EXPERIENCE
AND
REASON
1123
11. Junghans RP, Ahn YS: High-dose intravenous gammaglob-utin to suppress altoimmune destruction of donor platelets.
Am J Med 1984;76(suppl):204
12. Bussel JB, Hilgartnar MW: The usa and mechanism of action of intravenous immunoglobulin in the treatment of
immune haematologic disease. Br J Haematol 1984;56:1 13. Schiffer CA, Hogge DE, Aisner J, at at: High dose
intrave-nous gamma globulin in alloimmunizad platelet transfusion recipients, abstracted. Blood 1983;62(suppl):237a
Computed
Tomography
in an
Infant
with Salt Poisoning:
Relationship
of Hypodense
Areas
in Basal
Ganglia
to
Serum
Sodium
Concentration
The
pathogenesis
of the
intracranial
complica-tions of hypernatremia has been the subject of considerable research.’5 The purpose of this corn-munication is to report unusual appearances on
computed
tomographic
(CT)
scan
of the
brain
in
an infant
who
developed
hypernatremia
as a result
of salt
poisoning.
CASE
REPORT
The patient, a 6-month-old male infant, was admitted for investigation of seizures. He had been admitted to another hospital on the evening of Jan 25, 1983, because of several episodes in which he rolled his eyes and had generalized stiffening and back arching. Diazepam had
been given
intramuscularly,
and the infant
was then
given
intravenous (IV) fluids (50 mmol of sodium chloride and 33.3 g of dextrose per liter). Serum sodium level was not available before the start ofthe IV fluids. He had received 390 mL of this solution before transfer to University Hospital, Saskatoon on the morning of Jan 26, 1983.
Past History
The patient is the fourth child of healthy parents, his mother is North American Indian and his father is white. During the pregnancy, the mother drank large amounts of alcohol intermittently and smoked one-half pack of
cigarettes
daily.
The infant
was born
at
termand weighed
2,410 g. Apgar scores were 6 and 8 at one and five minutes, respectively. At age 1 month, allergy to cow’s milk was diagnosed. Since that time, the infant had been receiving
a meat-base
formula.
His developmental
milestones
were
delayed about 2 months behind his chronologic age.
Reprint requests to (B.F.H.) Department of Pediatrics, Univer-sity of Saskatchewan, University Hospital, Saskatoon, Sas-katchewan, S7N OXO Canada.
PEDIATRICS (ISSN 0031 4005). Copyright © 1984 by the American Academy of Pediatrics.
Course in Hospital
At the time
of admission,
the patient
weighed
5.74 kg (less than fifth percentile), his length was 65 cm (tenth to 25th percentile), and his head circumference was 41 cm (less than fifth percentile). The infant was lethargic and hypotonic, and deep tendon reflexes were absent.Serum
sodium
level was 130 mEqjL. The IV fluid infu-sion was continued, and by 8AM
on Jan 27, the infant was given a chicken meat-base formula. He had received 635 mL of this formula by 3:30PM
on Jan 28, when a CT scan of the brain was performed as part of the investi-gation of the cause of seizures. This showed low-density areas bilaterally in the putamen (Fig 1). Low density areas were not observed in the pontine region. At 1 1PM,
his temperature was 39.7#{176}C,and at 2AM
on Jan 29, he had seizures and was noted to have puffy hands and feet.He
had
taken
a further
320 mL of the formula since performance of the CT scan. The serum sodium level at 2 AM was 182 mEqjL. Urinary sodium level was 278 mEciJL. Because of these findings inquiries ware made as to the salt content of the meat-base formula, and it was found that 25 mL (430 mEq) of sodium chloride had beenadded
to the formula
instead
of the required
2.5 mL (43
mEq),
giving
the formula
a total
sodium
concentration
of
660 mEqjL. Appropriate IV fluid administration led to a gradual reduction of the serum sodium levels to 140 mEqj L over 48 hours. A CT scan on Feb 8 (Fig 2), showed resolution of the abnormalities noted previously. The subsequent course in hospital was uneventful. The infant remained generally hypotonic.
