sindrom diare pada malnutrisi.pdf
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139
TIlE A5IERI(AN JOURNAL OF CLINICAL NUTRITION
Vo). 22, No. 2, F’ebrirry, 1969, pp. t3I-I46
I’rinled in U.S.A.
Dehydration Syndrome in Malnourished
Iranian Children
MAHIN SADRE, M.D.,1 HAtsIts HEDAYAT, M.D.,1 MOHAMMAD GHARIIS, M.D.,�
ZARRINDOKHT GHAVAM, PH.D.,1 AND GONZALO DoNoso, M.D.�
ONE-THIRD of time children acimitted to
the pediatric wart!s in Teheran have
been simown to be suffering from severe
lmrotein-c�l0rie tnalnu tn lion (1). However,malnutrition as such is rarely time cause of
consultatioll or of admission, but rather an
intercttrrent disease, as upper or lower
respiratory infections in winter and diar-
rheal t!isease in spring anti summer. It
should 1)e pointed out, that nialnutrition
is so common timat in many cases it is not
eveti eimtered as a diagnosis in time pa-
tient’s file.
Diarrhea! disease in the malnourished
child produces a dehydration syndrome
that does not readily respond to the hydra-
tion measures that are adequate in nor-
mally nourished patients (2). Mortality
rates in hospitalized malnourished chil-
dren, many of them suffering from de-
hydration, Imas been estimated at 30-50%
in various parts of the world, including our
country (1, 3-6). This clearly points out
that dehydration in malnutrition is poorly
understooti and that the therapeutic meas-
mires employed are inadequate.
It has been ortr aim to study dehydra-
tion as it occurs in Iranian children suf-
fering from the different forms of protein-
calorie malnutrition, as a first step that
will permit a niore rational approach to its
treatment.
In timis paper, we present the results of
1 Food an(I Nutrition Iimstitute of Iran, Teheran,
Iran. 2 Professor of Pediatrics, Pahlavi Hospital,
University of Teheran. � Medical Nutritionist,World Healtim Organization.
bioclietnical analyses of blood anti mtiscle
of malnourisimed children suffering from
delmydration because of diarrhea! disease at
time moment of timeir atlmission and! prior
to any parenteral treatment. Also, time con-
dition of time discimarged patients, as seen
6 montims after timey were adimitted to the
hospital is reporte(i.
MATERIAI.S AND i’.IETHOI)S
Clinical Material
A total of 26 clmildren, 2-36 montims of age,
was studied. They were chosen fronm timose con-
sultimmg time outpatient clinic of Paimlavi Hospital
(University of Teheran) during time summer of
1967. Time criteria for selecting our patients
were: clinical evidence of dehydration (Sunken
eyes, decreased elasticity of time skin, depressed
fontanel, and dryness of mucous nmembranes);
a imistory of acute diarrhea and vomiting in the
premious 48 hr in a malnourisimed cimild; DO
obvious Signs of pulmonary, ear, nose, and
timroat infection, or of Specific iimfectious dis-
eases: and no parenteral therapy received during
time present episode. A diagnosis of kwaslmiorkor
was given when timere was edema accompanied
by imcpatomegaly aimd skin lesions. Time patient
was classified as marasmic when edema was not
preseimt aimd hepatonmegaly and skin lesions did
not occur conconmitalmtiy. No attempt was nmade
to standardize time various metimods of treatment
enmployed by the responsible pimysicians. These
treatnmemmts included (among others) use of: Dar-
row’s solution, Ringer solution, a Ringer-lactate
solution (1/6 isi) whole blood transfusions,
plasnma, serunm aibunmin, ammd protein lmydroly-
sates.
