Cerebral Salt Wasting Syndrome in Children
With Acute Central Nervous System Injury
Raquel Jiménez, MD, Juan Casado-Flores, MD, PhD, Monserrat Nieto, MD, and
María Angeles García-Teresa, MD
The purpose of this investigation was to describe the
causes, clinical pattern, and treatment of cerebral salt
wasting syndrome in children with acute central ner-
vous system injury. This retrospective study focused on
patients <15 years old diagnosed with cerebral salt
wasting syndrome, over a period of 7 years, in the
pediatric intensive care unit of a tertiary care hospital.
Selection criteria included evidence of hyponatremia
(serum sodium <130 mEq/L), polyuria, elevated urine
sodium (>120 mEq/L), and volume depletion. Four-
teen patients were identified with cerebral salt wasting
syndrome, 12 after a neurosurgical procedure (8 brain
tumor, 4 hydrocephalus) and 2 after severe brain
trauma. In 11 patients the cerebral salt wasting syn-
drome was diagnosed during the first 48 hours of
admission. Prevalence of cerebral salt wasting syn-
drome in neurosurgical children was 11.3/1000 surgical
procedures. The minimum sodium was 122 ⴞ 7
mEq/L, the maximum urine osmolarity 644 ⴞ 59
mOsm/kgH2O. The maximum sodium supply was 1
mEq/kg/h (range, 0.1-2.4). The mean duration of cere-
bral salt wasting syndrome was 6 ⴞ 5 days (range 1-9).
In conclusion, cerebral salt wasting syndrome can
complicate the postoperative course of children with
brain injury; it is frequently present after surgery for
brain tumors and hydrocephalus and in patients with
severe head trauma. Close monitoring of salt and fluid
balance is essential to prevent severe neurologic and
hemodynamic complications. © 2006 by Elsevier Inc.
All rights reserved.
Jiménez R, Casado-Flores J, Nieto M, García-Teresa MA.
Cerebral salt wasting syndrome in children with acute
central nervous system injury. Pediatr Neurol 2006;35:
261-263.
From the Pediatric Intensive Care Unit, Hospital Infantil Niño Jesús,
Universidad Autónoma, Madrid, Spain.
© 2006 by Elsevier Inc. All rights reserved.
doi:10.1016/j.pediatrneurol.2006.05.004 ● 0887-8994/06/$—see front matter
Introduction
Hyponatremia is a common finding in the postoperative
period in children with acute central nervous system
disease [1]. It can be secondary to excessive administra-
tion of hypotonic fluids and diuretics, syndrome of inap-
propriate secretion of antidiuretic hormone (SIADH),
cerebral salt wasting syndrome, hypothyroidism, renal,
hepatic, and adrenal insufficiency, and congestive cardiac
failure [2].
Cerebral salt wasting syndrome is characterized by
evidence of hyponatremia, excessive urine output, ele-
vated urine sodium concentration, and volume depletion.
It is important to distinguish cerebral salt wasting syn-
drome from syndrome of inappropriate secretion of anti-
diuretic hormone, as both present with hyponatremia in
patients with central nervous system injury [3].
This report describes the clinical pattern of 14 patients
with cerebral salt wasting syndrome and acute central
nervous system disease and its prevalence in postoperative
neurosurgical patients.
Subjects and Methods
This retrospective study involved patients ⱕ15 years old with a
diagnosis of cerebral salt wasting syndrome. During the last 7 years, 14
patients have been identified with cerebral salt wasting syndrome in the
pediatric intensive care unit of a tertiary hospital. The collected data
included age, sex, diagnosis, plasma sodium, urine sodium, urine
osmolarity, urine output, 24-hour fluid balance, and parenteral and
enteral sodium administration.
A diagnosis of cerebral salt wasting syndrome was made in children
with evidence of hyponatremia (plasma sodium ⬍130 mEq/L), accom-
panied by elevated urine sodium (⬎120 mEq/L), elevated urine osmo-
larity (⬎300 mOsm/kgH2O), excessive urine output (⬎3 mL/kg/h), and
a negative 24-hour fluid balance.
Communications should be addressed to:
Dr. Casado-Flores; Pediatric Intensive Care Unit; Hospital Infantil
Niño Jesús; Avenida Menéndez Pelayo 65; 28009 Madrid, Spain.
E-mail: jcasadof@line-pro.es
Received February 7, 2006; accepted May 10, 2006.
Jiménez et al: Cerebral Salt Wasting Syndrome and CNS Injury 261
Table 1. Clinical pattern of CSWS in 14 children