DISCUSSION
Although
the
patient
had
received
20
mEq
of
sodium chloride prior to transfer, he was
hypona-tremic
on
admission
to
University
Hospital.
The
reason
for
the
hyponatremia
was
not
clear,
but
it
was possibly related to the low levels of salt in the meat base that was used for his formula at home.
Meat
base
now
has
very
little
salt.
Thirty
hours
before
the
CT
scan
was
performed,
the
serum
so-dium
level
was
137
mEqjL,
and
11 hours
after
the
scan was performed it was 182 mEqjL. We presume that the low-density lesions in the basal ganglia
areas,
especially
the
putamen,
seen
on the
first
CT
scan (Fig 1) were related to hypernatrernia. They
had
disappeared
by
the
time
the
second
scan
(Fig
2)
was
performed.
The
contrast
between
gray
and
white
matter
is striking
and
may
be explained
by
differences
in
the
ultrastructure
of
these
tissues.
The
putamen
contains
densely
packed
neurons6
and
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www.aappublications.org/news
2.
Computed tomographic scan of brain 1 1 days r first scan, showing resolution of low-density areas in basal ganglia.1 124
PEDIATRICS
Vol. 74
No. 6 December1984
is much more vascular than the adjacent white matter, in which myelinated fibers make up the bulk of the tissue. Extracellular edema and blood vessel engorgement, which have been described in neuropathologic studies of salt poisoning,7 could account for the areas of low density observed in the
putamen on
CT
scan.
The
contrast
at areas
of
gray-white matter interface is analogous to the situation
seen in central pontine and extrapontine rnyeli-nolysis,8 which is observed most often when hypo-natremia has been corrected rapidly.9”
We are not aware of previous reports of these CT appearances in hypernatremia. However, similar changes have been noted in hypoxic and ischemic
12 exposure to adverse environmental agents,’3’6 and certain hereditary disorders.’7”8 Hanson’9 described hypodense areas in the white
matter in four children, including two with an ex-trapyramidal disorder and one who had galactose-mia.
Our
case
demonstrates
the
evolution
of cerebral
lesions that appear to be related to marked altera-tions in the sodium level of serum. Furthermore, it emphasizes the dangers of adding salt to
form-Fig 1. Computed tomographic scan of brain at time of hypernatremia, showing tow-density areas in basal gan-glia.
ula”20’2’
and
the
care
that
must
be
exercised
in
formula preparation, even in a hospital setting.
BRIAN F. HABBICK, MB, FRCP (C), FRCP (Glas), MRCP (Lond)
ALAN HILL, MD, PHD, FRCP(C) STANLEY P. K. TCHANG, MD, FRCP(C)
Departments of Pediatrics, Clinical Neurological Sciences, and Radiology
University of Saskatchewan,
Saskatoon, Saskatchewan, Canada
REFERENCES
1
.
Finbarg L: Pathogenesis of lesions in the nervous system in hypernatramic states: I. Clinical observations of infants.Pediatrics 1959;23:40-45
2. Finbarg L, Luttrall C, Redd H: Pathogenesis of lesions in the nervous system in hypernatremic states: II. Exparimen-tat studies of gross anatomic changes and alterations in the chemical composition of the tissues. Pediatrics 1959;23:46-53
3. Sotos JF, Dodge PR, Meara P, at at: Studies in experimental
hypartonicity: I. Pathoganasis of the clinical syndrome, bio-chemical abnormalities, and cause of death. Pediatrics
1960;26:925-938
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www.aappublications.org/news
EXPERIENCE
AND
REASON
1125
4. Ariaff Al, Guisado R: Effects on the central nervous systemof hyparnatremic and hyponatramic states. Kidney Int
1976;10:104-116
5. Finbarg L: Hyparnatremic (hypertonic) dehydration in in-fants: Current concepts. N EngI J Med 1973;289:196-198 6. Heimer L: The Human Brain and Spinal Cord. New York,
Springer-Verlag, 1983
7. Elton NW, Elton WJ, Nazarano JP: Pathology of acute salt poisoning in infants. Am J Clin Pat/wi 1963;39:252-264 8. Adams RD, Victor M, Mancalt EL: Central pontine
myati-nolysis: A hitherto undascribed disease occurring in alco-holic and malnourished patients. Arch Neurol Psychiatry
1959;81:154-172
9. Conger JD, McIntyre JA, Jacoby WJ: Central pontine mye-linolysis associated with inappropriate antidiuretic hormone secretion. Am J Med 1969;74:813-817
