CharacteristicsOsmolal State

Isonatremic Hyponatremic HypernatremicAge Any Any Often under 1 yr of age (any pos-

sible)Time of year Any Any, more in summer Most in winter months, especially

when humidity is very low insideFever and other Variable Variable, minimal nespina- High grade fever common; respi-

evidences of in- tory involvement usual ratory symptoms common withfectious etiology increased ventilatory rate

Anorexia Late in course of ill-ness

Minimal, good oral intakeof wated maintained

Marked early in illness

Vomiting Late manifestation Late or absent Early, may be coffee groundDiarrhea Moderate through-

outLong duration (3 or more

days)Variable

State of con- Normal May be obtunded Disturbedsciousness

Lethargy Variable Common Usual and markedHypenirnitability Unusual Unusual Marked to tactile, sound, and light

stimuliMuscle tone Normal Normal or weak Increased; nuchal stiffness some-

times present; muscle twitch-occasionally seen

Skin elasticity Poor Very poor Normal; skin may have a velvetyor uncommonly a doughyfeel

Skin turgor Diminished Poor GoodPulse rate Increased beyond

that caused byfever

Markedly increased Lroportionate to fever

Blood pressure Maintained orslightly low

Reduced, borderline ofcirculatory failure

Normal

Hyperpnea Variable Often, but variable Variable, sometimes marked andcontributory to water loss

dominate and hypennatnemia will ne-suIt. The presence of any factor thatpredisposes to insensible waterloss, high ambient temperature, lowhumidity, fever-especially high fe-yen, and hyperventilation all predis-pose to hypernatremia.

On examination deficient circula-tion points to loss of extracellularfluid. If the circulation is not severelyimpaired but there are signs refera-ble to the nervous system, particu-larly the identifiable combination oflethargy unstimulated and hypenirnit-ability to virtually any stimulus, a hy-pernatremic state should be sus-pected. Hypernatremic patients, in-stead of losing dermal elasticity inthe usual fashion, often have adoughy feel to their abdominal skin.

Even more commonly the skin willhave a somewhat velvety feel whichwe have found more reliable as anindicator of hypernatremia than themore traditionally described doughyfeeling. In hypernatremic states,there will be increased muscle toneoften including mild nuchal rigiditywhich is occasionally mistaken forthe nuchal rigidity of meningitis.

The definitive measurement forthis assessment is the level of so-dium in the serum. This is a bettermeasurement than the osmolalityper se because some substancesthat affect osmolality, eg, urea, donot influence body water distribu-tion.

This assessment point permits as-signment of a sodium concentration

to the deficit portion of the repairsolution. For most patients, thosewith isonatnemic dehydration, thiswill be 1 40 to 1 55 mEq/Iiter. Moresodium should be given if hyponatre-mia is diagnosed and less if hyper-natremia is present. Table 2 listsclinical associations frequentlylinked to different osmolan disturb-ances, whether as a cause, or aresult or even both.

3. Hydrogen Ion Disturbance

The history is helpful in detectinghydrogen ion disturbance. In infancyunless there has been vomiting withhigh obstruction, almost all disturb-ances produce acidosis and thenacidemia. Diarrhea is particularly


DEHYDRATION

pediatrics in review vol. 3 no. 4 october 1981 PIR 117

prone to cause this type of disturb-ance. The degree of acidosis or aci-demia is not easily gauged withoutlaboratory data. Hyperpnea is evi-dence of a compensatory phenom-ena and suggests acidosis. Thepresence of ketones in the urine issimilarly helpful. It should be remem-bered, however, that this latter lab-oratory change does not appear ininfants less than the age of 5 monthsfrom either starvation, or dehydra-tion, or both. Ketonunia in infantsless than 5 months old usually is asign of metabolic disease such asdiabetes or one of the aminoacido-pathies.

Measurement of the bicarbonateion or the complete blood gas bat-tery gives quantitative dimensions tothis disturbance. Although therapycould and sometimes should takehydrogen ion disturbance into ad-count, it should be remembered thatadequate attention to volume andcorrection of maldistnibution of waterwill usually enable the kidney andlung to do this task quite satisfacto-rily. During therapy the ions selectedshould either be chosen to be slowlycorrective or at least not to worsenthe disturbance. Remember the nor-mal pH of plasma and extracellularfluid is alkaline not neutral; there-fore, some base is usually properlyincluded even in maintenance so-lution.