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140
TABLE I
Son’e clinical characteristics in 26 malnourished patients suffering from dehydrati im
Age, -
months CX
Dehy- Pallor Skindration lesions
Per-\Vt, centagekg ideal
wt
2.4’ 48
3.5 44
2.8 42
5.5 50
4.0 35
4.5 47
Case
num-ber
2
34
a
6
7
8I)
10
11
12
13
14
15
it)
17
18
19
20
21
22
23
24
25
26
Name
ASA
ZB
ZE
sPAMA
RH
AB
AG
AH
AMI
MP
MK
KB
A4’AI()
FS
AN
MSA
MSA
AT
MO
ASO
FA
AK
i)A
MB
2
7
4
18
18
11
6
12
27
8
9
4
2
14
2
36
10
17
6
16
24
11
11
11
24
10
M
F
FF
M
F
M
M
F
M
F
F
F
M
F
M
F
F
F
M
M
F
F
M
M,
M
4-4
3.3
6.0
39
5-9
2.9
1.9
6.0
2.6
3-4
4.5
5.5
3-4
5.6
4.0
59
34
46
46
67
46
36
58
51
23
49
50
46
52
32
++
++
+++++
+++
+
++++
+
+++
+++++
+
+++++++++
++++++
+++
+++++++
+++
Hepa-tome-
galy
++
++
++
+
+++
++
+
+
+++
+++
+++++
++
+++
+++++++
++
+
+++
+++++
++
++
++++
+++
++
++
+++
+++
+++
++
++
++
++
+++
+
++
+++
+++
+++�
Edema, Edema,local general
+
+
- ++
+ -
- +++
+ -
++ -
+ -
+ -
- +++
- +++
- +++ -
+ -
Dis-
Other 2
days
No
No 9
No 26
No
No
Skin in- 16
fection
No I
No
Kerato- 34
mnalacia�
No
J aundice�
No 7
No
Otitis 14
�miedia
No 13
No 21
No
No
No 13
No 12
Eye in-
fection
No 8
No 11
12
No 7
No
Deathafter
1 day
1 day
8 hr
5 days
9 days
4 days
3 hr
9 days
3 days
1 day
3 days
2 days
5.9 59
4.7 50
5.8, 61
4.0� 32
3.8 41
Sadre et al.
Chemical Determinations
Blood samples and muscle biopsies were ob-
tained withmin 1 hr of admission and prior to any
timerapy. Blood was withdrawn from the jugular
or femoral vein and time following determina-
tions were carried out: Hematocrit and hemo-
globin (7), sodium and potassium (by flame
photometry in an EEL flame photometer),
calcium (8), cimloride (9), bicarbonate (10), phos-
phorus (11), total keto acids (12), total serum
proteins, and albumin (13). The biopsies (150-
500 mg) were obtained surgically from the del-
toid muscle. The samples were dried at 100 C
and timen extracted with light petroleum ether
in a micro-Soxhiet. The dry, defatted tissue was
ashed in a platinum dish at 450 C, the ashes were
taken up in a small quantity of nitric acid and
made up to a known volume. Sodium and po-
tassium were determined in the ash liquor by
flame pimotometry.
RESULTS
Table i shows the age, sex, weight, per-
centage idea! weight (14), and other clini-
cal characteristics of our patients on ad-
mission. In Table ii their blood values for
hemoglobin, hematocrit, sodium, potas-
sium, calcium, phosphorus, total keto acids
(as pyruvic), chloride, bicarbonate, total
serum proteins, and albumin are given.
Time sodium and potassium content
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Death Hb, g/Type within Hct, % 100 ml
4 days
Calcium, Chloride,niEq/ mEq/
liter liter
Bicar-bonate,mEq/liter
13.3
6.0
17.0
0.0
6.0
6.0
17.0
18.0
42.0
2.0
18.1
9.7
12.9
64
80
68
100
100
82
82
96
84.0
MM
M
MMM
MM
M
MMM
KK
KK
KKK
KKKKKK
K
+
+
+
++
+
+
+
+
CaseNumber
2
3
5
8
10
12
13
15
17
21
23
Avg
SD
SEM
4
6
7
9
11
14
16
18
19
20
22
24
25
26Avg
SD
SEM
P
Sodium,mEq/
liter
146
136
136
146
156
154
136
152
152
158
125
136
144.4
10.4
3.0
122
122
130
154
138
144
144
158
156
133
122
139
144
136
138.7
12.2
3.3
1 .28
N.S.