Minimum Plasma Maximum Urine Maximum Urine Diuresis Outcome

Age Diagnosis Sodium (mEq/L) Sodium (mEq/L) Osmolarity (mOsm/kgH2O) (mL/kg/h) (at PICU Discharge)

6 yr 2 mo astrocytoma 124 238 529 8 resolved

3 yr 6 mo astrocytoma 124 176 510 4.5 resolved
1 mo hydrocephalus 117 200 543 4.5 death
11 yr head trauma 129 211 762 5.4 nonresolved*
3 yr astrocytoma 98 225 626 10 death
15 yr astrocytoma 130 201 683 3.1 resolved
5 yr hydrocephalus 123 307 817 5.8 resolved
13 yr 2 mo astrocytoma 123 299 1132 3.1 resolved
4 yr 6 mo craniopharyngioma 124 283 731 15 resolved
15 mo hydrocephalus 123 197 480 4.3 resolved
11 yr head trauma 126 194 671 2.8 resolved
5 yr 9 mo choroid plexus tumor 129 146 471 4.8 resolved
12 mo hydrocephalus 123 285 789 11 resolved
8 yr 5 mo craniopharyngioma 119 104 284 4 resolved

* CSWS nonresolved, discharged with oral sodium supplementation.

Abbreviations:
CSWS ⫽ Cerebral salt wasting syndrome
PICU ⫽ Pediatric intensive care unit

Results charged with oral sodium supplementation. All patients

Cerebral salt wasting syndrome was diagnosed in 14
patients (9 males) whose mean age was 6.3 years ⫾ 4.6
(range, 1 month to 15 years).
The most common admitting diagnosis was brain tumor.
Of the 8 (57%) patients, 5 had astrocytoma, 2 had
craniopharyngioma, and 1 had choroid plexus tumor. The
second most common diagnosis was hydrocephalus (4
patients, 28.5%). Hydrocephalus was secondary to tuber-
culous meningitis (2 cases), intraventricular hemorrhage
(1 case), and sylvian aqueduct stenosis (1 case). All these
patients had undergone surgery (external drainage or
ventriculo-peritoneal shunt) before admission to the pedi-
atric intensive care unit. The other diagnosis was head
trauma (2 patients, 14.5%).
During the study period, 1229 postoperative neurosur-
gical patients were admitted to the pediatric intensive care
unit. The prevalence of cerebral salt wasting syndrome in
this group was 11.3 cases per 1000 neurosurgical patients.
Of the 14 patients, 11 (78.5%) manifested cerebral salt
wasting syndrome during the first 48 hours after admis-
sion, the rest between the third and the eleventh day.
The mean duration of the cerebral salt wasting syn-
drome was 6.3 ⫾ 5.4 days, range 1 to 19 days. All the
patients presented polyuria, with the mean highest diuresis
being 6.2 ⫾ 3.2 mL/kg/h (range 3-15 mL/kg/h), and
negative 24-hour fluid balance (mean ⫺39 ⫾ 32 mL/kg/
day).
Treatment consisted of volume and sodium correction
with a strict fluid and sodium balance every 2-4 hours. The
highest mean sodium supply was 1 mEq/kg/h (range,
0.1-2.4 mEq/kg/h). Parenteral replacement was adjusted to
each patient according to his or her urine losses, plasma
sodium, and fluid balance. Only one patient was dis-
responded to replacement therapy. Two patients died from
their central nervous system injury (brain tumor and
intraventricular hemorrhage).
Table 1 summarizes the clinical pattern of these 14
children with cerebral salt wasting syndrome.
Discussion
The incidence of postoperative hyponatremia has been
evaluated at 0.34%, and its mortality is significant [1]. The
main causes are the use of hypotonic fluids, syndrome of
inappropriate secretion of antidiuretic hormone, adrenal
insufficiency, extrarenal fluid losses, medication, and
cerebral salt wasting syndrome. Neurosurgical and head
trauma patients frequently present fluid and electrolyte
disturbances. Cerebral salt wasting syndrome is not a
common condition, but needs to be recognized because
these patients can develop hyponatremic encephalopathy
with catastrophic consequences.
Cerebral salt wasting syndrome prevalence and charac-
teristics in children are unknown. In this study, the
prevalence in postoperative neurosurgical practice was
high, 11.3/1000 cases. In their original report, Peter et al.
[4] described three patients with hyponatremia, increased
urinary sodium concentration, and excessive urine vol-
ume. Differentiation of this syndrome from syndrome of
inappropriate secretion of antidiuretic hormone is impor-
tant in children with acute brain disease. Both present with
hyponatremia as the basic symptom, but whereas cerebral
salt wasting syndrome presents inappropriately high urine
sodium concentration, excessive urine output, and nega-
tive fluid balance, syndrome of inappropriate secretion of
antidiuretic hormone is usually accompanied by increased

