ORIGINAL
ARTICLES
HYPERTONIC
DEHYDRATION
IN INFANCY
By William B. Weil, M.D., and William M. Wallace, M.D.
Departnent of Pediatrics of Western Reserve University School of Medicine and University Hospitals, Cleveland
(Submitted August 1, accepted August 24, 1955.)
This work was supported in part by a grant (RG-3754) from the National Heart Institute of the Na-tional Institutes of Health, U. S. Public Health Service.
ADDRESS: (W.M.W.) Babies and Children’s Hospital, 210:3 Adelbert Road, Cleveland 6, Ohio.
171
Pediatrics
VOLUME 17 FEBRUARY 1956 NUMBER 2
T
HE GLASSICAL study of Gamble, Ross,and Tisdall was the first to demonstrate
clearly that loss of body water was
accom-panied by loss of electrolyte in a proportion equivalent to its concentration in the body
ul These investigations form the
cornerstone of modern concepts of body
fluid physiology and parenteral fluid
tlier-apy. It is now generally appreciated that
losses of electrolyte and water are not al-ways strictly parallel. Under certain condi-tions loss of water may exceed that of elec-trolyte and, in consequence, lead to increase in the osmolarity of the body fluids. Con-rersely, electrolyte may be lost in excess of
water with subsequent decrease in the
osmolarity of the body fluids. In either
in-stance absolute deficits of both water and
electrolyte occur.
The terminology used to denote types of dehydration with reference to the osmo-larity of the body fluids is diverse and, at
times, confusing. Different terms have been
used by various in vestigators depending
upon the physical or chemical methods
used to identify the disturbance. The
pre-fixes hyper- and hypo- applied to the
suf-fixes tonicity, osmolarity, natrmia and elec-trolytemia all have equal force of meaning except for certain fine gradations in physio-logic concept. Since sodium salts, even
un-der the most abnormal conditions, consti-tute at least 90 per cent of the osmotically active particles in the extracellular fluid,
the sodium concentration of the serum is
an accurate, and the most generally
avail-able measure of the tonicity of the body
fluids. Concentrations of this ion below 130 mEq./l. are generally taken to indicate
hypotonicity and concentrations above 150
mEq./l., hypertonicity.
The concept that water loss may exceed
salt loss with consequent elevation of the osmolarity of the body fluids is not new. Re-peated references to it are found,
particu-larly in the pediatric literature. Salge, in 1911, pointed out that the osmolarity of the blood was often increased in diarrheal
dis-ease in infancy.2 Hamilton, Kajdi and Meeker found that the content of total base in the serum was elevated in 6 out of 25
WElL
Schwartz showed experimentally in
pup-pies that pure water deprivation, occurring while caloric and protein intake were nor-mal, led to concentration of the electrolyte
in the water of tissues and blood. Kerpel-Fronius called attention to “dehydration
be-cause of loss of water” in contradistinction to “dehydration because of loss of salt” and noted that serum electrolyte concentrations
were high in the former and low in the latter.5 This author stresses that
hyper-natremia is always accompanied
by
totalbody deficit of salt as well as deficit of
water and that the repair of this type of
de-hydration always requires administration of
both salt and water in the proper
propor-tions. Rapoport6 described 14 instances of
hypertonicity, all but 1 in infancy, and
stressed immaturity of renal function and excessive respiratory water loss as the cen-tral factors in the genesis of the increased
body fluid osmolarity. Prader and Rossi7
described a large number of patients, all
infants, in whom hypertonicity occurred
as-sociated with gastrointestinal disease, cen-tral nervous system lesions, hyperventila-tion, renal and endocrine disease. Finberg
and Harrison8 have recently described the
clinical and biochemical characteristics of this type of dehydration and noted the fre-quent associated signs of central nervous
system dysfunction.
The occurrence of hypertonicity of the body fluids in dehydration in infancy is relatively frequent. In 1953, 77 patients were admitted to Babies and Children’s
Hospital of Cleveland with dehydration as a prominent finding and in whom the con-centrations of sodium in the serum were measured before treatment was instituted. In 20 per cent of the
77
the values for sodium were in the hypertonic range, 10 per cent in the hypotonic range and the remain-ing 70 per cent in the normal range. Ex-amination of similar data of othersindi-cates similar distributions.3’ 9-11
The purpose of the present
communica-tion is to point out certain items of clinical
data that may serve to identify the hyper-tonic group of infants, to demonstrate some
of the pathologic physiology of the
condi-lion and to indicate optimal therapeutic
procedures.