13.90 11.1
34
35
46
47
33
50
3217
27
32
36
38
35-5
9.1
2.6
21
21
31
23
31
28
38
23
31
32
25
42
41
29.8
7.2
2.0
1 .75
N.S.a
Potas-sium,
mEq/liter
3.2
3.8
2.713.2
3.7
5.6
3.5
6.0
6.0
4.6
2.5
4.2
4.9
2.9
0.83
3.8
5.8
4-9
3.2
3.7
3.8
4-3
2.3
2.6
3-4
4. 1
2.9
2.6
2.0
3-5
0.96
0.25
2.07
0.05
8.4
8.2
7.5
14.0
9.0
13.5
8.9
5.2
9.4
10.6
11.0
12.0
9.8
2.5
0.73
5.6
5.5
8.1
6.6
7.8
9.1
11.0
8.1
9-4
9.0
7.712.2
11.5
8.6
2.1
0.58
1 .28
N.S.
5.6
6.6
6.6
5.8
1 .6
3.6
2.8
3.0
3.0
7.0
5.0
5.0
4.6
1 .8
0.51
5-9
3.6
4-9
11.9
4-9
3.0
5.0
8.0
9.2
2.5
1.7
5.0
5.0
6.7
4.8
2.2
0.58
0.25
N.S.
Phos-phorus,mg/tOO
ml
4.7
4.5
2.4
3.1
2.2
3-5
8.6
8.5
6.8
5.7
5.4
5.7
5.1
2. 1
0.61
2.2
4-7
4.0
3.2
6.2
5.3
5.6
3.2
5.1
4.6
1.9
1.4
5. 1
3-4
4.0
1.5
0.39
1.52
N.S.
Total Total Serumketo serum albu-
acids, proteinj mm,mliq/ g/iOO g/l0O
liter ml ml
6.4 4.0
0.95 6.9 3.5
0.33 6.6 3.4
0.72 6.6
0.17 4.8 2.7
0.28 6.6 4.5
0.46 7.2 3.8
0.16 6.3 3.3
0.46 7.5 3.80.41 7.2 3.8
0.34 6.6 1 3�4
0.46 6.6 3.4
0.44 6.6 3.6
0.23 0.67 0.46
0.07 0.19 0.14
0.22 3.0 1
0.21 4.7 2.0
1.18 4.20.32 4.8
0.34 3.6 1.2
0.36 4.8 1.6
0.69 4.8 1.8
0.36 4.6 2.4
0.24 3.9 1.8
0.54 I 4�5 2.9
0.70 3.9 1.8
4.5 2.0
4.2 1.5
0.32 3.6 , 1.8
0.46 4.2 1.9
0.26 0.55 0.46
0.10 0.15 0.12
0.12 10.6 9.6
N.S. 0.001 0.001
4.9054
84
76
90
102
118
81
101
102
95
90
91. 1
16.5
4.98
0.96
N.S.
3.2
4.0
6.0
27.0
6.0
6.0
12.0
10.0
16.0
6.0
23.0
7.7
15.5
18.0
13.1
12.2
4.8
1.3
0. 19
N.S.
Dehydration in Malnourished Children
TABLE II
Blood levels in 12 marasmic- and 14 kwashiorkor-dehydrated children
a N.S. = not significant.
141
(mEq/100 g of defatted, dry tissue) in
muscle biopsies, five from edematous and
five from nonedematous patients, is shown
in Table iii.
Table iv simows the condition of the dis-
cimarged patients, as recorded from a home
visit made 6 months after they were ad-
mmmitteti to time hospital. The weights on dis-
cimarge anti at time imoimme visit are also given.
