Saudi J Kidney Dis Transplant 2007;18(1):95-99

© 2007 Saudi Center for Organ Transplantation Saudi Journal

of Kidney Diseases
and Transplantation

Case Report

Cerebral Salt Wasting in a Patient with Head Trauma: Management with

Saline Hydration and Fludrocortisone
Akram Askar and Nauman Tarif

Department of Medicine, Division of Nephrology

King Khalid University Hospital, Riyadh, Saudi Arabia

ABSTRACT. Hyponatremia secondary to the syndrome of inappropriate anti-diuretic

hormone secretion is commonly observed in patients with various neurological disorders.
Cerebral salt wasting (CSW), although uncommon, has also been reported to frequently
result in hyponatremia. Here, we report a case of CSW in a patient with head trauma
without evidence of cerebrovascular injury or brain edema. He was diagnosed on the basis
of high fractional excretion of urinary sodium and uric acid along with extremely low
serum uric acid. Improvements in serum sodium levels after saline hydration and
fludrocortisone administration further supported the diagnosis, even in the presence of
normal brain and atrial natriuretic peptide levels.
Key Words: Hyponatremia, Cerebral salt wasting, SIADH

Introduction stroke etc. It occurs in up to 30% of patients

Hyponatremia is a common disorder that
occurs with a number of intracranial afflictions
including head injuries, tumors, infections,
Reprint requests and correspondence to:
Dr. Nauman Tarif
Consultant Nephrologist
Department of Medicine
King Khalid University Hospital
P.O. Box 2925 [38]
Riyadh 11461, Saudi Arabia.
e-mail: ntarif@yahoo.com
with subarachnoid hemorrhage (SAH). 1 The
syndrome of inappropriate anti-diuretic
hormone (SIADH) secretion is the cause of
hyponatremia in the majority of such cases. 2
Hyponatremia secondary to cerebral salt
wasting (CSW) has also been reported as a
result of various neurosurgical disorders,
although infrequently. 3-12 Confusion in
differentiating SIADH from CSW arises since
both results in similar electrolyte disturbances.
2, 13, 14
Herein, we report a case of a young
patient with head trauma, who was sub-
sequently diagnosed with CSW.
96
Case Report
A 17-year-old male was admitted to the
King Khalid University Hospital, Riyadh,
Saudi Arabia following a road traffic
accident. He suffered multiple injuries to
the face, chest, and pelvis and experience
closed-head trauma. He was unconscious
with a Glasgow coma scale of 7/15, had a
blood pressure of 100/60 mm Hg and pulse of
90 / min. He was resuscitated, intubated and a
computerized tomography (CT) scan revealed
an intact brain with no evidence of subdural
hematoma, SAH, intra-cerebral bleeding or
cerebral edema. Multiple facial bone fractures,
subcutaneous emphysema in the right chest
along with right lung contusion and multiple
pelvic bone fractures were noted. His baseline
investigations were normal with a serum
sodium (Na) level of 138 mmol/L. On day six
of admission, his serum sodium decreased to
120 mmol/L. Clinical evaluation at that time
revealed a central venous pressure (CVP) of 5
cm water; there was no evidence of edema
and oxygenation was maintained on 35%
FiO2. His urine output was around three liters
per day with a net negative fluid balance.
Pseudo-hyponatremia was excluded since he
had normal serum glucose, protein and lipid
levels and low serum osmolality. His urinary
Na was 229 mmol and urine osmolality was
630 mOsm/Kg. A diagnosis of hypovolemic
hyponatremia was made and saline infusion
was started. His serum Na rose to 136
mmol/L by day nine and subsequently
dropped to 123 mmol/L by day 15. Re­
evaluation of the patient showed that he was
normotensive with no peripheral edema and
his CVP line was removed. He still had a
urine output of 3-4 L/day. Urinary Na and
fractional excretion of Na [FENa] were high at
245 mmol/L and 2.2% respectively, along
with a high urine osmolality: of 783
mOsmol/Kg. A careful evaluation of his Na
Askar A, Tarif N
intake revealed that he received >700
mmol/L of Na from parenteral nutrition and
other intravenous fluids. His urinary
excretion of Na at the same time was also
of the same magnitude. A renal salt losing
state was therefore evident. Acute tubular
necrosis was excluded due to the absence of
any cause such as hypotension, medications
or sepsis. Thyroid function tests and serum
cortisol levels were also normal. A
diagnosis of CSW versus SIADH was
therefore entertained. The patient’s serum
uric acid level was found to be extremely
low at 56 mmol/L with a high fractional
excretion of urate [FEurate] of 55%. A trial
of fluid restriction from day 15 resulted in
an additional drop in serum Na to 116
mmol/L with low serum uric Acid and high
FEurate of 20%. Cerebral salt wasting was
confirmed and saline hydration was
initiated on day 20. Oral fludrocortisone 0.3
mg daily was added on day 24 and this
resulted in gradual improvement of serum
Na to 139 mmol/L by day 37. Under the
influence of fludrocortisone, the FENa
decreased while the FEurate remained high and
serum uric acid continued to be low (Table 1).
The brain natriuretic peptide (BNP) and atrial
natriuretic peptide (ANP) levels, tested at this
stage, were normal at 10 pg/ml (normal <17)
and 22 pg/ml (normal 5-43) respectively. The
patient was seen one month later in the
nephrology clinic with normal electrolytes and
serum uric acid. Fludrocortisone was tapered
and discontinued three weeks later. Repeat
investigations three weeks after discontinuation
of fludrocortisone were normal.
Discussion
Hyponatremia secondary to head trauma or
other central nervous system pathologies is well
known and mostly presents as SIADH. 2, 13, 14 In
1950, Peters et al described hyponatremia due
Cerebral Salt Wasting and Head Trauma 97