MATERIAL
AND
METHODS
From January, 1953, to March, 1954, any
child admitted to Babies and Children’s Hos-pital who was found to have a concentration of 160 mEq./l. or more of sodium in the serum
was considered for inclusion in the study. In 26 instances enough data were accumulated to be of value in documenting the general status and course of the patient. Initial determinations
of concentrations of sodium and chloride in the
serum were carried out in all, and of potassium, pH, total carbon dioxide and urea nitrogen in the majority. Pretreatment urines were oh-tamed in 11 instances and analyzed for sodium,
potassium and chloride. Complete balance data with respect to body weight, intake and output
of sodium, potassium and chloride were
ob-tamed on 5 patients. One of these, D.A., was studied by the balance technique during the onset of hypertonic dehydration. This infant was being observed to obtain data on normal
retentions of electrolyte and abruptly
devel-oped diarrhea of severe degree. Parenteral fluid
therapy was instituted before marked dehydra-tion had occurred but the data obtained docu-ment the fluid and electrolyte losses that result
in water deficit in relation to electrolyte. The
other 4 balances were measured in patients
with well established water deficits on admis-sion and were carried from the time of
admis-sion until clinical and chemical recovery were
apparent.
Concentrations of sodium and potassium
were determined by flame photometry.12 Con-centrations of chloride in stool and urine were determined by a modification of the method of
Wilson and Ball,13 and in serum by the method
of Van Slyke and Hiller,14 urea nitrogen in the
blood by the method of Archibald,15 blood pH by the method of Sendroy and Hastings16 and total carbon dioxide by the method of Van Slyke and Neil!.’7 Aliquots of fluids adminis-tered parentally were analyzed for their
con-tent of the various electrolytes.
CLINICAL
OBSERVATIONS
While clinical criteria are not infallible,
certain items of evidence obtained by
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TABLE II
Body bloke
Day Ut. Vol. Na K Cl
gm.
ml. mEq.( 1.
1 4960 836 5. 39. 33.
- 5O 83’) 21. 39. 33.
#{149}2
3 3076 638 5. 39. 33.
-
I HTPT
5 4741
1 5460 450 69. 1. 57.
- 2 .5741) 760 19. 0. 14.
3 .59i0 733 15. 0. 8.
.22
20
- 4 6000 773 16. 5. 10.
.5 5949 733 17. 27. 16.
- 6 5930
Urine Stool Serum
Vol. Na K Cl WI. Na K (1 Na K (1
ml. mEq./l. gm mEq., kg. mEq./l.
310 35. 75. 53. 151 38. 33. 4. 140
--
112370 38. 59. 56. 176 43. 43. 38. 140 111
306 0. 13. 48. 301 63. 49. 32. 138 110
83 65. 136. 10. 53 41. :18. 13. 143
--
--130 123
#{149} ii)9 3.3 145
iSO 101. 36. 107. 0
-
179 6.0 1384I172. 30. 85.
-
--
160-465 4I. 11.57. 0
-1 32 0
-
142 1 1 10:3.7 103
174
to raise the suspicion that hypertonic
de-hydration may be present and to indicate
the need for chemical and clinical correla-tion. Table I presents certain clinical and laboratory data concerning the patients ob-served. The great majority were infants
under 1 year of age. When the condition occurs in older children, certain specific
and unusual conditions are usually present. Gastroenteritis is usually the primary con-dition in the infant. The disease has usually
been severe and characterized by anorexia
and vomiting with subsequent minimal
in-take of fluid with continued formation of diarrheal stools. The oral administration of
isotonic or hypertonic salt solutions have been a common occurrence. Concomitant
renal disease was present in 3 of the
patients and mental retardation prior to the
acute illness was present in 4. Hyperventila-tion was evident in only 1 patient of the
present group.
All of the children presented clearly evi-dent signs of depression of the central nerv-ous system varying from lethargy to coma. Deaths occurred only in infants who were
comatose at the time of admission. All of the infants showed increased muscular tone,
amounting in many cases to marked
gen-eralized rigidity with opisthotonus. Deep
tendon reflexes were symmetrically
exag-gerated. The general appearance of the in-fant was in marked contrast to the alert, anxious and shock-like picture seen in the infant with salt depletion. The initial
ap-pearance of the infants and the frequent
occurrence of convulsions during the early phase of rehydration led to the performance of lumbar puncture and electroencephalog-raphy during the hospital course in a
num-ber of the infants. Whenever these were
performed, the protein concentration of the cerebrospinal fluid was elevated and the
electroencephalogram was abnormal. These
abnormalities did not persist in the
in-stances not ending in death. The possible correlation of the incidence of convulsions with the mode of therapy will be noted
later.