4. Intracellular Ion Losses

Whereas intracellular ion lossesinclude potassium, magnesium, andphosphate, from a clearly clinicalpoint of view it is usually only thepotassium loss that is important.Whenever there are losses of gas-trointestinal secretions, significantpotassium losses are likely to occur.The extent of these losses is knownfrom empirical data rather than fromany easy method of either estimatingor measuring with the current clini-cal laboratory. When the patient hashad longstanding diarrhea or vomit-ing, the potassium losses will belarge. If there has been polyunia, po-tassium losses will be predictablylarge as well. Measurement of potas-sium level in the serum may be de-ceptive because any diminution inthe glomerular filtration will cause

the potassium level to rise evenwhen the total body potassium islow. A high bicarbonate and a lowchloride level in serum suggest po-tassium deficit. This is true in relativeas well as absolute terms so that theexperienced clinician is occasionallygiven a clue by what seems an in-appropriate ratio of bicarbonate tochloride. The electrocardiogram un-fortunately reflects only the extra-cellular value of potassium and soadds no quantitative information.Phosphate and magnesium levelsare only occasionally of clinical im-portance in states of dehydration.

The important clinical principle isthat potassium must be provided toreplace tissue losses from diseaseand losses produced by the antici-pated high urine output during then-apy.

5. Skeletal Ions

Although phosphate and magne-sium may be included here as well,it is really the calcium ion that is ofimportance. Infants in the first weekor two of life frequently have im-paired calcium homeostasis so thatsuperimposed dehydration may tipthem to hypocalcemia. Hyperna-tremic states frequently producemild hypocalcemia; uncommonlythey may produce significant hypo-calcemia. Other factors that may dothis include high phosphate levels(often because of renal insuffi-ciency) and alkalemia, which is un-usual. Relative alkalemia, however,can be produced by treatment ofacidemia or acidosis, and rapid hy-dration may also produce a dilutionalstate. Either of these may predis-pose to hypocalcemia though notcommonly. In summary, the neonatalperiod and hypernatremic states arethe factors of most importance indisturbances of calcium ion duringdehydration.

IMPLEMENTATION INISONATREMIC ANDHYPONATREMIC DEHYDRATION

The clinical analyses just reviewedenables one to know both qualita-tively and quantitatively the amountof fluid required for repair and forother needs during an ensuing time

which will arbitrarily be one day. Be-fore implementation this informationmust be translated into a plan for therate of administration and for decid-ing whether each of the componentsis to be spread over the day orwhether there are times for specialemphasis for a given element of then-apy. Therapy in the first 24 hours inpatients with either isotonic constnic-tion of body fluids (isonatremia) orthose requiring slight modificationbecause of a hyponatremic state willbe considered here.

It is useful to divide therapy intophases, each with its own time seg-ment within the 24 hours. The daymay be divided into three segments:emergency, repletion, and early re-covery. When water is lost from thebody through the gastrointestinaltract, the loss ultimately involves allof the body compartments to somedegree. It follows then that watergiven during treatment must wind upin the various body compartmentsas well.

The emergency phase, then, hasas its emphasis replacement ofplasma volume. Most of the waterloss in isonatremic dehydration isfrom the extracellular fluid. Asidefrom the plasma, the other compo-nent of this water is the interstitialfluid which serves as the transportmedium for virtually all substancesactive in bodily functions. This spaceneeds early repletion, the secondphase, so that metabolic processesmay proceed normally. Finally, wa-ten and salts from cells, intracellularfluid, will need replacement to en-sure proper cellular function. Thethree body spaces indicated thenroughly correspond to the emphasisplaced during each of the threephases of therapy.

First, from the clinical assessmentscheme, the volume of fluid neededto repair the deficit may be estimatedas the amount required to recoverobligatory ongoing losses. Empiricaldata have indicated that it is appro-priate to give this combined volumeof fluid to the usual dehydrated pa-tient within the first 24 hours. Thusthere is a tentative volume to use inplanning therapy to which may beadded any continuing abnormallosses. From the earlier considera-tion of the pathogenesis of dehydna-



PIR 118 pediatrics in review #{149} vol. 3 no. 4 october 1981

tion it is also known how much so-dium to give during the first day anda qualitative concept of the amountof base and of potassium and cal-cium. It remains now to quantitatespecifically each ofthe elements andto divide up the administration in theseveral phases.

