The Management of Diarrheal Dehydration in Infants Using Parenteral Fluids

Fluid and Electrolyte Therapy

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The Management of Diarrheal Dehydration in Infants Using Parenteral Fluids

Ronald]. Kallen, MD*

It is a truism that an infant is more susceptible to dehydration, as a consequence of diarrhea, than an older child or adult. Although one might think that the higher proportional water content (expressed as a per cent of body weight) of infants tends to act as a buffer against the development of dehydration, this characteristic of infant body fluid composition has little protective value. The single most important factor predisposing to dehydration in infants is the high proportional turnover of body fluid, especially extracellular fluid. The increased susceptibility of infants to severe dehydration is depicted in Figure 1, reproduced from Gamble's classic work. 14 Using a somewhat different model, Kooh and MetcofP7 estimated that the turnover of fluid (daily fluid intake and outgo), as a proportion of extracellular fluid, is twice that of an adult. Except in the instance of a fulminant, secretory form of diarrhea, such as cholera, the development of dehydration is typically an incremental process, spread out over several days. This is the usual case in the most common etiologic form of gastroenteritis in the United States, namely that caused by rotavirus. Signs of dehydration develop when the cumulative effect of negative fluid balance, over several days, begins to exceed 5 per cent of initial body weight. Once dehydration is established, it remains for the physician to decide if rehydration is to be accomplished by oral or parenteral means. This article will focus on a systematic approach to decision making in the management of diarrheal dehydration by means of parenteral fluids, with special emphasis on infants. Hypothetical case simulations will be used to illustrate the principles outlined in the article. (See the Appendix for assessment and management of each case. Before consulting the Appendix, the reader may wish to formulate an assessment and management plan, which may then be compared with that described by the author.)

Case 1 A 3-month-old infant developed frequent, watery diarrhea 4 days before admission to the hospital. This was accompanied by low-grade fever, occasional vomiting, increasing lethargy and irritability, and decreased frequency of urination. *Director, Division of Pediatric Nephrology and Hypertension, Department of Pediatrics, Lutheran General Children's Medical Center, Park Ridge, Illinois

Pediatric Clinics of North America-Vol. 37, No.2, April 1990

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A recent weight, although healthy, was not available. At the time of admission, body weight was 5.3 kg; temperature, 38°C; blood pressure, 65/40; and heart rate, 140 beats per minute. The infant was lethargic and irritable. The anterior fontanel appeared scaphoid while the infant was recumbent. The eyes appeared slightly sunken. The buccal mucosa and tongue were dry. Skin turgor was decreased. A blood sample was drawn, and initial parenteral fluid administration consisted of 100 ml of isotonic saline solution. Shortly thereafter, the infant voided a small amount of dark, yellow urine. A few drops were obtained. Using a refractometer, the specific gravity was 1.030. The urine sediment showed a few hyaline and granular casts. Initial laboratory results were reported about 1 hour after the blood sample was drawn. Sodium, 136 mEq per liter Potassium, 4.9 mEq per liter Chloride, III mEq per liter Blood urea nitrogen (BUN), 31 mg per dl Creatinine, 0.8 mg per dl Venous blood pH, 7.22; pCO" 22 mm Hg; bicarbonate, 10 mEq per liter

Case 2 A 4-month-old male infant was admitted with a 4-day history of frequent watery diarrhea, increasing irritability, fever, and decreasing urination. He had been receiving a homemade oral electrolyte solution of unknown composition. Examination revealed an irritable infant with a blood pressure of 80/50; body weight, 5.4 kg; and temperature, 39°C. Skin turgor was moderately decreased and had a "doughy" feel. Laboratory results were as follows.

ee.

ee.

2000

-

1800 1600 1400

700

r-

500

INFANT, 7 KG.

.

300

z ~

100 oL....l--1---11""""

INFANT, 7 KG.

1200 1000 800

600 400 200

~

STOCl. oL.....J'--L......J"""1...

ADULT, 70 KG.

ADULT, 70 KG.

Figure 1. This figure, reproduced from Gamble's classic syllabus, depicts the higher proportional turnover of extracellular fluid in infants, compared to adults. The daily turnover of extracellular fluid in infants is three to four times greater than that for adults. The separate components of water balance are shown as bar graphs, for a 70-kg adult and a 7-kg infant. (From Gamble JL: Chemical Anatomy, Physiology, and Pathology of Extracellular Fluid. A Lecture Syllabus, Ed 6; Cambridge, Harvard University Press, 1954; with permission.)

DIARRHEAL DEHYDRATION IN INFANTS

267

Serum Sodium, 161 mEq per liter Potassium, 5.5 mEq per liter Chloride, 127 mEq per liter CO2 content, 13 mEq per liter Capillary blood pH, 7.28 Creatinine, 1.1 mg per dl Urine Specific gravity, 1. 028 Negative for blood and protein; sediment unremarkable

Case 3

An 8-month-old male infant was admitted after a 4-day history of fever and profuse, watery diarrhea. During this period, he drank "Hat" carbonated, cola-type beverages, but had little milk or solid food intake. Urine output was not noted for the 12 hours preceding admission. Physical examination disclosed a lethargic, limp infant with cool extremities. Blood pressure, 45/30, was difficult to obtain. The pulse was 160 beats per minute, with weak pulsation. The tongue and buccal mucosa were dry. Respirations were deep. The weight was 7.7 kg. During the examination, the infant had a generalized seizure, which was finally controlled with multiple dosages of diazepam. Serum Sodium, 113 mEq per liter Potassium, 4.8 mEq per liter Chloride, 82 mEq per liter CO2 content, 7 mEq per liter Arterial pH, 7.17 pC0 2 , 19 mm Hg BUN, 56 mg per dl Creatinine, 2.0 mg per dl Urine SpeCific gravity, 1.031 Sodium, 5 mEq per liter Creatinine, 50 mg per dl Sediment, a few hyaline casts

Further specific comments about assessment and management of these cases are in the Appendix.

INDICATIONS FOR PARENTERAL FLUID ADMINISTRATION

During the past decade, oral rehydration therapy has been promoted as an effective therapy for dehydration. Although data suggest that this may be effective in infants with mild dehydration, several indications remain for parenteral Huid therapy (modified from Finbergl l). 1. Evidence of impaired peripheral circulation or overt shock. 2. An infant weighing less than 4.5 kg or less than 3 months of age. 3. Inability to maintain an adequate rate of oral Huid intake, because o intractable vomiting, lethargy, or anatomic anomaly. 4. Failure to gain weight or continued weight loss despite Huid intake. Parenteral rehydration in the ambulatory setting is not widely practiced, but may be feasible and cost-effective.24

INITIAL MANAGEMENT

Intravenous access should be promptly established in any infant with a hint o circulatory compromise. Although hypotension may be indicative of overt shock, an