Despite the observation of large weight gains during rehydration, the initial
appear-ance of the infants was not that classically associated with dehydration. Skin turgor was deceptively normal, the eyeballs were
not sunken and signs of peripheral
circula-tory failure were never prominent. The
+
GM. MEO.
00 15
80 12
60 9
40 6
WATE R
SODIUM
POTASSIUM
CHLORIDE
llI
ri
3
H
20
0
20
40
Ii
60.9 DA RA
- WI. KG. 4.96 5.98 3.75 3.55 6.00
DAYS 4 3 5 5 4
Fic. 1. Cumulative balances calculated per kg. of body weight for water, sodium, potassium and chloride for 5 patients. The duration of the balance period in days is shown in the lower portion of the chart. The patient D.A. was studied during the development of hypertonic dehydration, the other patients (luring recovery. The ordinate presents separate scales for water and electrolytes, the scales being ad-justed so that 1000 gm. of water is equivalent to 150 mEq. of electrolyte.
ORIGINAL ARTICLES
currence of sclerematous or “putty-like”
skin was infrequent.
BALANCE
DATA
In Table II are presented the day by (lay data relating to the balances for pa-tients D.A. and R.A. The data for D.A.
con-cern the period of onset of dehydration and
for R.A. the period of recovery from this
state. In Figure 1 the cumulative balances for these 2 patients as well as for 3 others,
for whom data are not tabulated, are shown diagrammatically. The ordinate is scaled
sCparately for water and electrolyte, the 2
scales being adjusted so that 1000 ml. of
water is equal to 150 mEq. of electrolyte-the approximate concentration of total
cat-ion in extracellular fluid. Reference to Figure 1 shows that, during the
develop-ment of hypertonic dehydration in patient
D.A., water was lost in excess of sodium;
that there was an insignfficantly positive
balance of potassium and a markedly
posi-tive balance of chloride. The cumulative
balances shown for the
4
recoveries are,PH CH
with minor exceptions, mirror images of the “onset” balance. The balance patterns shown provide a reasonable explanation for
the serum electrolyte concentrations pre-sented in Table I. Water was lost in excess of sodium thus leading to concentration of this ion. Retention of chloride ion was noted and the serum concentration of chloride was
regularly elevated to a greater extent than
that of sodium. The relative chloride re-tention accounts for the decreased
concen-tration of total carbon dioxide in the blood and the depression of pH.
Figure 2 represents an attempt to
calcu-late the vicissitudes of the body fluid com-partments during onset and recovery from this type of dehydration. The figure was constructed as follows: Patient D.A. was assumed to have a volume of extracellular
fluid equal to 20 per cent and a total body water equal to 60 per cent of body weight at the beginning of the balance; the same relations were assumed to be true for R.A.
at the end of the recovery balance. Using
extracellu-PT. D.A.
ONSET Na
uEQ/L.L
2001
1501
PT. R.A RECOVERY
ECW ICW
lO0
50
.6
150-CL 12 5
BAL 4-49
- 67 MEQ BASE
100’
50
0
GL 103
BALC-5
Viifi;;
176 WElL HYPERTONIC DEHYDRATION IN INFANCY
0 .1 .2.3 .4 .5 .6 0 .i .2 .3 .4 .5 .6
VOL. (LI./KG.) VOL. (LI./KG.)
Fic. 2. Calculated distributions of water an(l cation between extraceilular water (EC\V) and
intra-cellular water (IC\\’) during onset and recovery from hypertonic dehydration. Tile concentration of
cation in EC\V is shown along the ordinate and volumes along the abscissa. The diagrams at the top of tile figure are for the beginning of the balance and at the bottom for the end of the balance. For iiiethod of calculation see text.