DISCUSSION
Dehydration in the malnourished pa-
tient can be due to a parenteral disease,
sucim as bronclmopneumonia, but it is nmuch
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19
22
27
43
26
27.4
22
24
42
28
44
32.0
24.8
25.4
23.0
28.6
20.6
24.4
18.0
27.0
6.5
31.3
14.5
19.4
Sadre et a!.142
TABLE lit
Sodiutim aimd potassium iim muscle biopsies of
10 dehydrated immalmmourished children,
nmEq 100 g dry, fat-free
Patient number Sodium Potassium
Marasmus
3
5
12
13
17
Mean
Kwashiorkor
4
6
14
16
18
Meamm
TABLE IV
Weight oim adnmission, discharge and after 6
nmonths imm six dehydrated nmaltmourished
children
Patient
number
Wt on admissionkVt on discharge\Vt after 6 months
of aelmission
kg�I
Per-centagel kg
ideal �vt�
Per-centageideal svt
kgPer-
centageideal wt
3 2.8 44 3.0 47 Died Died
6 4.5 47 5.4 56 6.0 54
9 6.0 46 6.2 47 6.4 45
16 3.4 23 4.4 30 4.5 29
19 3.4 46 3.5 47 Died Died
20 5.7 52 7.0 64 Died Died
more comimmon as a coimsequence of diar-
rheal disease. Time reason dehydration pre-
sents such an unfavorable prognosis and is
so difficult to correct is not clearly under-
stood1, but time following factors have been
thought to be responsible: abnormal dis-
tribution of water in the body compart-
ments (2, 15. 16); the larger surface area
per unit of body weight; alteration in the
biocimemical processes that supply energy
(17); dlepletion in magnesium and potas-
sium (18); (!isutrbances in time excretion of
water and solutes by the kidney (19, 20);
anti time like.
There is some disagreement on the
merits of hydration in time treatment of
malnourished patients. Some authors (21)
claim considerable success with the use of
a multielectrolyte hypotonic solution in
hyper- or hyponatremic patients. Otimers
(22) warn of the high risks involved in us-
ing hydration therapy in hyponatremic
malnourished patients. It is possible that
some of the discrepancies are due to the
predominance of kwashiorkor or marasmic
patients in the material studied. In this
way, marasmus, with early weaning to a
bacteriologically contaminated diet of poor
nutritional value, is by far the predomi-
nant type in subtropical countries (23-26).
On the other hand, kwashiorkor, with late
weaning to a diet very low in protein con-
tent, seems to be more common in the less
urbanized areas of tropical Africa and
America (27, 28). The differences that
have been reported to exist between the
two extremes of the protein-calorie mal-
nutrition spectrum such as liver damage,
edema, hypoalbuminemia, and anemia
could be thought to have some influence on
the biochemical picture of dehydration in
the malnourished child. However, in our
material, the type of malnutrition does
not have any bearing on the prognosis
(Table i). This observation is in agreement
with the findings of the Mexican authors
(29), who simply classify malnutrition ac-
cording to the percentage of ideal weight.
The age of the child and other clinical
characteristics, with the notable exception
of drowsiness, did not show a clear-cut
relationship with the outcome (Table i).
Drowsiness was present in seven of time
nine cases that died within 4 days of ad-
mission. A similar finding has been re-
ported by South African workers (30) and
by Chilean authors (31), who term dehy-
dration with drowsiness as “toxicosis” and
consider it to be a very bad prognosis.
Seventeen of the 26 patients studied were
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0
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-�1
.
.
.
.
.
.
Na KJ
Kwashiorkor
Nal K
Marasmus
Na K
Normal
Dehydration in Malnourisimed Children 143
1 year of age or younger. This points oimce
nmore to time predominance of malignant
immaimmutrition in time infant over that in time
prescimool child in lime urban areas of thedeveloping countries.
