Conclusion:
Hyponatremia may occur after severe traumatic brain injury that is why
an adequate treatment initiated on time is necessary in order to reduce
morbidity and mortality.
Keywords:
Cerebral Salt wasting, Hyponatremia, Syndrome of inappropriate
antidiuretic hormone, Traumatic brain injury
Introduction:
Cerebral salt wasting (CSW) syndrome is an uncommon cause of
hyponatremia in neurosurgical patients especially following traumatic
brain injury. Distinguishing it from the more familiar syndrome of
inappropriate antidiuretic hormone (SIADH) is crucial and it is vital to
make rapidly the right diagnosis in order to start an appropriate
treatment based on volume resuscitation and sodium restoration. Although
CSW has rarely been studied in the traumatic brain injury population
especially pediatric ones that is why we report a 15-year-old female
child with acute brain injury complicated of CSW managed by saline
hydration and fludrocortisone.
Written informed consent was obtained from the patient family for
publication of this case report and accompanying images. This manuscript
adheres to the SCARE guidelines.
Case presentation:
A 15-year-old female child was brought to the emergency department after
a motor vehicle accident (pedestrian struck by motor vehicle). She had
no significant past medical history and was not taking any regular
medications. Initial physical examination revealed neurological distress
with Glasgow come scale score of 4, decerebration and bilateral
mydriasis. Pulse rate was 100/min, blood pressure 120/65 mmHg,
respiratory rate 30/min and oxygen saturation 95%. Rapidly, she was
intubated and received osmotherapy with hypertonic saline.
Computed tomography revealed left fronto-temporal subdural hematoma
(6mm) with left temporal commitment and diffuse cerebral edema.
Neurosurgical opinion was sought. Therefore, she was admitted to
intensive care unit. Initial complete blood cell count and serum
biochemistry were without abnormalities and serum sodium concentration
was 140 mmol/L.
On day 6 of admission, the patient presented a significant increase of
urine output (more than 3mL/kg/h) with abnormalities in the transcranial
doppler ultrasonography. It was due to a low sodium level (124 mmol/L).
Possibility of cerebral salt wasting (CSW) and syndrome of inappropriate
antidiuretic hormone (SIADH) was considered. Urine osmolality and urine
sodium were 390 mosmol/L and 114 mmol/L respectively. She was also
hypovolemic so referred to the endocrinologist and nephrologist opinion,
CSW was the most suitable diagnostic.
Correction was started rapidly using hypertonic saline (2% saline) and
substantial volume replacement (equivalent of more than 3L/day of 2%
saline) in order to restore serum sodium to low normal levels within 48h
(sodium 135 mmol/L). Saline infusion (1.2% saline) was given as
maintenance fluid during his hospitalization. However, on day 12 of
admission, his sodium level continued to fall despite infusion of
hypertonic saline. That is why fludrocortisone was introduced initially
at 50 µg/day then increased to 150 µg/day. Introduction of this molecule
resulted in a fall in requirements for hypertonic saline. Although,
starting from day 25 of admission, serum sodium levels remained stable
around 135 mmol/L on fludrocortisone alone and she was discharged home
30 days post injury.
It worth noting that during his hospitalization, magnetic resonance
imaging of the brain was done objectifying an encephalitis treated by
antibiotics (Linezolid and Meropenem).
Fludrocortisone was continued for the next months. Serum sodium level
was 138 mmol/L after one month of treatment. Since she was discharged,
she has been followed by an endocrinologist.
Discussion:
Cerebral salt wasting is resulting in hyponatremia and poorly
hypovolemia caused by renal loss of sodium following intracranial
disorders (1) which was first described by Peters et al (2) in 1950. The
mechanisms leading to CSW remain an area of debate and one of the
hypothesis is that, after a brain injury, there is an increasing of
levels natriuretic peptides hormones which inhibit sodium reabsorption
and decrease release of renin (3).
It is important and complex to distinguish CSW from the syndrome of
inappropriate secretion of antidiuretic of hormone (SIADH) as treatments
are different. The combination of excess fluid and hyponatremia in SIADH
is treated by water restriction whereas in CSW hypovolemia necessitates
replacement of both water and sodium. It is crucial to treat
hyponatremia correctly because it can worsen cerebral edema or result in
seizure, however when it is sub-optimally treated, it would cause
osmotic demyelination (4).
CSW is most commonly studies in patients with aneurysmal subarachnoid
hemorrhage with high incidence of hyponatremia up to 57% according to
sherlock et al (5). Although, traumatic brain injury (TBI) could be
associated with hyponatremia, however literature studying CSW in TBI
population is poor with little information available on physiopathology
and outcomes. Furthermore, Leonard et al (6) found that incidence of CSW
in TBI patients was from 0.8% to 34.6% and it was developed within
days to two months post-injury. It occurs in patients of all ages but it
has been suggested that CSW takes a different course in children
compared to adults. Nine pediatric cases of CSW due to TBI were
published in the literature as well as we know (Table 1). Three patients
developed CSW two days post traumatic (7–9), two developed CSW after
one week (8,10) and four developed CSW between two weeks and two months
post traumatic (11–14).
Concerning the management of CSW, it is based on the correction of
intravascular volume depletion and hyponatremia. However, close
monitoring of saline sodium level is crucial in order to prevent overly
rapid correction of hyponatremia (15). Moreover, pharmacological
intervention could be necessary in some cases especially Fludrocortisone
which is recommended as a potential therapeutic option. Misra et al (16)
proved that Fludrocortisone may result in earlier normalization of serum
sodium in patients with cerebral salt wasting as a part of tuberculous
meningitis.
Conclusion:
Hyponatremia could be present after traumatic brain injury. Every
clinician should be aware of the importance of making the right
diagnosis on time and distinguishing CSW from SIADH which they have
opposite treatment. So, we reported this case in order to emphasize the
role of initiating appropriate treatment rapidly in reducing morbidity
and mortality of hyponatremia.
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