DIFFERENT
STAGES
OF
INFANTILE
MALNUTRITION
By E. KERPEL-FRONIUS, M.D., F. VARGA, M.D.,
J.
V#{246}N#{246}CZKY, M.D., AND K. KuN, M.D. P#{233}cs,HungaryI
T WAS found in a previous study’ that circulation is seriously impaired in severeinfantile malnutrition. This fact led to an inquiry as to how far the diminished circulation satisfies the metabolic needs of the malnourished infant.
In this endeavour oxygen consumption, circulation time, cardiac output and the
arterio-venous O2-difference were determined simultaneously in groups of undernourished infants.
METHODS
The malnourished infants were divided, according to the gravity of their clinical condition, into
3 groups. The first group covers cases of severe “dystrophy,’ ‘ the second those of severe “atrophy”
and the third, cases of ‘‘athrepsia’ ‘
(
“decomposition’ ‘)
. The classification was made according to theclassical descriptions of Finkelstein’ and Marfan.’ The average age of the infants was the following: normals, 4 mo, ; dystrophia group, 5.5 mo.; atrophia, 3.5 mo. ; athrepsia, 3 mo. The severely “dystrophic” group was 31%, the “atrophic” and “athreptic” groups 40% underweight.
02 consumption was determined according to Kestner4 and Schadow’ in experimental periods of I hr. duration. Circulation time was measured with Congo red dye.’ Oxygen in the blood was mess-ured according to Van Slyke.6 An estimate of cardiac output was attempted, using a modification of
. .
‘
02 consumption . . .the Fick principle: (cardiac output =
,
)
‘ The difficulty of applying this method inarterior-venous 02
infancy lies in obtaining the 02 content of mixed venous blood. Catheterization of the right heart
in badly ailing infants presents some dangers. In the calculations, therefore, the present authors have used the 02 content of cerebral venous blood obtained by puncturing the sinus longitudinalis. On the basis of the data which follow it is felt that this modification, however open to criticism, does not significantly alter the results: 1. The 0 content of sinus blood in normals is remarkably con-stant, and only slightly lower than mixed venous blood.” 2. In 2 normal infants cardiac output was
only about 10% lower when calculated from cerebral venous blood instead of mixed venous blood. 3. In 2 dehydrated infants cardiac output values, calculated from sinus, or from heart blood, showed a fairly good agreement.8 4. Changes in cardiac output and in circulation time, as will be seen from
the data, show a close agreement in all normal and pathologic cases.
EXPERIMENTAL DATA
All the data are summarized in chart 1.
The height of the columns represent the 02 transported to the tissues per minute (i.e.,
cardiac output x vol.
%
of arterial 02). The blackened portion of the column represents 02 consumption. All values are calculated to a surface area of 1.73 m2. Individual valuesare represented by circles; the columns show the mean values. The mean values for the
arterio-venous 02 difference and circulation time can be read at the top of each column.
In the normal infant 02 transport is double the amount consumed. In the adult 02
trans-port is higher, in view of the higher blood hemoglobin (and blood 02) content and
somewhat larger cardiac output. In the severely dystrophic group 02 consumption is
From the Department of Pediatrics, University of P#{233}cs,P#{233}cs,Hungary. (Received for publication Sept. 27, 1950.)
624 E. KERPEL-FRONIUS, F. VARGA,
J.
VONOCZKY AND K. KUNsomewhat higher and so is 02 transport. Circulation time and arterio-venous 02 difference
are unchanged. It is a well established fact that basal metabolism generally rises in
malnu-trition, especially if calculated/kg. actual weight.9” The increase, as is shown in this chart, is still apparent when basal metabolism is related to body surface. In clinically more severe forms of malnutrition metabolism appears, however, to be ‘‘normal’ ‘ or even
decreased.12,13 The data reveal that in progressively severer stages grave disturbances set
in, affecting both oxygen consumption and circulation. In severe atrophy 02 consumption decreases, so does 0 transport, the diminution in transport, however, being somewhat
greater. In athrepsia 02 transport is dangerously close to 02 consumption, the
arterio-venous 02 difference is broadened, circulation time doubled. Thus, while in atrophia
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ici circulcFton
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Dl diff.VoI.% ;7 6.7 107 7.1 -45
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ill
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CHART 1
circulation is more or less adjusted to decreased metabolic needs, in athrepsia circulation collapses far below the metabolic needs of the wasted body. There appears,
superim-posed upon the slowing up of circulation characteristic of severe atrophia, a real failure
of circulation, involving a condition of anoxia of the stagnating type.