Jar and that osmolar equality exists between
the 2 compartments, the serum concentra-tions and balance of chloride have been used to calculate the changes in intra- and extracellular fluid by the method described
by Darrow. Volume of fluid is plotted along the abcissa and concentrations along the ordinate. By this method of calculation
it is evident that the volume of the chloride space remains relatively unchanged from normal during onset and recovery; the water lost is almost entirely from the intra-cellular fluid. During the onset of the
proc-ess of intracellular dehydration, cation (pre-sumably sodium since potassium balance
was little changed) is transferred to the chloride space and during recovery with-drawn from this space. Finberg and Harri-son,8 using the same method of calculation
for a single 24-hour balance period, found no cation shift. Calculation of the balance data for the first 24-hour period in the 4
recoveries presented here gives a similar
result. Presumably shift of cation occurs
only during the later and definitive phases of the repair and is dependent upon final
adjustment of chloride balance and
extra-cellular chloride concentration.
URINE
COMPOSITION
AND
RENAL
FUNCTION
While oliguria was the rule in the
pa-tients studied, it was possible in a number of instances to examine the urine prior to administration of fluid. Concentrations cf
electrolytes and specific gravities of these samples are given in Table I. Only in the
salt-loaded infants do the concentrations of
sodium and chloride ions in the urine ex-ceed their plasma values. Generally, concen-trations of sodium and chloride in the urine are low. Despite the dehydration, the
on
2
patients (#13 and #20). In both in-stances the clearance values were less than 10 per cent of normal on the initial day andhad returned to normal by the time of ap-parent clinical recovery. The high
concen-trations of urea nitrogen in the blood given
in Table I indicate that similar low
clear-ance values were probably present in the
majority of patients.
DISCUSSION
When dehydration is produced in normal
individuals by simple deprivation of water either in the presence or absence of a
nor-ma! caloric intake, elevation of the
concen-tration of sodium in the serum inevitably
u41#{176} Gamble2#{176} and Peters2’ have
pointed out the physiologic utility of this
occurrence for prolonging survival time in
dehydration. As dehydration proceeds, both the concentration of sodium and the total
amount of sodium in the urine declines and the concentration of the ion in the plasma
rises. Under the stimulus of the
hyperna-tremia, antidiuretic action increases, urinary
water loss is curtailed, and urine concentra-tion becomes maximal. Simultaneously, the
hypernatremia leads to osmotic transfer of
water from the intra- to the extracellular compartment, thus serving the function of sustaining the declining extracellular and
plasma volume. In this process potassium is transferred to the extracellular fluid and
excreted in the urine, and a negative
bal-ance of potassium occurs. Hypernatremia
thus becomes the instrument by which the
declining supply of body water is redistrib-uted and conserved in the interests of main-tenance of circulating volume.
The sequence of events and the physio-logic adaptation of the infants under
dis-cussion are, in part, analogous to those just outlined. Water deficit occurs through the combined effects of low intake and the loss
of hypotonic fluid from the skin, lungs and
intestinal tract. The concentration of sodium
in the plasma is high and in the urine low. However, unlike the normal response, maxi-mal concentration of the urine does not regularly occur and significant loss of
intra-cellular cation does not appear to take place. In the majority of instances where it was possible to measure the specific gravity
of the urine before treatment, it was found
to be below that expected in infants of
this age undergoing simple water
depriva-tion.2224 The balance data indicate no
sig-nificant changes in potassium balance.
Ob-viously renal dysfunction of an intrinsic
nature was present in these infants. That
this failure was transient was indicated by the subsequent clinical course of the infants
and by the return of the urea clearance to normal.
The oliguria and critical clinical
condi-tion of these infants makes study of the
renal defect difficult. A number of factors must play a role. Because of immaturity of renal function, infants of this age group
may be unable to respond adequately under
conditions of maximal stress.2527 McCance
and 9 have studied renal
func-tion during dehydration in infancy and found little change in glomerular filtration rate. However, U/P ratios for a number of
substances were not as great as in adults with comparable dehydration. Calcagno and
Rubin4 compared the renal function of in-fants dehydrated by fluid restriction with others dehydrated from diarrhea and
vomit-ing. They observed greater depression of filtration rate, urea clearance and U/P ratios in the sick infants than in those with similar weight loss resulting from simple fluid
re-striction. Similarly, McCance and Widdow-son3#{176}noted a tendency toward hypotonic urine, low sodium and chloride clearances and a fall in urea clearance as much as 5
times as great as the fall in inulin clearance in patients dehydrated as a result of illness. It is possible that the disturbance in
osmolar-ity of the body fluids may act to impair renal function in a manner analogous to that seen in hypotonicity of the body fluids.3’
The failure to excrete potassium in re-sponse to cellular dehydration may indicate
tubular immaturity32 or renal incompetancy.