Emergency

An emergency phase is to be im-plemented only if there is significantcirculatory deficit. If such is not pres-ent, the emergency phase is repne-sented only by a more rapid rate ofinitial infusion during the repletionphase on it may even be omittedwhen no circulatory manifestationsof any sort are detectable; eg, notachycardia. The emphasis for theemergency phase is restoration ofthe plasma volume. The simplestway to do this is to infuse a fluid thatcontains either protein on other sub-stances that will have the same on-cotic properties as plasma albumin.Thus, single donor plasma on a so-lution of 5% albumin or any otheranalogous fluid is ideal. The volumeof water in this infusion will, at leastfor an appreciable ieniod of time,remain intravascular and accom-plish the intended goal. Empirically,it was learned long ago that one caninfuse 20 mI/kg of plasma on 5%albumin to a dehydrated patientwithout risk of clinical consequencefrom overexpansion of the plasmavolume. This then has become onestandard way to implement theemergency phase. Subsequently, itwas learned that one may also useaqueous solutions for this purposeand avoid the expense and hazardsof protein solutions, yet accomplish-ing the desired goal. In neonates andmalnourished infants, the albuminsolutions are preferred for the emer-gency phase as well as for hypen-natremic patients in shock.

In other patients aqueous solu-tions prove to be equally satisfactoryduring the emergency phase, but thevolume given must be greater toachieve a similar effect on plasmavolume-theoretically four times asmuch. When an aqueous solution isto be used, different authorities haverecommended various solutions. Iprefer the use of solutions contain-

ing glucose to Ringers lactate so-lution though both have been usedsuccessfully. In fact, even when us-ing albumin solutions I immediatelyfollow administration of that solutionwith 10% glucose in water, 20 ml/kg, also very rapidly. These two in-fusions together can usually be ad-complished within one hour, a totalof 40 mI/kg, a volume which is thensubtracted from the proposed totaldays volume to ascertain how muchmore is needed. If an aqueous solu-tion alone is to be given initially, a10% glucose solution to which isadded 75 mEq/Iiter of sodium, 55mEq/Iiten of chloride, and 20 mEq/liter of bicarbonate (on other base) isrecommended. This solution, 40 mI/kg, is administered over approxi-mately the same one-hour interval.Either of these alternatives consti-tutes the emergency phase.

Those who use Ringers lactate or0.9% sodium chloride (so-called normal on physiologic saline)recommend 40 to 50 mI/kg again inapproximately one hour. I prefer hy-pentonic glucose to be used becausethis substance not only providessubstrate for the nutrition of starvingcells but also temporarily pulls ad-ditional water to the extracellulanfluid, even into the vascular fluid,and thus initiates urine formation abit more rapidly.

In assigning the emergency fluid,either to the deficit or maintenanceportion of the allotment, the task isobvious. Simple plasma on albuminsolutions contain sodium and there-fore should be assigned to the deficitfraction. Glucose water without so-dium belongs to the estimated main-tenance portion. A solution with 75mEq/Iiten of sodium is half deficitand half maintenance. If one were touse Ringers lactate on 0.9% salineall of it should be assigned to thedeficit fraction.

Repletion

The duration of the repletionphase, together with the emergencyphase if any, should be one third ofa day on eight hours. The emphasisfor this phase is restoration of theinterstitial fluid. The volume to begiven is such that 50% of the tenta-tively assigned days volume will be

administered within eight hours.During this phase there is no pointin using 1 0% glucose, but rather 5%glucose which serves well as thestock solution. The sodium contentis adjusted according to the esti-mated sodium need and can rangein concentration from 40 to 80 mEq/liter. Assuming that urine formationhas become clinically visible it istime to add panenteral potassium. Asafe concentration that will preventthe clinical effects of potassium de-pletion is 20 mEq/Iiten. Chloride ionand base may be distributed accord-ing to the clinical assessment of thehydrogen ion status of the patient.

Early Recovery

The emphasis in this phase is re-placement of the intracellular fluid.The rate can be slowed and thephase lasts for the remaining twothirds of the day or 1 6 hours. Thecomposition fluid is similar to onidentical with that of the precedingphase. Table 3 shows the foregoingtherapeutic implementation for a pa-tient who is presumed to have a def-icit of 1 00 mI/kg (1 0% of bodyweight) with an isotonic dehydrationand who requires an emergencyphase. An oral glucose-electrolytesolution may be substituted at thispoint for any patient who can acceptit.