The significance of these changed relations between 02 supply and consumption in
wasting can be better understood when compared with other conditions involving de-creased 02 consumption. The last two columns show conditions found in hypothyreosis and in severe dehydration. In the case of a cretin 2 years of age of the size of a young infant, decrease in 02 consumption was paralleled by an approximately equal decrease
in circulation. Slowing of circulation (i.e., decrease in cardiac output) seems to be
adjusted to the smaller call of the tissues for 02. The similarity to atrophia is striking. This is not so in severe dehydration. Serious circulatory shock is evidenced by the fact that
the margin between 02 transport and consumption almost completely disappears; the
arterio-venous 02 difference is enormously broadened, circulation is very slow. Thus, low
02 consumption is clearly secondary to primary failure of circulation. Tissues of normal
maximal utilisation of each cubic centimeter of 02 transported to the tissues is insufficient to bring about a normal consumption. A state of severe stagnating anoxia is created,
in-volving ‘‘toxic” symptoms : loss of consciousness and acidosis.7’8
Returning now to athrepsia, low 02 consumption is clearly the result of two processes:
1. The metabolic need of the tissues has diminished during the preceding long process of
“atrophy’ ‘ and inanition. 2. Circulatory failure adds its effect to the former process by
further decreasing 02 consumption. In spite of very low 02 consumption and circulatory
failure, the athreptic infant is less anoxic and ‘‘toxic’ ‘ than the dehydrated one, because
its metabolic need is slighter.
COMMENT
An analysis of the mechanism leading to the slowing of circulation in severe
malnutri-tion is not the purpose of this paper. The same facts were observed in wasting starving
adults by Govaerts’4 and in the famous Minnesota experiments.’5 The heart is certainly
wasted in all marantic conditions ;115 electrocardiographic changes were described in adults and infants.16 But in the terminal stage of malnutrition, athrepsia, there is more than
an adjustment of circulation to lowered metabolism ; the rapid deterioration of circulation
is clearly connected with hemoconcentration ; plasma volume decreases, the red count and
hematocrit increase.’7 Rapid weight-loss is known to be characteristic of this condition.2’3
Clinically, the high mortality of marantic infants in intercurrent infections appears
con-nected with poor circulation. Intercurrent pneumonia, by lowering arterial 02 capacity,
will add its effects of ‘‘anoxic’ ‘ anoxia to those of the ‘‘stagnating’ ‘ anoxia characteristic of
the athreptic condition. Diarrhea leading to dehydration will rapidly cause deterioration of
the precarious circulation and increase pre-existing stagnating anoxia. It is thus
compre-hensible that intercurrent infections, in spite of ample use of antibiotics, lead to high
mortality rates in severely wasted infants.17
SUMMARY
The relation of 02 consumption to circulation was studied in varying stages of infantile
malnutrition. In severe “dystrophy” 02 consumption and circulation are somewhat
increased. In severe “atrophy” both cardiac output and 02 consumption fall to lower
values, the lowered metabolic need of the tissues, however, being met by even a slower circulation. The condition is similar to that found in hypothyreotic patients. In athrepsia
circulation collapses far below the metabolic need of the wasted organism; anoxia of the
stagnating type ensues. Anoxia is, however, milder than in severe anhydremic circulatory
shock, because the metabolic need of the tissues has decreased during the long atrophic
and inanition period that preceded the terminal, athreptic stage of malnutrition. The poor
circulation of the severely marantic infant may be an important factor in the high mortality
rate when such patients suffer intercurrent infections, especially in pneumonia and
diar-rhea! disease.