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apparently normal blood pressure can be maintained in infants with compensated22 shock. Delayed capillary refill time, exceeding 3 seconds, may indicate a precarious circulatory state,13 although scant validation of this test as a reliable sign of perfusion status has occurred. 16, 26 The signs of impending shock include muscular hypotonia, lethargy, mottled appearance, cool skin, and irritability reflecting extreme thirst in infants. An infant with impending shock must be rapidly evaluated and managed as an emergency. Treatment must be initiated without delay, even if laboratory results are not yet available. Urgent volume expansion, up to 20 ml per kg, during 30 to 60 minutes, must be implemented as soon as circulatory access is accomplished, using an isotonic crystalloid or isotonic, iso-oncotic colloid-containing solution (see elsewhere in this issue). Although isotonic "normal" saline is frequently effective for this purpose, it does have the theoretic disadvantage of a nonphysiologic balance of sodium and anion. Because the accompanying anion consists solely of chloride, the attendant "dilution acidosis" may exacerbate a pre-existing metabolic acidosis. This is a consequence of the fact that the infusion of saline further dilutes the extracellular bicarbonate concentration. It is preferable to use a solution that contains a more physiologic distribution of anion-perhaps two thirds of chloride and one third of bicarbonate or lactate. Ringer's lactate solution is a close approximation. Once the infant has attained a stable hemodynamic status, the next phase of management begins with a systematic assessment of the infant and laboratory results. FIVE-POINT ASSESSMENT Before proceeding, it is assumed that a careful history has been taken, with special emphasis on frequency, consistency, and estimated volume of diarrheal stools, the composition and volume of oral intake, presence or absence of fever, frequency of vomiting, a recent body weight, and frequency of urination. All infants with dehydration should be systematically evaluated, following a simple outline (Table 1). The consideration of each of these five points provides a data base of pertinent information as a platform for further management decisions. This kind of assessment is best done by posing a set of five questions. 1. Does a Significant volume deficit exist, and what is the magnitude of that deficit? 2. Does an osmolar disturbance of body fluids exist? 3. Does an acid-base disturbance exist? 4. Does a disturbance of potassium metabolism exist? 5. What is the state of renal function? Although the overall strategy is to arrive at an integrated plan for treatment, each of these points will be considered separately. Does a Volume Deficit Exist? For all practical purposes no laboratory tests enable one to assess severity of dehydration. The term dehydration, used in the context of this discussion, refers Table 1. The Five-Point Assessment of Dehydration POINT OF ASSESSMENT

METHOD

Volume deficit Osmolar disturbance Acid-base disturbance Potassium Renal function

History, physical examination Serum sodium concentration Blood pH, peo 2 , and bicarbonate Serum potassium (?) Blood urea nitrogen, creatinine, urine-specific gravity (or osmolality), urine sediment examination

•

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DIARRHEAL DEHYDRATION IN INFANTS

Table 2. Severity of Dehydration as Per Cent of Preillness Body Weight MILD

(%)

MODERATE

5 4-5

DelF Robson23

(%)

10 6-9

SEVERE

(%)

15 10 or more

to a decrease in the volume of body fluid and should be expressed as a per cent o initial body weight. The term per cent dehydration is often used loosely an computed as a per cent of the body weight on admission. This is conceptuall incorrect because empirically derived data for measured fluid and electrolyte deficit are given in terms of body weight at the time ofrecovery,s which is an approximatio of the preillness weight in infants without an underlying nutritional disorder. I the usual clinical setting, a recent preillness weight is typically not available Therefore, the assessment of volume deficit is critically dependent on a bedside hands-on examination, evaluating the infant for physical signs of dehydration. A useful scheme, summarized in Tables 2 and 3, yields a relatively crude, semiquan titative estimate of extent of dehydration. Although the estimate of severity o dehydration in terms of mild, moderate, and severe lacks real precision and, a indicated in Table 2, minor differences occur in definition, it is useful as a startin point. The aim of this estimate is to arrive at an approximation of the body flui deficit in volumetric terms (in milliliters). This is done by first estimating the initia body weight, in kilograms, based on the clinical assessment of severity of dehydra tion, using the following formula. x body weight, admission

100 100 - per cent estimate dehydration

Nevertheless, a recent study suggests that a clinical estimate of the severity o dehydration, based on physical signs, is inexact and subjective. 's This study foun that resident physicians overestimated the degree of dehydration by a factor of two Moreover, certain "classic" signs used for arriving at an estimate of the severity o dehydration, such as sunken eyes, dry mouth, and absence of tears were not a reliable as observation of decreased peripheral perfusion and skin turgor.

Table 3. Severity of Dehydration Based on History and Examination MILD

Pulse SystoliC blood pressure Urine output Buccal mucosa Anterior fontanel Eyes Skin turgor Skin

MODERATE

SEVERE

Full, normal rate Normal

Rapid Normal, low

Rapid, weak Shock

Decreased Slightly dry Normal Normal Normal Normal

Markedly decreased Dry Sunken Sunken Decreased Cool

Anuria Parched Markedly sunken Markedly sunken Tenting Cool, mottling, acrocyanosis

Adapted from Dell RB: Pathophysiology of dehydration. In Winters RM (ed): The Bod Fluids in Pediatrics. Boston, Little, Brown, 1973, p 142; Robson AM: Parenteral fluid therapy In Behrman RE, Vaughan VC III, Nelson WE (eds): Textbook of Pediatrics, ed. 13 Philadelphia, WB Saunders, 1987, p 196.

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Does an Osmolar Disturbance of Body Fluids Exist? The simple laboratory test that answers this question is the concentration of sodium in serum. Based on the serum sodium concentration, the type of dehydration has been conventionally classified as follows. Hypotonic (hyponatremic) dehydration: Isotonic (isonatremic) dehydration: Hypertonic (hypernatremic) dehydration:

<130 mEq per liter 130-150 mEq per liter > 150 mEq per liter

It is not necessary to measure or estimate serum osmolality. It is important to emphasize that the serum sodium concentration, by itself, provides no useful information as to the overall state of body fluid balance. It is generally accepted that most instances of dehydration occur without a disturbance of body fluid osmolality, resulting in isotonic (or isonatremic) dehydration. Because the presence or absence of an osmolar disturbance of the body fluids has an important bearing on the composition of the final parenteral fluid used for treatment, however, the serum sodium concentration must be known. The presence or absence of an osmolar disturbance may be suspected in some cases, based on physical examination, even before laboratory studies are completed. In hyponatremic or hypernatremic dehydration, the disproportionate loss of water and solute may produce certain characteristic signs. For example, in hypernatremic dehydration, as water is lost in disproportionately greater amounts than solute (Table 4), a redistribution of fluid occurs between the intracellular and extracellular fluid compartments. The net effect is that the extracellular and intravascular fluid compartments are relatively well preserved. Such infants are not as likely to have circulatory instability, despite an actual weight loss of a severe degree. Moreover, the hypertonicity of the body fluids in the subcutaneous tissues alters the retractility of the skin, causing the characteristic doughy consistency. As noted in Table 4, infants with hyponatremic dehydration have disproportionately greater losses of solute relative to water. The immediate impact of the loss of extracellular ions is that intravascular volume is severely compromised, as fluid translocates into the intracellular fluid compartment to maintain osmotic equilibrium. The ill appearance of such infants, who may have clinical shock, belies the relatively modest weight change. Experience has shown that most cases of dehydration have proportional losses of solute and water. A rough distribution of the frequency of the different forms of dehydration is: isonatremic, 80 per cent; hypernatremic, 15 per cent; and hyponatremic, 5 per cent. 23 Recent experience suggests, however, that the incidence of hyponatremia may be increasing even as the occurrence of hypernatremia is decreasing. 9. 12 Does an Acid-Base Disturbance Exist? The determination of acid-base parameters of a venous blood sample suffice for this purpose. Several factors converge in the etiology of the usual acid-base Table 4. Typical Fluid and Electrolyte Deficits in Dehydration

Isonatremic H ypernatremic Hyponatremic

WATER

SODIUM

POTASSIUM

(mllkg)

(mEq/kg)

(mEq/kg)

100-120 100-120 100-120

8-10 2-4 10-12

8-10 0-4 8-10

From Robson AM: Parenteral fluid therapy. In Behrman RE, Vaughan VC III, Nelson WE (eds): Textbook of Pediatrics, ed 13. Philadelphia, WB Saunders, 1987, p 194.