Elkinton and Winkler33 have shown that
transfers of cellular potassium do not occur
TABLE III
AVERAGE CONTENT OF ELEcTROLYTE AND WATER OF NORMAL AND I)IAIGUIE.&L STOOLS AS DETERMINED BY VARIOUS AUTHORS
Type of Oral Intake
Number of Samples
mEq./l. of JVoter
Na K
Per Cent (f
---I Water in
Stools
Normal
Stools
Milk Mixture
Milk Mixture Milk Mixture
11
6 6
19 26
22
l)iarrheal Stools
Milk Mixture
Milk Mixture Fasting Fasting
10
14
7
6
41
59
64
46
Reference
52 49
61
29
27
44
49
80 36
88 11
37
93 36
97 38
93 11
37
WElL HYPERTONIC DEHYDRATION IN INFANCY
* Electrolyte determined on supernathnt after ceiitrifugation.
that thirsted subjects did not lose as much
potassium as might be expected from the rise in osmolarity. Retention of chloride to
a greater extent than sodium, as found in the patients studied here, has been
pre-viously noted.”
Whatever the combined renal factors are, extrarenal occurrences play an equally po-tent role in the genesis of the abnormal
con-centrations. A number of factors act in
uni-son to cause deficits of water in excess of
electrolyte. These are loss of water from the
skin and lungs, loss of hypotonic stools and,
in some instances, ill-conceived administra-tion of sodium chloride. Presumably the
excessive water deficit occurs at a rate
in-compatible with complete renal adjustment of electrolyte concentration by the kidney.
In the normal infant approximately one-half of the daily water expenditure from the body is from the skin and lungs, while in febrile states both the absolute and relative amounts are greatly increased. Even when
sweating occurs with varying degree of loss of electrolytes, the fluid lost is always
hypotonic. Hyperventilation causes
in-creased loss of water from the lungs and has been implicated as a major factor in the production of loss of water in excess of salt
in such infants.6
It has not been generally appreciated that the sodium concentration of stool water is invariably below the concentration of this
ion in extracellular fluid while the
potas-sium concentration is six- to fifteenfold that
of extracellular fluid. The sum of these
uni-valent cations is always less than the total cation concentration of the body fluids. The
concentration of chloride ion is always less
than the sum of sodium plus potassium. Diarrhea! stools tend to be somewhat less
hypotonic and to contain a slightly greater percentage of water than do normal stools.
The most significant difference is in the total daily volume. Stools from fed and
fasted infants with diarrhea are also
gener-ally similar. Support for these statements is
presented in Table III. These ionic char-acteristics of stool lead to a loss of water in
excess of univalent electrolyte, and of fixed
cation in excess of fixed anion with
subse-quent production of fixed anion acidosis. The administration of excessive quantities
of sodium chloride played a role in the
gene-sisof the hypertonicity in 8 of the 26 cases. In 7 of these, isotonic or hypertonic solutions
of sodium chloride had been given the
in-fants to drink in place of milk mixtures. In each case a hypotonic solution had been
in-tended but erroneous directions given the mother in regard to its preparation.* The
practice of rehydration with isotonic so-dium chloride solution parenterally and the
#{176}One level teaspoon (5 to 6 gm.) of sodium
treatment of dehydration and acidosis with
enemas of 2 to 3 per cent solutions of
sodium bicarbonate are still encountered as factors in the causation of hypertonic
de-hydration.
-Deviations from normal concentrations of sodium in the serum in various diseases of
the central, nervous system have been re-peatedl reported and have led to specula-tion concerning hypothalamic regulation of
the concentration of this ion in body fluids. Increased concentrations were first men-tioned by Allott’#{176}and the role of the central
nervous system in relation to hypernatremia
has recently been reviewed by Welt.4#{176} Several authors have observed low urea
clearances and low concentrations of
so-dium and chloride in the urines of such pa-tients.414’ In the patients described here, the infant with cerebral hemorrhage (No.
24) may belong in this etiologic category. It is clear that many instances of
hypernatre-mia associated with disease of central
nerv-OUS system stem from the simple inability
of the patient to express thirst and to take
fluids adequately in response to this
stimu-lus. Whether abnormalities of the central
nervous system represent cause or effect is
often difficult to assess. In the majority of
the present group the disappearance of cen-tral nervous system signs with return of the sodium concentration to normal would
indicate that the symptoms were secondary to the hypernatremia. Finberg and Harri-son8 in their study of hypernatremia found that concentrations of calcium in the serum
were regularly decreased prior to and after therapy and suggest that the central nervous
system signs may be related to
hypocalce-mia.