REFERENCES
1. Kerpel-Fronius, E., and Varga, F., Dynamics of circulation in infantile malnutrition, PEDI-ATRICS 4:301, 1949.
2. Finkelstein, H., S#{228}uglingskrankheiten, ed. 4, Amsterdam, Elsevier, 1938.
3. Marfan, A. B., Les affections des voies digestives dans Ia premiere enfance, Paris, Masson & Cie,
1930, vol. 2.
626 E. KERPEL-FRONIUS, F. VARGA,
J.
VONOCZKY AND K. KUN5. Schadow, H., Grundumsatz und spez.-dynamische Wirkung bei gesunden Siiuglingen im
Ver-gleich mit den Befunden bei Erwachsenen und alteren Kindern, Jahrb. f. kinderh. 126:50, 1930.
6. Van Slyke, D. D., in Peters, J. P., and Van Slyke, D. D., Quantitative Clinical Chemistry,
Balti-more, Williams & Wilkins Company, 1932.
7. Kerpel-Fronius, E., Varga, F., and Kun, K., Cerebral anoxia in infantile dehydration, Arch. Dis.
Childhood 25:156, 1950.
8. Kerpel-Fronius, E., Varga, F., V#{246}noczky, J., and Kim, K., Anoxia in infantile dehydration, Acta
paediat. 40:10, 1951.
9. Talbot, F., Severe infantile malnutrition, Am. J. Dis. Child. 22:358, 1921.
10. Levine, S. Z., Wilson, J. R., and Gottschall, G., Respiratory metabolism in infancy and in
childhood: Respiratory exchange in marasmus; Basal metabolism, Am. J. Dis, Child. 35:615,
1928,
I 1. Fleming, G. B., and Hutchinson, H., Study of metabolism in undernourished infant, Quart. J.
Med. 17:339, 1924.
12. Garot, L., Contribution
a
l’#{233}tudedes troubles du mtabolisme clinique dans Ic d#{233}nutritiun gravedu nourrisson. III. M#{233}moire,Rev. franc de p#{233}diat.9:273, 1933. 13. Fouet, A., Le metabolisme basal du nourrisson, Thesis, Paris, 1924.
14. Govaerts, P., and Lequime, J., Pathogenic des oedemes de carence, Presse med. 27: 386, 1943. 15. Keys, A., Henschel, A., and Taylor, H. L., Size and function of human heart at rest, in
semi-starvation and in subsequent rehabilitation, Am. J. Physiol. 150:153, 1947.
16. McCulloch, H., Studies on heart in nutritional disturbances in infancy, Am. J. Dis. Child. 20:486,
1920.
17. Kerpel-Fronius, E., Varga, F., Kun, K., and V#{246}n#{246}czky,J., Beitrag zur Klinik und pathologischen Physiologic der S#{228}uglingsatrophie und Dekomposition, Acta med. Hungarica, to be published.
SPANISH ABSTRACT
Estudio del Consumo de Oxigeno en Relaci#{233}n la Circulaci#{243}n
en Diferentes Grados de Desnutrici#{243}n
El consumo de oxigeno en relaci#{243}na la circulaci#{243}n fu#{233}estudiado en estados variables de des-nutrici#{243}n. El consumo de oxigeno y Ia circulaci#{243}n estuvieron aumentado en las distrofias severas. En las atroflas severas, tanto el volumen cardiaco como el consumo de oxigeno disminuyeron a valores mas bajos, sin embargo, las necesidades metabolicas de los tejidos fueron llenadas gracias a una circulaci#{243}n aCm mas lenta. Un estado similar es encontrado en los pacientes hipotiroideos. En los
estados atrepsicos las necesidades metabolicas del organismo desnutrido no pueden llenarse debido
al colapso circulatorio, lo que da lugar al desarrollo de una anoxemia. Esta anoxia es menos severa
que Ia observada en el shock circulatorio anhidremico, debido a que las necesidades metabolicas
est#{225}ndisminuidas durante los periodos prolongados de atrofia y inanici#{243}n que anteceden Ia fase final
o atreptica de la desnutrici#{243}n. Se estima que Ia circulacion deficiente de los niflos con marasmo severo
puede ser un factor importante en Ia alta mortalidad observada en estos pacientes cuando desarrollan infecciones intercurrentes, especialmente pneumonias y diarreas.