T

271

DIARRHEAL DEHYDRATION IN INFANTS

disturbance accompanying diarrheal dehydration (i.e., acute, simple metabolic acidosis). The pure effect of bicarbonate loss in diarrheal stool is metabolic acidosis with a normal anion gap (8-16 mEq per liter), typically associated with hyperchloremia. Some infants with decreased appetite may have increased acid production, however, because of a breakdown of body protein and fat as a consequence o calorie deprivation. The effect of this process may be an accumulation of organic acid anions, and a rise in the measured anion gap. Moreover, in the instance o severe dehydration and renal hypoperfusion, underexcretion of acid, with accumulation of acid anions, further compounds the acidosis. Although, in a typical case, metabolic acidosis is a "simple" or "pure" process, the assessment of an acid-base disturbance, especially in infants with complicated illness, should include consideration of a "mixed" acid-base disorder. This is most conveniently accomplished by plotting pH, pC0 2 , and bicarbonate concentration on a graphical depiction of the Henderson-Hasselbalch equation (i. e., an in vivo acid-base nomogram).23 In this nomogram, the displacement depicted for metabolic acidosis represents a composite of empirically derived data from four separate studies. 3 One of these studies includes data from children with "pure" metabolic acidosis, in which the displacement o pC0 2 is given by the following regression equation. 1 pC0 2 (mm Hg)

=

1.54 x [HC03 - )

+ 8.36

± 1.11

This equation may be used in lieu of the above-cited nomogram to assess whether or not a mixed acid-base disorder is present. A mixed acid-base disorder (i. e., a metabolic acidosis without an appropriate ventilatory adjustment) is an unusual occurrence in the typical case of diarrhea dehydration. The most common mixed acid-base disorder, metabolic acidosisrespiratory acidosis, might be anticipated in an infant with chronic lung disease or respiratory depression, however. In this instance, a plot of data on the nomogram shows that the pC0 2 is higher than expected for a simple metabolic acidosis. Does a Disturbance of Potassium Metabolism Exist?

Available data, based on recovery balance studies, show that potassium deficits, in infants with moderate isotonic dehydration, range between 8 to 10 mEq per kg (see Table 4). This is not surprising because diarrheal stool contains substantia quantities of potassium. 17, 19 It can be estimated that a 5-kg infant, with a 2- or 3day illness generating up to 200 ml of stool per kilogram per day, in the absence o potassium intake, would sustain a deficit of about 40 mEq (or 8 mEq per kg). This estimate agrees closely with empirically measured data in infants with isotonic dehydration of moderate severity, as noted in Table 4 (8 to 10 mEq per kg). Because potassium is an intracellular ion, as the intracellular stores of potassium become depleted, a parallel decline in the volume of intracellular fluid occurs. This is probably the case in the typical instance of rotaviral diarrhea, in which the dehydration develops during several days. By contrast, a more fulminant, secretory diarrhea (as in cholera) engenders significant volume deficits during hours rather than days because the intestinal losses consist mainly of extracellular ions. 19 Because the duration of illness is relatively brief, such patients sustain somewhat lower potassium deficits,19 Moreover, the preponderant depletion of extracellular fluid in these patients is reflected by the clinical observation that shock is a common occurrence. Data as to potassium deficits also enable one to make a crude estimate of the partition of fluid deficit between extracellular and intracellular fluid compartments, For example, because similar deficits of sodium and potassium (see Table 4) exis in infants with isotonic dehydration of moderate severity (100-120 ml per kg), and the concentrations of sodium (in extracellular fluid) and potassium (in intracellular fluid) are similar, the deficit may be partitioned equally between the intracellular

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and extracellular fluid compartments. 29 For example, an infant with a preillness weight of 10 kg and an estimate of 12 per cent dehydration (120 ml per kg), has a total deficit of 1200 ml:600 ml representing extracellular losses, and 600 ml derived from intracellular fluid. Nevertheless, the serum potassium concentration is of limited value because a close correspondence does not always exist of the serum level with the state of body stores, which is mainly in the intracellular fluid. Moreover, the serum potassium concentration is influenced by acid-base balance. 2 It is generally accepted that metabolic acidosis may obscure frank hypokalemia, which might otherwise have reflected total body potassium depletion (see elsewhere in this issue). In the final analysis, the serum potassium concentration is of little practical value, except in the instance of acute renal failure. Although acute renal failure practically never occurs, even in dehydration of moderate or severe degree, prerenal azotemia is common. In the usual instance, at the time of admission to the hospital, the serum potassium level, if elevated, provides foreknowledge as to the possibility of acute renal failure and the need to proceed cautiously with potassium repletion. What Is the State of Renal Function? In the typical situation, infants with diarrheal dehydration present with oliguria at the time of admission. This is often reflected by a history of decreased urination. It is imperative to distinguish prerenal azotemia from acute renal failure quickly (Table 5). In the context of this discussion, acute renal failure is defined as suppression of renal excretory function associated with renal tubular cell injury (acute tubular necrosis). Although the dehydrated infant is often oliguric, and may not void for several hours, it is only necessary to collect a small quantity of urine. The specific gravity can be measured, using just a few drops of urine, by means of a refractometer. A drop of the urine sediment can be examined for the presence or absence of renal tubular cell casts. In most instances, oliguria reflects prerenal azotemia and is an appropriate, physiologic response to dehydration. An occasional infant with profound dehydration and shock, however, may have had prolonged renal hypoperfusion with consequent ischemic renal tubular cell injury. In such infants, the specific gravity is relatively low, given the state of dehydration and the urinary sediment may contain renal tubular cell casts. In the instance of established acute renal failure, it is imperative that fluid and potassium administration be modified accordingly. It deserves emphasis to state that the BUN is not a reliable index of renal function, because it is affected by multiple factors including dietary protein load, level of tissue breakdown, and variable rates of back diffusion of urea across renal tubular cells. Serum creatinine is a better index, but its concentration is a function of age and muscle mass. 27 Before the age of 2 years, the normal serum creatinine is in the range of 0.3 to 0.5 mg per dl. Because an inverse, proportional relationship exists between serum creatinine and creatinine clearance (an approximation of glomerular filtration rate),'5 a serum creatinine of 0.8 mg per dl in an infant is indicative of a glomerular filtration rate that is about one half of normal. Table 5. Physiologic Oliguria Versus Acute Renal Failure

Urine output Urine-specific gravity Microscopic examination of sediment FE (Na) index

PHYSIOWGIC OLIGURIA

ACUTE RENAL FAILURE

Decreased >1.020 No specific findings

Decreased 1.010-1.012 Renal tubular cells (singly or casts) >2-3%

<1-2%

"!'

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DIARRHEAL DEHYDRATION IN INFANTS

The distinction between oliguria on a prerenal basis and acute renal failure is reliably made by measuring the sodium and creatinine concentration in simultaneous samples of blood and urine. The index of fractional excretion of sodium, FE(Na), is then calculated as follows.

and PINa) are the concentrations of sodium in urine and plasma, and U IC ,) and are the concentrations of creatinine in urine and plasma. In infants, prerenal azotemia is generally indicated by an FE(Na) index less than 1 to 2 per cent. Acute renal failure is indicated by an FE(Na) index greater than 2 to 3 per cent. UlNa)

PIC,)