One patient in the present series (No. 20) has maintained a persistent hypernatremia
for more than 1 year. Normal concentrations
may be produced only by forced hydration.
She now appears mentally retarded. Her response to a water load administered
orally is blunted and infusion of hypertonic
saline solution produces only a partial anti-diuresis. She does respond to pitressin. Urea
clearance values are at the lower limits of
normal and a normal amount of titratable acidity is produced after infusion of phos-phate.
Water deprivation associated with
dia-betes insipidus as well as the feeding of large quantities of protein in the face of increased water expenditure will eventually
produce high degrees of hypernatremia.’
Patients 22, 23, 25, and 26 (Table I) pre-sented instances in which such etiologic
fac-tors played a role. Hypernatremia is
en-countered during the postanuric phase of
lower nephron 4546
In view of the water deficit without
ac-companying electrolyte loss, the primary
consideration in rehydration therapy would
seem to be the parenteral administration of
electrolyte-free fluid in appropriate quanti-ties. Experience with the therapy of this type of disturbance, however, has shown
that the rapid restoration of body fluid os-molarity using glucose solutions is
fre-quently accompanied by severe convulsive disturbances. Presumably water intoxication
occurs in these infants even at supernormal concentrations of sodium in the serum. In several instances in which convulsions
oc-curred, the administration of sufficient hypertonic salt solution to restore the
orig-inal concentration of sodium was accompa-nied by cessation of the central nervous
system disturbance. Correction of the
ab-normal concentrations should be gradually
accomplished over a 1- to 2-day period.
Optimal rehydration is best accomplished using solutions containing 50 to 65 mEq./l.
of sodium and 35 to 45 mEq./l. of chlo-ride administered at the rate of
approxi-mately 180 ml./kg. of body weight/24 hours. Such a solution can be prepared
using 1 part of one-sixth molar sodium
lac-tate, 2 parts 0.9 per cent solution of sodium chloride and 4 to 6 parts of 5 per cent solu-tion of glucose. The concentrations are simi-lar to those recommended for routine use by
Butler and associates.4749 The absence of potassium deficit and the frequency finding
of the first 24 to 48 hours of therapy, the
abnormalities in the concentrations of
elec-trolytes have been adequately corrected, a
satisfactory urine volume had been
estab-lished, and the infants are able to tolerate dilute milk mixture administered orally.
SUMMARY
Dehydration, biochemically characterized
by increased concentrations of sodium and chloride in the extracellular fluid, is a
fre-quent result of diarrhea in infants. The genesis of the hypematremia and
hyper-chioremia lies in the relatively greater ex-penditure of water than electrolyte via skin,
lungs, stool and urine. The significance of these events in terms of distribution of body water and cation are discussed. The water
deficit in these infants is primarily intra-cellular. Cation deficits are minimal.
The majority of infants with this type of
dehydration present certain clinical signs
that should serve to make the clinician
aware of the abnormality of concentration. These infants show varying degrees of de-pression of central nervous system varying from lethargy to coma. Convulsions are fre-quently observed during the course of the disturbance. While dehydration, as
meas-ured by water retention during recovery, is invariably present, the traditional signs of water deficit are deceptively absent.
Dilute solutions of electrolyte are
indi-cated in repair. Rapid adjustment, however, of the concentration abnormality appears to accentuate the central nervous system dis-turbance. Repair is best carried out in a leisurely manner over a 2- to 3-day period.
REFERENCES
1. Camble,
J.
L., Ross, C. S., and Tisdall, F. F.: The metabolism of fixed base during fasting.J.
Biol. Chem., 57:633,1923.
2. Salge, B.: Die physikalischen Erscheinun-gen des Blutes beim gesunden und
kranken Saugling. Ztschr. Kinderh., 1:
126, 1911.
3. Hamilton, B., Kajdi, L., and Meeker, D.: The acidosis of acute diarrhea in in-fancy. Am.
J.