262 PEDIATRIC NEUROLOGY Vol. 35 No. 4

but not high urine sodium, oliguria, and positive fluid
balance. Fluid and salt restriction is the treatment for
syndrome of inappropriate secretion of antidiuretic hor-
mone, but this would increase morbidity in cerebral salt
wasting syndrome in which fluid and sodium replacement
are required [5]. A retrospective study of electrolyte
disturbances in 195 children with acute central nervous
system diseases identified 20 (10.3%) children with hypo-
natremia, seven of whom were diagnosed with syndrome
of inappropriate secretion of antidiuretic hormone and the
other nine with cerebral salt wasting syndrome [3].
Monitoring of plasma and urine sodium, urine osmolar-
ity, diuresis, and fluid balance allows us to promptly
identify these patients and to adjust water and salt replace-
ment to their needs.
All of the patients in the present study had a negative
24-hour negative fluid balance, but it was not clinically
significant. Signs of diminished fluid volume (e.g., ortho-
static hypotension, tachycardia, sunken eyes, dry mucous
membranes) were not significant. We do not think that a
negative fluid balance is necessary to make the diagnosis
of cerebral salt wasting syndrome because if the fluid
balance is monitored frequently, the fluid can be replaced
promptly, thus preventing the onset of volume depletion.
The response to saline infusion also helps to distinguish
between the two syndromes: in cerebral salt wasting
syndrome, sodium administration corrects volume deple-
tion and hyponatremia [6], whereas in the syndrome of
inappropriate secretion of antidiuretic hormone it would
be of limited or no benefit.
Serum antidiuretic hormone and atrial natriuretic pep-
tide are not helpful in distinguishing between syndrome of
inappropriate secretion of antidiuretic hormone and cere-
bral salt wasting syndrome [2]. Plasma atrial natriuretic
peptide levels are frequently high in some patients with
cerebral salt wasting syndrome but not always [7-9]. This
peptide causes natriuresis, diuresis, vasodilation, and sup-
pression of renin and aldosterone secretion [10]. The
concentration of atrial natriuretic peptide in the brain is
10,000 times less than in the heart [11], making it unlikely
that brain secretion of atrial natriuretic peptide is respon-
sible for cerebral salt wasting syndrome. Serum antidi-
uretic hormone is usually high in syndrome of inappropri-
ate secretion of antidiuretic hormone and low in cerebral
salt wasting syndrome, but many factors can promote its
secretion, including stress, pain, and intracranial pressure.
Patients in the postoperative period of an intracranial
disease are at a higher risk of developing cerebral salt
wasting syndrome, especially those with brain tumor,
hydrocephalus requiring surgery, head trauma, and, as
described elsewhere, tuberculous meningitis [12,13].
In conclusion, a significant number of neurosurgical
patients manifest cerebral salt wasting syndrome, fre-
quently during the first 48 postoperative hours. To recog-
nize and treat it promptly and appropriately, fluid and
sodium balance must be carefully monitored. With correct
treatment (fluid and salt replacement), severe neurologic
and hemodynamic complications can be prevented.
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