FURTHER MANAGEMENT Once the five-point assessment has been completed, further management hinges on posing a set of three additional questions. What kind of solution should be administered? How rapidly should the deficit be replaced? How much solution is needed? What Kind of Solution? In the ensuing discussion, the "kind" of solution refers to the composition of the final solution to be given during the initial 24 hours of treatment. Although it is common practice to break down overall fluid administration into 8- or 12-hour periods, the principles are the same. Experience has shown that infants with isotonic dehydration of moderate severity, and without acute renal failure, typically receive parenteral fluids of similar electrolyte composition. The composite parenteral fluid must take into account estimates of body fluid volume deficit as well as usual maintenance fluid requirement (see article elsewhere in this issue). It is assumed that the overall fluid requirement does not include replacement fluid for ongoing pathologic losses owing to continuing diarrhea or vomiting. In a typical infant with moderate, isotonic dehydration, once parenteral fluid therapy is begun, diarrhea often subsides rapidly, and further ongoing losses need not be considered. The final parenteral fluid stereotypically contains 50 to 60 mEq per liter of sodium. Based on the assumptions that the fluid deficit is 10 per cent of body weight, that ongoing losses are minimal, and that the rate of deficit replacement (see later discussion and Table 6) is in accord with usual practice, the selection of the type of solution is done using a decision-tree approach (Fig. 2), based on the serum sodium concentration. This schema evolved from the author's experience with the "osmolar replacement" method of management, as described by others. 4, 17 This experience has shown that most cases can be treated by means of the schema indicated in Figure 2. Dehydration of greater severity (up to 15 per cent) would modify these figures somewhat. This decision-tree schema further assumes that initial volume Table 6. Rate of Deficit Repletion as Cumulative Per Cent 0-12 Isonatremic H ypernatremic Hyponatremic

HOURS

12-24

HOURS

50 25

100

75

100

50

24-48

HOURS

100

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Serum [Na+j

~

>150 mE/L

1

130-150 mE/L

Sodium

30-40 mE/L

1

0.2 %NaCi/5% 0

concentration

50-60 mE/L

1

0.33%NaCI/5%D

1

120-130 mE/L

in

final

1

<120 mE/L

solution

70-80 mE/L

!

0.45" NaC1/5" 0

80-100 mE/L

1

0.45" NaC1/5" 0 +

Bicarbonate* (Na+ =34 mE/U

(Na+ = 56 mE/U

(Na+=

n

mE/L)

* 0.45% NaC1/5% (1000 mil + NaHC~, 23 mE Figure 2. This decision-tree is used to select the appropriate parenteral fluid for treatment of infants with diarrheal dehydration of moderate severity, based on knowledge of the serum sodium concentration. (In the figure, "5%D" refers to 5% dextrose solution.)

expansion with an isotonic solution, of up to 1 to 2 per cent of body weight (10-20 ml per kg), has occurred. It should be noted that a parenteral fluid selected using the schema in Figure 2 is a composite of both deficit and maintenance components for water and electrolyte. For infants weighing less than 10 kg, the daily maintenance water requirement is 100 ml per 100 calories metabolized. Because infants in this weight category metabolize about 100 calories per kg per day, the maintenance water requirement can also be expressed as 100 ml per kg per day. As will be analyzed further subsequently, this is probably an overestimate for dehydrated infants receiving parenteral fluids and in whom diarrhea has abated. The usual requirement for sodium and potassium is about 1 to 3 mEq per kg per day. Expressed in terms of caloric expenditure, the maintenance requirement of both sodium and potassium is about 2.5 mEq per 100 calories per day (see elsewhere in this issue). Dehydrated infants have low fractional excretion of both sodium and potassium in the urine, however, and a more realistic estimate of their maintenance needs is about 1 mEq per kg per day for each cation. These estimates have been factored into the derivation of the schema shown in Figure 2. As a caveat, it should be noted that the recommendations for isotonic and hypotonic dehydration (see Fig. 2, Table 7) are based on the osmolar replacement method. In the instance of hypertonic dehydration, however, similar computations yield a final composite solution with an unacceptably low sodium concentration. In this instance, Figure 2 incorporates the recommendation of Finberg'" 10 as to the sodium concentration of the final parenteral fluid. In the final analysis, a need exists to have available each of four different kinds

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DIARRHEAL DEHYDRATION IN INFANTS

Table 7. Sodium Concentration of Parenteral Solutions Used for Rehydration

TYPE OF DEHYDRATION

Isonatremic H ypernatremic Hyponatremic H yponatremic*

DESIRED SODIUM CONCENTRATION

TYPE OF SOLUTION

SODIUM CONCENTRATION

(mEqIL)

(%)

(mEqIL)

50-60 30-40

0.33 0.2

34

70-80

0.45

77

56

90-110

*Not commercially available (see text).

of solutions, as shown in Figure 2 and Table 7. Three of these solutions are commercially available (0.2 per cent, 0.33 per cent, and 0.45 per cent saline with dextrose). However, because a solution containing about 100 mEq per liter of sodium is not readily available, an appropriate formulation can be done in either of two ways. 1. Equal volumes of 0.9 per cent saline and 0.33 per cent saline (with 5 per cent dextrose) yield a final sodium concentration of 105 mEq per liter in 2.5 per cent dextrose. 2. Add 23 ml of 1.0 molar (8.4 per cent) sodium bicarbonate to 1000 ml of 0.45 per cent saline, with dextrose yielding a solution containing approximately 100 mEq per liter of sodium, 77 mEq per liter of chloride, and 23 mEq per liter of bicarbonate. Although potassium deficits vary, depending on the duration, severity, and type of dehydration (see Table 4), three principles should guide the administration of potassium. 1. Potassium administration should not begin until the infant has voided, and assurance is given that renal function is adequate. 2. Potassium repletion should be accomplished gradually during at least 2 days. 3. The rate of intravenous potassium administration should not be greater than 4 mEq per kg per day so as not to exceed the rate-limited uptake of potassium by cells, and thereby avoid hyperkalemia. Because the usual potassium maintenance requirement in the hospitalized, dehydrated infant is about 1 mEq per kg per day, the net effect is that this rate of administration (4 mEq per kg per day) provides up to 3 mEq per kg per day toward repletion of the potassium deficit. If the potassium deficit in a typical infant with isotonic dehydration is 9 mEq per kg (see Table 4) then, if parenteral fluids are the sole source of intake, the preceding rate of administration will accomplish full repletion by 72 hours. Generally, these goals are accomplished by adding potassium chloride to the final parenteral solution at a concentration of 20 to 25 mEq per liter. Related to the question concerning what kind of solution to use is consideration of whether or not sodium bicarbonate should be added. This decision rests on three further considerations. 1. Is the process causing metabolic acidosis a reversible, self-limited one? Is there a mixed acid-base disorder? 2. Is renal function temporarily impaired (prerenal azotemia), or has acute renal failure superVened? 3. Is the metabolic acidosis of such severity that immediate intervention is warranted? In most infants, as parenteral fluid therapy proceeds, metabolic acidosis tends to correct spontaneously, and it is not necessary to add sodium bicarbonate to the treatment program. Metabolic acidosis, however, may not be self-limiting in a postshock infant with acute renal failure. Because spontaneous recovery from

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metabolic acidosis is unlikely in this instance, it is necessary to treat acidosis with parenteral sodium bicarbonate actively, especially if blood acid-base parameters approach the severe range. It has been our practice to define severe metabolic acidosis as an arterial pH less than 7.20 and a bicarbonate concentration less than about 8 mEq per liter (a pH of 7.20 reflects a 50 per cent increase in hydrogen ion concentration, relative to pH 7.40, i. e., approximately 60 mEq per liter versus 40 mEq per liter). This definition is not arbitrary but is based on the behavior of the pH displacement curve in "pure" metabolic acidosis (Fig. 3). This figure was constructed from the observed relationship between changes in serum bicarbonate and peo 2 in acute metabolic acidosis. 1 pCO, (mm Hg)