THERAPEUTIC MANAGEMENTFOR HYPERNATREMICDEHYDRATION

Because the pathophysiology ofhypennatnemia has distinct featuresseparating this form of dehydrationfrom the more common varieties, theprinciples of therapy must accom-modate the differences. Mild hypo-calcemia occurs in approximately20% of patients. Hyperglycemia, oc-casionally severe, also occurs inperhaps one third of patients. Theplan of therapy must consider thesedisturbances.

Restoration of hydration follows adifferent path when moderate hyper-natremia is present. The objective oftreatment is to replace fluid volume,to restore water distribution, and toconnect the complicating disturb-ances. At first glance therapy seems


TABLE 3. Scheme for First 24 Hours of Rehydration for Isotonic Dehydration of an lnfant*Period 1 Period 2 Period 3 Total

Phase Emergency Repletion Early RecoveryDuration #{189}-ihr 6-7 hr 16 to 18 hours 24 hoursEmphasis for res- Plasma volume Extracellulan fluid Intracellular fluid All compartments

tonationFluid composi- A. Plasma or 5% albu- 5% glucose with Na 5% glucose with Na Na 9 mEq/kg, K 3

tiont mm + 10% glu-cose

B. 1 0% glucose withNa 75, C1 55,HCO3 20 mEq/li-ten

40, K 20, C1 40,and base 20mEq/liter

40, K 20, C1 40to 45, and base1 5 to 20 mEq/Iiter

mEq/kg, Cl 8.5mEq/kg

Amount (mI/kg A. 20 mI/kg of each 60 mI/kg 1 00 mI/kg plus any 200 mI/kgof body solution totaling 40 additional abnormalweight)f mI/kg

B. 40 mI/kglosses

* Estimated deficit = 1 0% of weight(i 00 mI/kg). Estimated ongoing losses = 1 00 mI/kg.t Use either plan A or B in period 1.

mm H2O

150

140

130

#{149}120

20 mI/kg

90 Ijb 2OI J I I I I J

40 60 80 100 120TIME IN MINUTES

:1_g 3 Effect on CSFpressure ofarapid intravenous infusion of 5% glucose in water, 20 ml!

kg. Same pressure increase will occur at any base line CSFpressure. This phenomenon, whensymptomatic, is called water intoxication.

DEHYDRATION

pediatrics in review vol. 3 no. 4 october 1 981 PIR 119

to be the simple replacement of wa-ten. In fact, careful attention to thecontent of solution used and to therate of administration reveal that im-portant special measures must betaken. Two other circumstances alsorequire comment: the presence ofoligunia influences decision making,and finally, salt poisoning should beconsidered as a separate entity.

Most patients with hypennatnemicdehydration are not severely oligunicowing to the relatively expandedplasma volume. This group may thenbe considered first. If one were toinfuse plain 5% glucose water intothese patients, the risk would becerebral swelling-actually waterintoxication. This results from thepresence of endothelial cell tightjunctions in the CNS. Just as rapidinfusion of hypertonic salt results inbrain shrinkage, so does rapid infu-sion of isotonic glucose water causebrain swelling. Glucose rapidlycrosses the blood-CNS barrier byactive transport so that unlike thered cell, the brain does not necog-nize glucose as an osmol, at least atphysiologic levels of glucose, butdoes react to sodium and chlorideions as relatively impermeable be-cause of the tight junctions.

When 5% glucose water is infusedrapidly intravenously the CSF pres-sure rises (Fig 3). The increase inmillimeters of water is the same fora given infused volume and rate ne-gardless of the initial pressure. The

increase in pressure is from swellingof the brain cells, not an increase ininterstitial fluid, ie, not edema. Brainswelling affects a number of nervoussystem functions frequently result-ing in convulsions. For some yearsafter hypernatremic dehydrationwas described and recognized din-

ically, convulsions were commonlyseen during therapy, because rapidwater replacement was attempted.

This circumstance led many cen-tens to suggest adding 75 mEq/literor more of sodium salts to initialtherapy. This will reduce risk of con-vulsions but adds to the sodium bun-


Considerations(in Order)

TABLE 4. Regimen for Therapy of Hypernatremic Dehydration

1. Volume

Action

2. Glucose content

3. Sodium content

4. Potassium con-tent

5. Anion content

a Estimate the patients deficit by clinical meansfirst (mI/kg) and multiply by weight (kg) for to-tal sum.

b. Estimate 48 hr worth of maintenance waterfollowing usual clinical rules.

c. Add a + b for tentative volume of solution for2 days.