Time only biochemical sign consistent
with time type of malnutrition was hypo-
aibuminemia, whicim was present in all the
patients suffering from kwashiorkor (Table
it). Hematocrit and hemoglobin levels
were Imiglmer in time marasmic patients, but
time difference was not statistically signifi-
cant. Near norlnal values have been re-
ported for albunmin and lmemoglobin in the
nmarasmic chiltl (32, 33), whereas anemia
and hypoalbuminemia are a constant find-
ilmg imm kwasimiorkor (34). Severe anemia,
with imemoglobin levels of less than 7 g/
100 ml, was present in four of our patients,
but diti not seem to play any role in their
chances for survival (Tables i and mm). Hy-
pernatremia, with figures over 152 mEq/
liter, was present in six cases and hypo-
natremia, with values under 130 mEq/
liter was seen in four patients. Alterations
in the sodium content of serum, especially
ilyponatremia, have been reported as a
sign of bad prognosis (22, 35). In our
series, imowever, time children that presented
abnornmal sodium values did no worse than
timose with sodium levels witimin the
imormal range. Hypernatremia was not con-
sistently associated with increased hemato-
crit values, such as would suggest Imypo-
voleimmia, witim time possible exception of
case 10 (Table ii).
Patients suffering from kwashiorkor had
lower potassium levels, in both serum and
muscle, than marasmic patients (Tables
ii and III). However, time difference was
only significant for serum, possibly because
of time low number of muscle biopsies.
Hypopotassemia was present in five kwa-
simiorkor cases but in only two marasmic
cimildren, and hyperpotassemia was found
imm four marasmic patients. The very high
potassium content (13.5 mEq/iiter) in pa-
tient 5 occurret! together with a very low
Fic. 1. Sodium ammd potassium in muscle of de-
hydrated malnourished children. Comparison with
nornmal values (36).
chloride value and imo deternminable bi-
carbonate. The patient died a few imours
after admission. Such imigh levels of potas-
sium imave been recorded in agonic mal-
imourishied patients by otimer autimors (2).
No consistent relation could be demon-
strated between sodium ammd potassium
levels in time serum with those in time
muscle. Time extent of time potassium de-
pietion in muscle cannot be judgeti from
time level of timis element in time serum. The
muscle biopsies simoweti a higher content
of sodiumlm anti lower potassititmm than nor-
nmal muscle. Time pattertm itm timese two
electrolytes is altereti, probably more in
kwasimiorkor tlman in tmmarasmus, as can be
seen frotmm Fig. 1 in wimich outr results are
compared with timose given by Dubois et
al. (36) for normal cimildren. Timese authors
found no marked loss of potassium in the
nmuscle of dehydrateti patietmts witim nor-
mal nutritioimal status.
It is not clear to us if time clmammges founti
in the muscle electrolytes are brougimt
about by deimydration, or wimetimer delmy-
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144 Sadre et a!.
dration simply aggravates a preexisting
abtmormaiit�. Similar alterations as re-
ported here imave been found in marasmic
children sumfferi ng from dehydration (37).
Also. decreased concentration of potassium
aimtI an increase in sodhum have been
simowtm to exist in patieimts suffering from
U mmcommlpl i ca ted kwashiorkor (38).
Disturbances in time mechanisms that
supply energy to time cell imave been re-
porteti imm immalmmutrition (17). These could
be responsible for aim inadequate perform-
ance jim time ostimotic work that keeps p0-
tassiunm inside andi time sotiium outside time
cell, explainimmg thereby time changes found
in time nmuscle of our patients.
Some of time children studied had very
low calcenmia, but mmone showed evidence of
tetanv. It is possible timat acidosis, which
increases time percentage of ionic calcium,
can account for lack of this sign.
Time acid-base composition of time serum
in many of otmr patients showeti a con-
siderable gap between the sum of the
anions and the cations. It appeared pos-
sible that timis gap could be related, at
least imm part, to atm increase in keto acids.
However, time level in timese compounds did
mmot differ significantly from that found in
a series of eigimt normmmal children of com-
parable age, i.e., 0.45 ± 0.07 versus 0.32 ±
0.02 mEq total keto acids (as pyruvic) per
liter. Hypocimloremia with very low bi-
cari)onate levels and lmigh amounts of un-
deterimmined anions was frequent in our
material. Acidosis with somewimat similar
cimaracteristics may be encountered in pro-
found metabolic alterations sucim as the
diial)etic coma.