=

1.54

X

[HC0 3 - ) (mEq per liter) ± 8.4

For all practical purposes, the curvilinear relationship depicted in Figure 3 can be considered to have a zone of gradual pH displacement and a zone of rapid pH displacement. The point on the curve at which the zone of rapid pH displacement begins corresponds to the acid-base parameters mentioned earlier. As metabolic acidosis becomes increasingly severe and plotted data move into the steeper portion of the curve, any further perturbation (for example, a decline of serum bicarbonate as little as 1 mEq per liter) produces a highly leveraged further displacement of pH.21 To mitigate against further displacement, provision of exogenous sodium bicarbonate should be considered. (See later discussion on the dose of sodium bicarbonate to be administered.) If it is deemed necessary to add sodium bicarbonate to the final fluid regimen, then an appropriate realignment of the sodium concentration, in relation to anion, should be made. As an example, for a near-physiologic 2:1 relationship of chloride to bicarbonate, in a solution containing 50 to 60 mEq per liter of sodium, 17 ml of 8.4 per cent sodium bicarbonate added to 0.2 per cent saline (34 mEq per liter of sodium) will yield a final solution with a sodium concentration of about 51 mEq per liter and a chloride concentration of 34 mEq per liter. [H+]

pH

nano fq/L 100

pCO, ~ 1.54 x [HCO-] + 8.4 7.00

90

80

7.10

70

60

50

7.30

40

7.40

30

5

10

15

20

PLASMA BICARBONATE, mEqlL

25

30

Figure 3. This figure, based on data from children with metabolic acidosis, 1 depicts the displacement of pH as serum bicarbonate declines. The "zone of rapid pH displacement"' (pH less than 7.20) has a slope that is several times greater than the "zone of gradual pH displacement" (pH 7.20 or higher). As the pH moves through the "zone of rapid pH displacement," a further decline of serum bicarbonate, of as little as 1 or 2 mEq/L, produces a highly leveraged further decrease of pH.

277

DIARRHEAL DEHYDRATION IN INFANTS

As a general principle in the treatment of metabolic acidosis, the initial dos of sodium bicarbonate, if given as a bolus, is calculated to achieve an increase o the serum bicarbonate concentration of 5 mEq per liter. Because the usual estimat of the effective volume of distribution of infused sodium bicarbonate is 50 per cen of body weight, the dosage is as follows. 5 mEq per liter X 0.5 liter per kg = 2.5 mEq per kg

In view of the leveraging effect of the hyperbolic relationship depicted in Figure 3 the therapeutic effect of this dose is greatly amplified. For example, in the instanc of a severe metabolic acidosis (pH, 7.15; plasma bicarbonate, 6 mEq per liter pC0 2 , 18 mm Hg [see Figure 3]), an increase in bicarbonate concentration of a little as 5 mEq per liter (from 6 to 11 mEq per liter) changes the pH to 7.3 (provided that the pC0 2 does not change significantly during the short time tha sodium bicarbonate is infused). Thus, a modest dose of sodium bicarbonate yield blood acid-base parameters that now reside on the portion of the curve that depict a more gradual pH displacement. How Rapidly Should the Deficit Be Replaced?

The extent and rapidity of deficit repletion varies, depending on whether o not an osmolar disturbance is present. For many years, the traditional teaching wa that less than 100 per cent replacement of the volume deficit should be accomplishe during the first 24 hours of treatment. In recent years, as oral rehydration therap has come into widespread use, the aim of treatment has generally been to accomplis full repletion within the first 8 to 24 hours. Experience has shown that this is safel accomplished in infants with isotonic and hypotonic dehydration. However, th pace of replacement therapy should be more gradual in infants with hypertoni dehydration, in accord with Finberg's recommendation. 8. 10 The rationale for mor gradual replacement therapy in hypertonic dehydration is to prevent undue fluid shifts into cells of the central nervous system (relative water intoxication) if th extracellular sodium concentration declines too rapidly. The usual guideline is t aim for a rate of decline of serum sodium of about 0.5 mEq per liter per hour, o 12 to 15 mEq per liter per day. The recommendations for the rate of defici repletion have been consolidated in Table 6 and Figure 4. How Much Solution Is Needed?

The total volume to be infused includes the following components: defici replacement, usual maintenance needs, and replacement of ongoing losses. A

Figure 4. This figure depicts the rate of repletion of water, sodium, and potassium deficits. Repletion of water and sodium in isotonic and hypotonic dehydration is shown to be either uniform during the initial 24 hours (heavy solid line) or, especially in the instance of hypotonic dehydration, 75% repletion within 12 hours, with the balance given in the remaining 12 hours of the first day (light solid line). Water and sodium repletion in hypertonic dehydration (dashed line) is accomplished uniformly over at least 48 hours. Potassium repletion occurs over at least 72 hours (dotted line).

100

CumulBtJve per cent repletion

80

60 ,

.....

~'

40

,'

"

",' "

/
..... .......... .

.....

.,'

.....

_

bID/hypo·

-

bID/hypo· Hypertonic·

....... PoIIIaium

",'

0/'"

o

48 60 72 12 24 36 Time since ststt of repletion (hours) *Water, sodium for iso-hypo-& hypettonic dehydratio

278

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adjustment is made for initial volume expansion. In practice, the estimation of total infusate volume is best accomplished using a tabular schema and a "fill-in-theblanks" approach (Table 8 and Fig. 5). The component of overall intake for deficit repletion must take into account recommended rates of correction. Using case 1 as an example (see Appendix for a more detailed discussion), the aim is to achieve 100 per cent repletion at the end of 24 hours. Therefore, 600 ml is entered in the appropriate blank on the form (see Table 8). The component of intake covering the maintenance fluid requirement is usually about 100 ml per kg per day for infants weighing less than 10 kg. The figure, 100 ml per kg per day, derives from the following separate components of the total maintenance requirement: insensible water loss (approximately 30 ml per kg per day), renal water losses (60 ml per kg per day), and stool (10 ml per kg per day). Because each of these discrete components of the composite maintenance fluid requirement may be uniquely affected by illness, each will be considered separately in the discussion that follows (also see elsewhere in this issue). The previously cited estimate (100 ml per kg per day) is probably a generous allowance, because it assumes that the renal solute load is unchanged and that urinary solute concentration is 300 mOsm per kg water. Because the obligatory urine volume is given by the equation .

I

U rme vo ume

(I· d ) Iters per ay

renal solute load (mOsm per day) urine concentration (mOsm per kg water)

= ---------'----"---'-'--

the infant in our example, case 1 (weighing about 5 kg), excreting 20 mOsm per kg per day of solute,'7 at a concentration of 300 mOsm per kg water, would require 0.333 liters of urine per day (or 333 ml per day). Therefore, the component of maintenance fluid requirement that covers the renal water requirement is as follows. Renal water requirement

333 ml per day 5.0 kg

= ----"--"'67 ml per kg per day

In actuality, however, hospitalized infants receiving parenteral fluid therapy, may not have had their usual dietary intake for several days, and are avidly conserving sodium and potassium with a consequent reduced renal solute load. One reasonable estimate is 10 mOsm per kg per day.'7 At the same time, volume Table 8. Separate Components of Overall Intake First 24 Hours of Treatment for Each Case Example COMPONENT

Maintenance* Deficit Ongoing losses Subtotal Initial bolus Remaining fluid needed

CASE 1 Volume (ml)

CASE 2 Volume (ml)

CASE 3 Volume (ml)

640 600

660 300

900 1300

1240 -100 1140

960

2200 -300t 1900

960

*Includes an allowance for fever, cases 1 and 2. tIncludes initial volume expansion (160 ml), bolus of 3 per cent saline (100 ml), and bolus of NaHC0 3 (40 ml) as discussed in Appendix.