Use 2#{189}(2%-3%) to obviate later possible prob-lems with hyperglycemia.

Allow 80-1 00 mEq/liter for deficit fraction of fluidand none for maintenance portion. Resultantconcentration is usually 20-35 mEq/Iiter. Usethis concentration of sodium or simply estimateat 25 mEq/Iiten.

Generally, maximum safe amount for IV infusionon about 40 mEq/Iiter.

Sodium plus potassium advised equals 60-75mEq/liter of cation. Distribute anions betweenchloride and base in accordance with clinicaljudgment. Ifdesired, start with more base andchange to more chloride after 6-12 hr. Do notuse HCO3 as base because of calcium to beadded. Use acetate on lactate along with chlo-

6. Calcium content

7. Rate of adminis-tration

ride.One amplue of 10% calcium gluconate for every

500 ml of infusate.1/48 of volume/hr for 48 hr. In infant, usual volume

will be 275-350 ml/kg/48 hr or 6-7 mI/kg/hr.


PIR 120 pediatrics in review #{149} vol. 3 no. 4 october 1981

den, frequently while excessive in-sensible water losses are in prog-ness, thus aggravating hypennatne-mia. Such therapy also frequentlyproduces visible edema in patients,leading to prolongation of the recov-ery period. An alternative to increas-ing concentration is to slow the rateof infusion which will also avoid con-vulsions, but at risk of being too slowin repairing dehydration, again withsuboptimal outcome.

A compromise resolution to theseproblems can be found, in part, byconsidering that a high potassiumintake would offset cerebral swellingand some of the potassium wouldenter depleted cells (mostly musclecells) carrying water into them. Atthe same time water is delivered tothe patient at a slow even rate. Thisregimen is appropriate provided thepatient has no initial serious circu-latory deficiency. The repair solution

is constructed with consideration ofvolume to be administered for 48hours and of glucose content, so-dium content, potassium content,anion distribution, calcium additive,and rate of administration. Table 4demonstrates a method for analysisof each of these points for use in apatient with hypernatnemic dehydra-tion, but not in shock, and who pro-duces visible urine. Shock, oligunia,and salt poisoning are consideredseparately.

Shock

If the patient has circulatory im-pairment (shock), first infuse 20 mI/kg of 5% albumin solution (singledonor plasma, plasma without im-munoglobulin, on whole blood are allsatisfactory). Sodium content inthese fluids up to 140 mEq/liten isnot important since nearly the whole

volume will remain intravascular. Ifthe patient is producing urine, pro-ceed as in the general manner givenabove.

Anuria

If the patient, even though not inhypotensive shock, has no apparenturine, try a rapid infusion of 5% al-bumin. If urine then enters the blad-den, proceed as before. If no urineenters the bladder, give furosemide,1 mg/kg. If urine flow occurs, pro-ceed as above; if not treat the patientwithout potassium in the infusion.Increase the sodium concentrationto 50 mEq/Iiten, slow the rate byreducing the volume to be adminis-tered, subtracting half the mainte-nance allowance from the 48-hourtotal.

Salt Poisoning

In the event of massive salt poi-soning (plasma concentration of so-dium >200 mEq/liten) use penito-neal dialysis to remove excess so-dium chloride. For the dialyzing so-lution use 8% glucose with no elec-trolyte, 1 00 mI/kg, two on threetimes at approximately one-hour in-tervals. Simultaneously be sure tomaintain an intravenous solution todeliver a volume of repair and main-tenance solution as above. The hy-penglycemia induced by this methodoffsets the removal of sodium andprevents water intoxication. As theglucose is metabolized, water slowlyenters cells.

Insulin is not advisable for any hy-pennatnemic patients with hypergly-cemia because rapid removal of glu-cose by metabolism is the physio-logic equivalent of rapid water infu-sion.

In summary, the best treatmentseems to be a slow infusion relativelylow in both glucose and sodium andhigh in potassium with added cal-cium. For the past 12 years this reg-imen has been highly successful andhas not produced complicating con-vulsions.


DOI: 10.1542/pir.3-4-1131981;3;113Pediatrics in Review

Laurence FinbergTreatment of Dehydration in Infancy

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DOI: 10.1542/pir.3-4-1131981;3;113Pediatrics in Review

Laurence FinbergTreatment of Dehydration in Infancy

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