Dis. Child., 38:314, 1929.4. Hamilton, B., and Schwartz, R.: The
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D., MacLachlan, E. A., andSPANISH ABSTRACT
Deshidrataci#{243}n
Hipert#{243}nica
en la Infancia
En Ia mayorIa de los casos de deshidrataci#{243}n como resultado de diarrea, Ia p#{233}rdida de agua y su contenido electrolItico se realiza en tal forma que Ia concentraci#{243}n electrolitica de los lIquidos org#{225}nicos queda dentro de lImites normales. Sin embargo, en el 20% de niflos di-arreicos la p#{233}rdida de agua excede la de los electrolitos y las concentraciones i#{243}nicasde los lIquidos aumentan enormemente; a tal
con-dici#{243}nse le llama deshidrataci#{243}n hipert#{243}nica.
Este tipo de deshidrataci#{243}n se manifiesta con smntomas y signos clInicos definidos que ayudan a identificarlo e indican Ia necesidad de una correlaci#{243}n quimico-clInica; se observa de pre-ferencia en lactantes menores de un aflo y solo en condiciones especiales en ni#{241}osmayores. En las formas moderadas los lactantes presentan letargo y falta de respuesta a! medio; en los grados m#{225}sseveros de hipertonicidad, hay coma profundo. Generalmente se encuentra adem#{225}s hipertonla muscular exagerada, a menudo hasta alcanzar niveles convulsivos.
A pesar de observarse aumento notable de peso durante la rehidrataciOn, el aspecto inicial de estos pacientes no es el asociado a la deshi-drataciOn; Ia turgencia de la pie! es normal, los globos oculares no se encuentran hundidos y nunca aparecen claros los signos de insufi-ciencia circulatoria perif#{233}rica. La ausencia de manifestaciones de deshidrataciOn y las evi-dentes alteraciones del sistema nervioso central, conducen a un diagnOstico inicial de infecciOn del sistema nervioso central u otro de igual
gravedad y a menudo retardan el empleo de
una terapia hidrica adecuada. A la puncidn
lumbar Ia inica anormalidad que se encuentra
regularmente es el aumento de las proteinas
en el lIquido cefalorraquideo. El electroen-cefalograma est#{225}difusamente anormal.
Las p#{233}rdidas de agua en exceso de los
elec-trolitos son el resultado de una combinacidn de factores: baja ingestion de agua por la
anorexia y los vOmitos; administraci#{243}n fre-cuente a! ni#{241}ode sueros salinos, isot#{243}nicos o hipert#{243}nicos, como parte de una terap#{233}utica ma! calculada; p#{233}rdidas excesivas de agua por la piel, los pulmones y la via gastrointestinal; como estos pacientes no concentran
adecuada-mente la orina, acenhian a(in m#{225}sIa deshidrata-ci#{243}n.La incapacidad para concentrar la orina
parece ser un defecto traixsitorio y desaparece cuando los ni#{241}osson rehidratados. Los estudios de balance en cierto niimero de lactantes
mos-traron que la p#{233}rdidade agua es sufrida casi
completamente por el liquido intracelular. Hay
escasa p#{233}rdidao ganancia de sodio o potasio
del organismo durante Ia instalaci#{243}n o Ia
recu-peraciOn del cuadro; Ia retenciOn clorurada es
exagerada, sin embargo mas bien durante In genesis de este estado, pero se pierde al
exterior durante su recuperaci#{243}n.
La terap#{233}utica de estos ni#{241}ospuede
rea-lizarse mejor con soluciones parenterales
con-teniendo de 50 a 60 mEq. de sodio por litro;
los sueros con potasio parecen estar contraindi-cados. Deben evitarse los ajustes r#{225}pidos de las concentraciones electrolIticas por n’iedio de ad-ministraciOn de suero glucosado, pues tal
con-ducta tiende a acentuar los trastornos del
sis-tema nervioso central. Los signos y sIntomas del
sistema nervioso central desaparecen cuando
se normalizan las concentraciones plasm#{225}ticas.
INTERLINGUA ABSTRACT
Dishydratation
Hypertonic
in
le
Prime Infantia
In le majoritate del casos de dishydratation resultante de diarrhea, aqua con le electrolytos continite in illo es perdite per le corpore in un tal maniera que le concentrationes electro-lytic del fluidos del corpore remane intra Ic limites del norma. Sed in circa 20 pro cento del infantes con diarrhea le perdita de aqua excede le perdita de electrolytos, e Ic concen-trationes ionic del fluidos corporee se monstra grandemente augmentate. Le stato resultante ha essite designate como dishydratation
hyper-tonic. Iste typo de dishydratation exhibi certe specific signos e symptomas clinic que servi a
identificar le disturbation. Istos require le
esta-blimento de correlationes chimic e clinic. Il se tracta de un condition que occuri-e
predominantemente in infantes de minus que
un anno de etate. In infantes de plus alte etates
illo occurre solmente sub conditiones inusual.