279

DIARRHEAL DEHYDRATION IN INFANTS

depletion stimulates high rates of secretion of antidiuretic hormone (ADH) and the renal concentrating mechanism is maximally invoked, provided that intrinsic renal damage does not occur (as is the case in acute renal failure). Assuming a urinary solute concentration of 800 mOsm per kg water, the daily urine volume is as follows. Urine volume (liters per day) = =

10 mOsm per kg per day X 5 kg 800 0 k m sm per g water 0.0625 liters per day

= 62 ml per day

Under these circumstances, a urine output as little as 62 ml per day may appear to be an alarming degree of oliguria but is, in fact, physiologic. The renal water requirement is 62.5 ml per day

---""---'- =

5.0 kg

12.5 ml per kg per day

or only 0.5 ml per kg per hour. Thus, the actual renal water requirement may be as little as one fourth to one fifth of the usual allowance (60 ml per kg per day). Of course, once parenteral fluid administration proceeds, the hypovolemic stimulus to ADH secretion is down-regulated and urine output increases moderately, thereby increasing the urinary component of the maintenance fluid requirement. In the absence of diarrhea, the component of the usual maintenance fluid requirement attributed to stool water is relatively low, 5 to 10 ml per kg per day. For an infant weighing about 5 kg, assuming that diarrhea rapidly diminishes once parenteral fluid administration begins, and using 10 ml per kg per day as an estimate for stool water, this component is as follows. 5 kg x 10 ml per kg per day

=

50 ml per day

Thus, in the afebrile infant with dehydration, and without continuing diarrhea, the maintenance fluid requirement is as follows. Insensible water loss Urine Stool

30 12 10 52

ml ml ml ml

per per per per

kg kg kg kg

per per per per

day day day day

Note that this figure is nearly one half of the usual allowance (100 ml per kg per day). Insensible water loss in infants, which approximates 30 ml per kg per day, may need to be adjusted upward if fever is present. The usual adjustment is 10 ml per °C per kg per day.'7 In using this adjustment, however, it is assumed that, on the average, the temperature is elevated throughout the course of the day. In the example of case 1 (see Appendix), the assumption is that the mean temperature elevation, during the first 24 hours of hospitalization, is 1°C. Taking into account the presence of low-grade fever, the calculation of maintenance fluid requirement becomes Insensible water loss Increment for fever Urine Stool Total

30 10 12 10 62

ml ml ml ml ml

per per per per per

kg kg kg kg kg

per per per per per

day day day day day

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If the infant continues to have profuse diarrhea, which usually occurs at rates 5 to 10 times greater than usual, then a separate allowance should be made, as a line item entry on the form (Fig. 5), for ongoing losses. In this instance, a convenient adjustment is to select the solution with the next higher level of sodium, indicated in the hierarchy in Figure 2. For example, if an infant had isonatremic dehydration, the appropriate initial solution is 0.33 per cent saline (with dextrose). If the infant continued to have voluminous diarrhea during the first several hours of treatment, however, then the solution should be changed to 0.45 per cent saline (with dextrose). How Long Should Parenteral Fluid Therapy Continue? Any infant receiving parenteral fluids should be closely monitored, especially in terms of changes in hemodynamic vital signs, body weight, urinary output and specific gravity, and serum electrolytes. Any departure from other than the expected course of recovery should alert the physician to the possibility of inadequate treatment. Most infants with diarrheal dehydration, once begun on parenteral fluid therapy, have rapid subsidence of diarrhea. Presumably, this is an effect of "bowel rest." Although advocates of oral rehydration therapy claim that persistent diarrhea is not an indication for switching to parenteral fluid therapy, it is a common observation that such infants have increased stool output compared to those receiving parenteral fluids. 25 This does not argue against successful oral rehydration therapy, however. It is simply incumbent on physicians to assure that such infants ingest greater volumes of fluid. Indications of a successful course of therapy include the following. 1. Steady weight gain, compared with the weight on admission, especially if diarrhea continues. 2. Stable vital signs, if these were compromised on admission, and subsidence of physical signs of dehydration. 3. Progressive decline of urinary specific gravity to 1.010 or less, and a concomitant increase in urine output. A specific gravity of 1.010 (or urine osmolality of 300 mOsm per kg water), in the absence of renal tubular injury, indicates that the person is probably euvolemic and isonatremic. 4. Improvement in metabolic acidosis, if initial values were displaced. 5. Progressive improvement in azotemia. Repletion of extracellular fluid will improve renal perfusion with a consequent

COMPONENT

VOLUME(ml)

----------'------------------1

DEFICIT

600

I

310 MAINTENANCE i _________~---------~ ONGOING LOSS SUBTOTAL (MINUS) INITIAL BOLUS REMAINING FLUID NEEDED

o 910 -100

810

Figure 5. The "fill-in-theblanks" worksheet is used to arrive at a total volume of final composite solution.

281

DIARRHEAL DEHYDRATION IN INFANTS

rapid decline of BUN and creatinine. The failure of a progressive decline in BUN concentration, during rehydration, may be a clue to the presence of underlying intrinsic renal disease. One study showed that the decline of BUN during parenteral fluid therapy, in infants without intrinsic renal disease, approximated first-order kinetics, with a mean halftime of about 15 hours (range, 6-24 hours).5 Thus, as a general index of efficacy of therapy the BUN might be measured 24 hours after initiation of treatment, at which time it should be at least one half of the initial value. After 48 hours, the BUN is expected to be about one fourth of the initial value, or even lower. A halftime of decline of BUN exceeding 24 hours may indicate the presence of intrinsic renal disease. If an infant has sustained more severe renal injury and has a course suggesting acute renal failure, the urinary specific gravity will not be a helpful index. Moreover, once euhydremia is achieved, further parenteral fluid administration should be reduced to rates appropriate to the management of acute renal failure. Although probably little indication exists for venipuncture to obtain a follow-up set of blood electrolyte studies in the usual infant following a typical course of recovery, any infant with acute renal failure requires regular monitoring of clinical and biochemical status.

CONCLUSION The systematic approach to parenteral fluid therapy of dehydration in infants, described in this article, can be reduced to a set of questions. As the physician considers these questions, a rational plan of care will evolve, based on a substrate of physiologic considerations. Selection of the most appropriate parenteral fluid is guided by a decision-tree approach, using the serum sodium concentration.

Appendix Case 1 Assessment

1. The description of this infant suggests dehydration of moderate severity (see Tables 2 and 3). Initial rehydration during the first hour of parenteral fluid administration should consist of isotonic volume expansion, at 20 ml per kg: 20 ml per kg

X

5.3 kg = - 100 ml

For our case example, based on well-developed signs of dehydration (Tables 2 and 3), if the estimate was 10 per cent, and the weight on admission was 5.3 kg, the computation is done by setting up a simple ratio and solving for a single unknown, x (preillness weight):

x - 100 5.3

90

x = 530/90 = 5.9 kg The next step is to estimate the actual deficit (in milliliters) by taking the difference between the estimated pre illness weight and admission weight:

5.9 kg (preillness weight) - 5.3 kg (admission weight) 0.6 kg (estimated deficit) The difference, 0.6 kg of body weight, translates to a fluid deficit of 600 m\. This is a valid assumption if the acute weight loss is equated with fluid loss, without consideration of loss of