Table 1: Day to day changes in serum and urine electrolytes and fluid balance from the day of admission
to the ICU till correction of hyponatremia.
Day Blood Urine Fluid Balance
Sodium Urea Creatinine Uric Sodium Osmo­ FENa+ FEUrate Intake Output
(mmol/L) (mmol/L) (micromol/L) Acid (mmol/L) lality
1 138 5.8 65 - - - - - 3450 2310
4 136 3.3 51 - - - - - 3900 3790
5 128 4.8 52 - - - - - 4260 3400
6 120 5.1 49 - 229 630 - - 4365 4140
9* 136 2.8 44 - - - - - 3770 3740
15 123 6.9 46 56.6 245 783 2.2% 55% 3250 4500
19 120 4.4 42 25 - - - 19% 3200 4500
20** 116 4.2 33 - - - - - 2700 1700
26 125 4.5 54 63 99 - 0.59% 33% - -
30 138 4.6 44 133 - - 15% 1800 2300
37 139 5.2 53 169 80 938 0.63% 18% 650 + 800+
* = Improvement of serum Na after saline infusion.
** = Fludrocotisone was added

to salt wasting in three patients with cerebral
disease, seven years prior to the description of
SAIDH by Schwartz. 3, 15 CSW was regarded
as a rare entity, although several case reports
and case series in both adult and pediatric
patients have been reported. 3-12
Common to SIADH and CSW is hypo­
natremia, increased urinary Na excretion and
high urinary osmolality, as seen in our patient.
SIADH however, is a relatively volume
expanded state with inappropriately high ADH
levels. 2 In contrast, patients with CSW have
appropriately high ADH levels secondary to
the volume depletion that results from Na loss.
2, 13, 15
Evaluation of volume status may be
difficult in general as discussed by Chung et
al in their review of the subject. 16 Patients in
the intensive care unit setting could be
assessed by the measurement of their CVP. A
high urine output will further support salt
losing nephropathy rather than SIADH. This
point was stressed in the previous publications
as a clue to the diagnosis. In our patient, urine
output continued to be more than 3-4 liters per
day. 13, 15
Definitive diagnosis can be made by
documenting elevated levels of the natriuretic
peptides; ANP and BNP, although this may
not be a universal finding in all patients. 13,17,18
In our patient, the levels were within the
normal range as observed by other authors
as well. 13,18
Proximal tubular function defects in
patients with SIADH and CSW may also
help in differentiating the two conditions.
Blood urea nitrogen (BUN) increases in
patients with volume contraction as is seen
in CSW, whereas in patients with SIADH
with volume expanded state, the BUN is
usually on the lower side. This, however, is
not always observed and not very helpful. 2
This was evident in our patient (Table 1), in
whom the BUN levels remained in the
normal range and occasionally decreased
despite the presence of volume depletion.
Increased excretion of uric acid in patients
with SIADH is also the result of a defect in net
uric acid reabsorption in the proximal tubule.
19,20
The cause of this defect is unlikely to be
volume expansion and remains elusive.
Patients with AIDS and other neurological
disorders have also been found to have higher
fractional excretion of uric acid [FEurate] even
in the absence of, or even after correction of,
hyponatremia as reviewed in detail by
Maesaka. 2 The differentiation between
SIADH and CSW can therefore be made by
the observation that FEurate continues to be
98
high even after correction of hyponatremia
in the latter condition. 21,22 In our patient,
the FEurate was 55% initially and 18% even
when serum Na had been corrected to139
mmol/L (Table 1).
Management of SIADH and CSW are quite
different. Although both conditions require
high salt intake, volume restriction is required
in SIADH while volume expansion is required
in CSW. Wijdicks et al did a retrospective
analysis of 134 patients with subarachnoid
hemorrhage, of whom 17 patients were
diagnosed with SIADH. Fifteen of these
patients deteriorated after fluid restriction and
thus might have had CSW. 4 Appropriate
management of CSW is fluid replacement
with saline and addition of fludrocortisones,
similar to the treatment course undertaken for
our patient. 2, 13, 14, 23 Interestingly, in our
patient, the FENa decreased significantly to
<1%, likely under the influence of
fludrocortisone, while the patient maintained
high FEurate and increased serum Na levels.
Another interesting aspect in our patient was
the absence of any obvious cerebrovascular
injury or edema contributing to CSW
development. Following a detailed literature
search, we found one case report similar to our
patient who presented with CSW without
evidence of cerebrovascular injury or brain
edema. 11
In conclusion, hyponatremia secondary to
CSW in patients with various neurosurgical
disorders, even in the absence of obvious
injury, is not a rare occurrence. Diagnosis can
be established by the presence of volume
depletion and high fractional excretion of Na
and urate along with high urine osmolality.
The BNP levels, if available, may support the
diagnosis. Management requires salt and water
repletion along with fludrocortisone. It is
therefore important to monitor patients with
head trauma even in the absence of obvious
injury for prompt diagnosis and management
Askar A, Tarif N
of potentially dangerous electrolyte
abnormalities.
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