Time cimloride level in time serum was a
sign of some progmmostic value in our pa-
tients. Timus, all eigimt of the cimildren that
imad cimlorenmias of 95 mEq/liter or higher
sui-vivet!, wimereas all timree that presented
figures of less than 70 d!ied!. Bicarbonate
levels ms-ere associated with prognosis more
or less in time sanme way: seven of the eight
patieimts ms-itim figures above 17 mEq/liter
surviveti, and all timree that showed the
lowest levels died.
Time results shown in Table mmclearly in-
dicate that the biochemical picture in de-
imydration in time malnourished child can
vary considerably from patient to patient.
The tieath rate in our series was 46%. It
would seem timat to obtain better survival
rates, a therapy directed to improve the
metabolic disturbance found in each in-
tiividual case should be considered. This
means increasing the existent laboratory
and nursing facilities that are far from
adequate. From time economic point of
view timis is justifiable if a larger number
of patients can be saved timan at present
whim this directed therapy, a probable but
still unproven proposition.
In our series, each child that is dis-
chargeti alive represents an average of 17
patient-days. At a cost of $5/patient-day,
each success represents $85. The doubtful
value of timese “successes” can be seen from
time figures shown in Table iv. Out of six
patients that were discharged from theimospitai and could be located, three had
died before 6 months. The nutritional con-
dition of those found to be alive 6 months
after admission, as jut!ged from their per-
centage of ideal weight, was nearly as bat!
as on (iiscimarge. Timeir chances of survival
into adulthood would appear to be rather
small and even if they did survive their
pimysical and intellectual development
could be considerably impaired (39).
Because of the imigh cost of hospitaliza-
tion and time higim demand for beds, the
deimydrate(I malnourisimed patient is dis-
cimargeti as soon as imis acute episode is over,
witim practically no recovery in his nu-
tritional state (Tables m and iv). A cimance
for inmproving it should be provided at
Centers for Nutritional Rehabilitation
(40), wimere costs can be mutch lower timan
in time hospital.
It appears to us that without proper
facilities for the treatment of dehytiration,
and witimout a definite improvement in time
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Dehydration in Malnourished Children 145
nutritional status of time patient before he
is returned to his environment, the effi-
ciency of Imospitalizing and treating the
dehydrated malnourished child, measured
in money spent for each full recovery, will
continue to be very low.
SUMMARY
A study was made on some of the clinical
and biochemical characteristics of dehydra-
tion consecutive to diarrheal disease as it
occurred in 26 malnourished Iranian chil-
tlren, 2-36 montims of age.
No significant difference could be shown
to exist between the blood levels of hemo-
giobin, sodium, calcium, phosphorus, chlo-
ritie, bicarbonate and total keto acids
exhibited by the marasmic (12) and kwa-
shiorkor (14) patients. Significantly, higher
total serum proteins, albumin and potas-
sium were found in the marasmic children.
Muscle biopsies in malnourished pa-
tients of the kwashiorkor (5) and marasmic
(5) type revealed a higlmer content of
sodium and a lower content of potassium
than reported in tue literature for the
nmuscle in normal children.
Clinically, the only sign consistent with
bad prognosis was drowsiness. Biochemi-
cally, low bicarbonate and low chloride
levels were associated with a fatal out-
come.
The intrahospital immortality was about
50%. Of the patients discharged alive that
could be traced 6 montims after leaving the
lmospital, three had died and the other
tlmree did not show any improvement in
timeir nutritional condition. These facts
point to time poor economic efficiency of
treating time dehydrateci malnourisimedl pa-
tients under present conditions.
We gratefully ackmlowlcdge the help received
from Dr. R. Moazanmi and Dr. J. Salamati for the
facilities offered for tmospitalization and care of the
p2mticnts. Our thanks also go to the staff of theSurgical Ward No. 1, Pahlavi Hospital, especially to
I)ms. M. Mir, A. Mir and H. Ahrari for performing
the muscle biopsies. We thank Misses M. Kamker,
A. Nevisi, A. YouSefi, ammd P. Hamedi, and Mr. S. A.
Zeidi for help in the chemical determinations.
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