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Appendix Continued body tissue. This is a reasonable premise in most previously well, adequately nourished infants with typical gastroenteritis and diarrhea. 2. In our example, the serum sodium is 136 mEq per liter, indicating that the infant has an isonatremic (isotonic) dehydration. 3. Although a venous blood sample provides no useful information regarding the oxygenation status of the blood, it is a reasonable approximation of the acid-base status. In the management of an actual case, it is rarely necessary to do an arterial puncture. The caveat is that the pH and bicarbonate of a venous sample, drawn without stasis, will be slightly lower than arterial values; the peo 2 will be slightly higher. The values in our case example, plotted on an acid-base nomogram (such as that in Fig. 5-7 of Robson23), fall within the band for metabolic acidosis. This generally means that one is dealing with a "simple" or "pure" metabolic acidosis, without the superimposition of a second or third primary acid-base disorder, although exceptions may exist. In our example, the ventilatory adjustment of peo 2 is appropriate for the lowering of the bicarbonate concentration. This is also evident on inspection of the pH and peo z because the latter, 22, is numerically similar to the digits to the right of the decimal point of the pH value, 7.22."° In our case example, the acid-base results do not fall in the zone of rapid pH displacement (see Fig. 3). Moreover, it is likely that the metabolic acidosis is a self-limited, reversible process, especially because the infant does not have acute renal failure. 4. In our case example, the serum potassium is 4.9 mEq per liter. This does not tell us much other than we need not be concerned, for the moment, about hyperkalemia if the infant was anuric. We can reach no conclusion about the state of body potassium stores or the extent of depletion, however. Moreover, because this infant has a metabolic acidosis, the serum potassium is somewhat higher than might otherwise have been the case. 5. The specific gravity, 1.030, indicates that the urine is concentrated. The absence of renal tubular cells in the urine sediment suggests that the infant has pre renal azotemia and a physiologic oliguria. Management 1. In view of isonatremic dehydration, using the decision tree (see Fig. 2), the appropriate solution is 0.33 per cent saline (with dextrose). Because the metabolic acidosis is not in the range of rapid pH displacement, and it is likely to be a self-limited disturbance, it is not necessary to add sodium bicarbonate to the regimen. Potassium chloride is added to yield a final concentration of 20 mEq per liter of potassium. 2. As indicated in Figure 4, 100 per cent of the deficit may be replaced in the first 24 hours (600 ml, see Table 8). 3. The allowance for maintenance fluid needs should include an adjustment for fever. Assuming an average temperature elevation of l°e during the course of the first 24 hours, 50 ml is added to the usual requirement (100 ml per kg per day, or 590 ml for a preillness weight of 5.9 kg), for a total of 640 m!. The total volume of parenteral fluid is: 600 ml (deficit) + 640 ml (maintenance), for a subtotal of 1240 m!. Subtracting the volume used for initial volume expansion (approximately 20 ml per kg, or 100 ml), the total remaining to be given is 1140 ml (see Table 8). Once the total volume of infusate is determined, the actual hourly rate of administration, beginning 1 hour after admission, for the remaining 23 hours of the first hospital day, is readily computed. In our example (case 1), 1140 ml per 23 hours = 50 ml per hour.

Case 2 Assessment 1. This infant, with physical signs of body fluid depletion, in the absence of circulatory compromise, suggests dehydration of moderate severity. With an estimate of a 10 per cent decline of preillness body weight, the fluid deficit is:

x - 100 5.4

90

x (preillness weight) = 6.0 kg

283

DIARRHEAL DEHYDRATION IN INFANTS

Appendix Continued The fluid deficit, by subtraction, is: -

Preillness weight Admission weight

6.0 kg 5.4 kg 0.6 kg

Thus, the fluid deficit is 600 ml. 2. This infant, with a serum sodium of 161 mEq per liter, has hypernatremic dehydration. 3. The acid-base parameters suggest metabolic acidosis. In view of intact peripheral circulation (absence of shock or cool skin temperature), the capillary blood pH is a good approximation of arterial blood pH. Because the peo, was not given, and in the absence of clinical evidence of other primary acid-base disturbances, it is readily derived from an acidbase nomogram 23 or using the equation cited earlier: peo, = 1.54 x 13

+

8.36

= 28 mm Hg

Note that the anion gap is elevated, 21 mEq per liter, suggesting that, in addition to bicarbonate loss in the stool, insufficient calorie intake probably caused increased organic acid production with accumulation of unmeasured anions. 4. The serum potassium, 5.5 mEq per liter, is slightly elevated, which may represent the combined effects of acidosis, catabolic breakdown of tissue, and some decrease in renal excretory function (see later). 5. The serum creatinine, 1.1 mg per dl, is a nearly threefold increase, indicating that renal perfusion is low, and glomerular filtration rate is about one third of normal. The specific gravity is appropriately high. The oliguria is consistent with prerenal azotemia. Management 1. In view of hypernatremia, the appropriate solution (see Fig. 2) is 0.2 per cent saline (with dextrose). Assessment of the acid-base disturbance suggests that exogenous sodium bicarbonate is not necessary. The final solution should contain potassium chloride, 20 mEq per liter. 2. The deficit, 600 ml, will be replaced uniformly during 48 hours, so as to minimize the risk of central nervous system dysfunction. During the first 24 hours, 300 ml will be allocated. 3. In addition to deficit repletion (300 ml) during the first 24 hours, the maintenance fluid requirement (100 ml per kg per day or 600 ml for a preillness weight of 6.0 kg) for this febrile infant should be adjusted in anticipation of an average temperature elevation of about l°e throughout the rest of the first day (60 ml). The total maintenance requirement is 660 ml. The overall total for the first 24 hours is 960 ml (see Table 8).

Case 3 Assessment 1. This infant has definite circulatory compromise, suggesting dehydration of a severe degree. The estimate is 15 per cent of preillness body weight. The preillness weight is:

x

100

7.7

85

x (preillness weight) = 9.0 kg Fluid deficit: 9.0 - 7.7 = 1.3 kg or 1300 ml 2. The serum sodium indicates hyponatremic dehydration. The history noted that the infant consumed carbonated beverages. None of the usual beverages have significant concentrations of sodium and are unsuitable for replacement of fluid losses in infants with diarrhea. 30 3. The acid-base parameters indicate the presence of a severe metabolic acidosis. Plotting the parameters on a nomogram shows that the disturbance is a "simple" one with an appropriate ventilatory adjustment. The anion gap is increased, 24 mEq per liter, consistent

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Appendix Continued with acid anion retention owing to impaired renal excretory function (see later). Because the acid-base parameters place this patient in the zone of rapid pH displacement (see Fig. 3), consideration should be given to intravenous administration of sodium bicarbonate. 4. The serum potassium is normal. Potassium supplement should be withheld until the infant has voided, however, and the urine assessed for the possibility of acute renal failure. Generally, voiding soon after initiation of parenteral fluid therapy indicates improvement in renal perfusion. 5. Despite profound oliguria, examination of the urine suggests a physiologically appropriate prerenal azotemia. This is confirmed by calculation of the FE (Na) index: 0.18 per cent of filtered sodium, indicating avid renal tubular sodium reabsorption. Management 1. The decision tree (see Fig. 2) suggests that a solution with a sodium concentation or about 100 mEq per liter is appropriate. The urgent treatment of the infant on admission, however, dictates that the final solution be modified. In view of the impaired state of the peripheral circulation, the infant received initial volume expansion with isotonic saline, 20 ml per kg, or about 160 ml. After the laboratory report was received, it was concluded that the seizures on admission were probably a consequence of hyponatremia. The infant received 3 per cent saline, according to the formula (body weight on admission rounded to 8 kg): Amount of sodium (mEq) = desired change in sodium (mEq per liter) x 0.6 x body weight (kg) = (10 mEq per liter) X 0.6 liter per kg x 8 kg = 48 mEq At the end of the infusion of 3 per cent NaCI, the serum sodium should be 123 mEq per liter. The desired increment in serum sodium concentration (10 mEq per liter) is in accord with the recommendation of Sterns,28 6 to 12 mEq per liter. Because hyponatremia in dehydrated infants is an acute process, more rapid correction of a low serum sodium concentration may not entail the risks of demyelination seen in adults and attributed to excessively rapid correction of chronic hyponatremia. Because 3 per cent saline has 0.5 mEq sodium per ml, 100 ml of solution provides 50 mEq of sodium. This was administered during 3 hours. At the end of this period, laboratory measurement should confirm that the serum sodium has increased to about 123 mEq per liter. At this level of serum sodium concentration, the appropriate solution is 0.45 per cent saline (with dextrose) (see Fig. 2). An additional consideration pointing to the use of 0.45 per cent saline, rather than a solution with 100 mEq per liter of sodium, is the additional sodium load required for the treatment of severe metabolic acidosis. Because the blood acid-base data for this patient fall in the zone of rapid pH displacement, exogenous sodium bicarbonate is indicated. Assuming a desired increment in bicarbonate concentration of 5 mEq per liter, the usual formula for calculation of the dose is used, with body weight on admission rounded off to 8 kg: mEq of sodium bicarbonate = desired increment of bicarbonate x 0.5 x body weight (kg) = 5 mEq per liter x 0.5 liter per kg X 8 kg = 20 mEq This amount of sodium bicarbonate is provided by 40 ml of the 0.5 molar (4.2 per cent) solution, administered during 30 to 60 minutes. The final composite solution should contain potassium chloride, 20 mEq per liter. 2. Up to 100 per cent of the estimated deficit may be replaced within the first 24 hours (see Fig. 4). The estimate of deficit was 1300 ml. 3. The subtotal (maintenance, 900 ml per day + deficit, 1300 ml = 2200 ml) is adjusted by subtracting the volume of solutions already received: Initial volume expansion Volume of 3 per cent saline Volume of NaHC03 Subtotal