In leve casos le infantes es lethargic e
irre-sponsive; in sever casos de hypertonicitate illes es profundemente comatose. Un augmentate
tono muscular, frequentemente de grados proxime a nivellos convulsive, se incontra
regu-larmente. In despecto del observation de
(lel rehydratatioii, le apparentia initial de iste infantes non es usualmente lo que on associa
con dishydratation. Le turgor cutanee es de-ceptivemente normal; le globos ocular non es
infundate; e le signos de disfallimento del
cir-culation peripheric es nunquam prominente.
Le absentia de signos de dishydratation e le
evidente affection del systema nervose central
duce generalmente al diagnose initial de un
infection del systema nervose central o de un
altere catastrophe e causa frequentemente un
1)ostPonimento del uso de un adequate therapia n fluido. Quando un punctura lumbar es
execu-tate, un elevation del nivello proteinic in le fluido spinal es regularmente discoperite como
Ic sol anormalitate. Le electroencephalogramma
es diffusemente anormal.
Iste genere de deficit de aqua in excesso de electrolyto resulta de un combination de plure factores. Le ration de aqua es basse in
conse-quentia de anorexis e vomito. Iso- o hypertonic solutiones salin ha frequentemente essite ad-ministrate a iste patientes como parte de un mal-cogitate therapia, e le perdita de aqua
via le pelle e le pulmones e a transverso Ic
tubo gastrointestinal es considerabile. In plus, iste infantes non succede a adequatemente
con-centrar le urina, e assi Ic dishydratation es
accentuate ancora plus. Le incapacitate a con-centrar le urina pare esser un defecto transiente
iue dispare quando Ic infantes es rehydratate.
Studios de balancia esseva executate in un
numero de infantes. Iste studios monstra que
Ic deficit de aqua occurre quasi integremente a! costo del fluido intracellular. Durante le disveloppamento del condition e durante Ic recuperation ab illo Ic natnum e Ic kalium del
corpore monstra pauc perdita o augmento. Del altere latere, un satis marcate retention de chloruro es manifeste durante Ic genese del condition. Illo se perde externemente durante Ic recuperation.
Le therapia de iste infantes se face Ic melio
per medio de solutiones parenteral que contine
50 a 60 mEq de natrium per litro. I! pare que
Ic uso de solutiones continente kalium es plus tosto contra-indicate. Le rapide adjustamento del concentrationes electrolytic per medio del administration de solutiones de glucosa debe
esser evitate proque iste procedimento tende a accentuar Ic disturbation del systema nervose
central. Le signos e symptomas del systema nervose central dispare quando Ic concentra-tiones plasmatic ha retornate a nivellos normal.
PNEuxI0NIA iN NEWBOHN INFANTS, Alexander J. Schaffer et al. (J.A.M.A., 159:663, October 15, 1955.)
The occurrence of pneumonia in newborn infants has been recognized by pathologists for many years. The authors are of the opinion that pediatricians have not recognized this condition as often as they should and that early diagnosis will permit successful
treatment. The authors refer to a form of pneumonia which may develop in utero 01 in the first few hours of life in contrast to the forms of pneumonia well known to
occur later in the neonatal period from a variety of established etiologic agents. The organisms found in the pulmonary inflammation in the fetal lung usually are
those conimonly found in the maternal vagina. The pathogenic mechanisms which
per11it these organisms to invade the fetal lung are discussed. Pneumonia in the early neonatal period usually occurs in cases where membranes rupture more than
6 hours before delivery, who were the products of prolonged and complicated labors,
01 in premature infants. Details of treatment to he instituted in newborn infants demonstrating signs indicative of pneumonia are discussed. The authors suggest that
pneumonia is a sole cause of death in 6 to 9 per cent of all stillborn or newborn infants. Infants affected with pneumonia at birth commonly show signs of illness such as would be expected from pneumonia, although the manifestations may be subtle and all the usual symptoms and signs are not regularly present. The authors state that if pediatricians were to be suspicious of the diagnosis of pneumonia in the
newborn and observe the symptoms described, the diagnosis would be made more