10. Tomlinson BE, Pieridas AM, Bradley WG: Central myati-nolysis: Two cases with associated electrolyte disturbance.
Q
J Med 1976;45:373-3861 1. Laurano R: Pontina and axtrapontine myetinolysis following rapid correction of experimental hyponatremia. Trana Am
NeurolAssoc 1981;106:98-101
12. Murray RR, Kapila A, Btanco E, at al: Cerebral computed tomography in drowning victims. AJNR 1984;5:177-179
13. Sawada Y, Ohashi W, Maemura K, at at: Computerized tomography as an indication of tong-term outcome after acute carbon monoxide poisoning. Lancet 1980;1:783-784 14. Kim KS, Weinberg PE, Suh JH, at at: Acute carbon
mon-oxide poisoning: Computed tomography of the brain. AJNR
1980;1:399-402
15. Matsuo F, Cummins JW, Anderson RE: Neurological seque-laa of massive hydrogen sulfide inhalation. Arch Neurol 1979;36:451-452
16. Aquilonius SM, Bergstrom K, Enoksson P, at at: Cerebral computed tomography in methanol intoxication. J Comput Assist Tomogr 1980;4:425-428
17. Seleklar K, Kansu T, Ziteti T: Computed tomography in Wilson’s disease. Arch Neurol 1981;38:727-728
18. Hall K, Gardnar-Madwin D: CT scan appearance in Leigh’s disease (subacute necrotising encephalomyelopathy).
Neu-roradiology 1978;16:48-50
19. Hanson PA: Metabolic origin of hypodanse areas of white matter on CT scan, abstract ad. Meeting of the Child
Nau-rology Society, Salt Lake City, October 7-9, 1982 20. Miller N, Finbarg L: Paritoneal dialysis for salt poisoning.
N Engi J Med 1960;263:1347-1350
21. Finberg L, Luttrall CN: Mass accidental salt poisoning in infancy. JAMA 1963;184:187-190
COMPUTER
LUDDISM
. . .
A data
processor
is the
useful
tool
of a university
which
has
long
since
become a knowledge factory-churning out grades and essays, students andscholars.
Nowadays,
the
bits
of arcana
produced
by most
scholarship
are
not
in
themselves
significant;
rather,
their
purpose
is to support
the
continuous
cycling
of data
upon
which
the
smooth
functioning
of the
university
rests.
What
is
important, in such a case, is that everyone find something to say, some fact or idea to use as currency in a professional exchange of thought. The interest of what is said matters little. Indeed, so long as we view knowledge as consisting
of “bits”-facts,
texts,
critical
attitudes-that
can
be collected
and
bartered,
moved from one place or head to the other, then the computer offers us an
extraordinarily efficient way of coding and storing what we “know.” Rather
than
having
transformed
the
university
or the
kinds
of thinking
that
take
place
there,
the
computer
has
instead
allowed
the processing
of “knowledge”
to become
yet more technically precise and controlled. The computer has not contested
any
of our
old
notions
about
thinking;
instead,
it has
served
as a new
vehicle
for an outdated
sense
of the
mind
as a warehouse
of ideas.
From Harris J: Computer Luddism. Et Cetera 1984;41:56-60.
Submitted by Student
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