160 100 40 300

ml ml ml ml

285

DIARRHEAL DEHYDRATION IN INFANTS

Appendix Continued Hence, the remaining portion of the subtotal to be administered is:

2200 ml 300 ml 1900 ml The final solution is a composite of the maintenance (100 ml per kg per day for a preillness weight of 9.0 kg or 900 ml per day) and the balance of the deficit (excluding the bolus administration of 0.9 per cent saline, 3 per cent saline, and 4.2 per cent NaHC0 3). Thus 1900 ml remains to be administered (see Table 8). If the "bolused" solutions were given during the first 3 hours, the rate of infusion of the composite solution during the remaining 21 hours of the first day is:

1900 ml per 21 hours

=

90 ml per hour

Now that the total volume remaining to be administered is known (1900 ml), one can double check the appropriateness of 0.45 per cent NaCI as the final composite solution (rather than a solution having a higher sodium concentration, as dicated by Fig. 2). The overall sodium load dictated by the algorithm in Figure 2 should be corrected for the amount of sodium administered in the form of boluses: Overall sodium load (per Figure 2) = 2200 ml x 100 mEq per L = 220 mEq Total of sodium already received: Initial bolus of 160 ml of 0.9 per cent NaCI

+ Bolus of 40 ml of 4.2 per cent NaHC0 3

+

Bolus of 100 of 3 per cent NaCI Total sodium already received

25 20 50 95

mEq mEq mEg mEq

Total sodium remaining to be administered is: Overall sodium requirement Minus sodium already received Total remaining to be given

220 mEq 95 mEg 125 mEq

This amount of sodium will be contained in the remaining volume of fluid, 1900 ml (or 1.9 liters). Thus, the final sodium concentration of the composite solution should be:

125 mEq =::.....:c=-", 1. 9 liter

=

66 mEq per liter

Thus, the selection of 0.45 per cent NaCI as the final composite solution, containing 77 mEq per liter of sodium, is a close approximation of this patient's requirements.

REFERENCES 1. Albert MS, Dell RB, Winters RW: Quantitative displacement of acid-base equilibrium in metabolic acidosis. Ann Intern Med 66:312, 1968 2. Androgue HJ, Madias NE: Changes in plasma potassium concentration during acute acidbase disturbances. Am J Med 71:456, 1981 3. Arbus GS: An in vivo acid-base nomogram for clinical use. Can Med Assoc J 109:291, 1973 4. Boineau MD, Lewy JE: Maintenance fluids and the management of diarrheal dehydration. Pediatr Ann 10:280--288, 1981 5. Brill CB, Uretsky S, Gribetz D: Indication of intrinsic renal disease in azotemic infants with diarrhea and dehydration. Pediatrics 52:197-205, 1973

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6. Darrow DC, Pratt EL, Flett J Jr, et al: Disturbances of water and electrolytes in infantile diarrhea. Pediatrics 3: 129-156, 1949 7. Dell RB: Pathophysiology of dehydration. In Winters RW (ed): The Body Fluids in Pediatrics. Boston, Little, Brown, 1973, pp 134-154 8. Finberg L: Hypernatremic (hypertonic) dehydration in infants. N Engl J Med 289:196, 1973 9. Finberg L: Dehydration and osmolality. Am J Dis Child 135:997-998, 1981 10. Finberg L, Kravath RE, Fleischman AR: Water and electrolytes in pediatrics. Philadelphia, WB Saunders, 1982 11. Finberg L: Repair and prevention of dehydration by intravenous fluids. In Brunell PA (ed): Diagnosis and Management of Acute Diarrhea. Report of the Thirteenth Ross Roundtable on Critical Approaches to Common Pediatric Problems. Columbus, Ohio, Ross Laboratories, 1982, p 71 12. Finberg L: Too little water has become too much. Am J Dis Child 140:542, 1986 13. Finberg L: Oral rehydration: Finding the right solution. Contemp Pediatr 4:61-67, 1987 14. Gamble JL: Chemical Anatomy, Physiology and Pathology of Extracellular Fluid: A Lecture Syllabus, ed 6. Cambridge, Harvard University Press, 1954 15. Kassirer JP: Clinical evaluation of kidney function-glomerular function. N Engl J Med 285:385, 1971 16. Knopp RK: Capillary refill: New concerns about an old bedside test [editorial]. Ann Emerg Med 17:990, 1988 17. Kooh SW, Metcolf J: Physiologic considerations in fluid and electrolyte therapy with particular reference to diarrheal dehydration in children. J Pediatr 62:107-131, 1963 18. Mackenzie A, Barnes G, Shann F: Clinical signs of dehydration in children. Lancet 2:605, 1989 19. Mahalanabis D, Wallace CK, Kallen RJ, et al: Water and electrolyte losses due to cholera in infants and small children: A recovery balance study. Pediatrics 45:374-385, 1970 20. Narins RG, Emmett M: Simple and mixed acid-base disorders: A practical approach. Medicine 59:161, 1980 21. Narins RG, Cohen JJ: Bicarbonate therapy for organic acidosis: The case for its continued use. Ann Intern Med 106:615-618, 1987 22. Perkin RM, Levin DL: Shock in the pediatric patient: 1. J Pediatr 101:163, 1982 23. Robson AM: Parenteral fluid therapy. In Behrman RE, Vaughan VC III, Nelson WE (eds): Textbook of Pediatrics, ed 13. Philadelphia, WB Saunders, 1987, pp 191-207 24. Rosenstein BJ, Baker MD: Pediatric outpatient intravenous rehydration. Am J Emerg Med 5:183, 1987 25. Santosham M, Daum RS, Dillman L, et al: Oral rehydration therapy of infantile diarrhea: A controlled study of well-nourished children hospitalized in the United States and Panama. N Engl J Med 306:1070-1076, 1982 26. Schriger DL, Baralf L: Defining normal capillary refill: Variations with age, sex, and temperature. Ann Emerg Med 17:932, 1988 27. Schwartz GJ, Haycock GB, Spitzer A: Plasma creatinine and urea concentrations in children: Normal values for age and sex. J Pediatr 88:828, 1976 28. Sterns RH: The treatment of hyponatremia: Unsafe at any speed? Am Kidney Found Nephrology Letter 6:1, 1989 29. Weil WB Jr: A unified guide to parenteral fluid therapy: 1. Maintenance requirements and repair of dehydration. J Pediatr 75:1-12, 1969 30. Wendland BE, Arbus GS: Oral fluid therapy: Sodium and potassium content and osmolality of some commercial "clear" soups, juices, and beverages. Can Med Assoc J 121:564, 1979 31. Winters RW: Principles of Pediatric Fluid Therapy, ed 2. Boston, Little, Brown, 1982

Address reprint requests to: Department of Pediatrics Lutheran General Children's Medical Center 1775 Dempster Street Park Ridge, IL 60068