Letter to the Editor
Hyponatremia in Stroke and Response to Saline Infusion
Dear Editor,
Cerebral salt wasting (CSW), also known as renal salt
wasting, is a hyponatremic state that mimics all of the
laboratory findings observed in the syndrome of inap-
propriate antidiuretic hormone (SIADH) secretion. The
only clinical difference is the state of the extracellular
volume (ECV) being hypovolemic in CSW and euvolemic
or hypervolemic in SIADH. CSW is defined as ECV de-
pletion due to a renal sodium transport abnormality with
or without high urinary sodium concentration, the pres-
ence of hyponatremia, or cerebral disease with normal
adrenal and thyroid functions.1
We have read with great interest the paper written by
Kalita et al on CSW as the main cause of hyponatremia
after acute stroke (either ischemic or hemorrhagic).2 Al-
though we found valuable information about the evaluation
of hyponatremia in patients suffering acute stroke, we
are concerned about the diagnosis criteria used in this
prospective study to distinguish on clinical grounds CSW
from SIADH. These criteria may bias and contribute to
the high prevalence of CSW found by Kalita et al,2 mainly
due to the inadequacy of the approach used to deter-
mine the ECV in their cohort. We would like to highlight
some relevant points about evaluation of hyponatremia
in this group of patients.
First, the clinical assessment of volume status in pa-
tients with hyponatremia has a limited sensitivity and
specificity, with only approximately 50% of patients cor-
rectly identified.3
Second, in some patients with SIADH, serum sodium
improves with the infusion of isotonic saline; this re-
sponse can be predicted with the initial urine osmolality
(UO) lower than 530 mOsm/kg. In a landmark study by
Musch and Decaux, only patients with an initial UO greater
than 530 mOsm/kg had worsening hyponatremia in re-
sponse to isotonic saline infusion.4
Third, ideally the clinical suspicion of hypovolemia
should be confirmed by appropriate laboratory assess-
ment. Although hemoconcentration was listed as one of
the diagnostic criteria, the authors did not report on actual
hematocrit levels of patients diagnosed with CSW.2 Other
laboratory evaluations like the fractional excretion of urate
1052-3057/$ - see front matter
© 2017 National Stroke Association. Published by Elsevier Inc. All
rights reserved.
Journal of Stroke and Cerebrovascular Diseases, Vol. 26, No. 6 (June), 2017: pp 1391–1392
(FEurate) should also be used. A FEurate exceeding 11%
is consistent with either SIADH or CSW. However, by
repeating FEurate after correction of hyponatremia with
any therapeutic method (such as water restriction or
administration of hypertonic saline), it is possible to dis-
tinguish SIADH from CSW, because it will normalize to
4%-11% in SIADH and will remain >11% in CSW.5
Additionally, authors state in their introduction that dif-
ferentiating between CSW and SIADH is important because
of the differences in the management approach. However,
in this population of patients (either with acute isch-
emic or hemorrhagic stroke), managing “true” SIADH
patients with water restriction might increase the risk
of brain herniation and other adverse neurologic out-
comes. As recently proposed by Sterns and Silver, 6
hypertonic saline rather should be used in these set-
tings. Hence, although the criteria for differentiating
between these 2 hyponatremic syndromes might not be
optimal, this should not affect the decision to adminis-
trate salt.
Based on these arguments, we advise to interpret with
caution the conclusion that CSW is the main cause of hy-
ponatremia after either acute ischemic or hemorrhagic
stroke. Different groups should confirm this observation,
but more importantly, better diagnostic criteria should
be used to assess ECV and to distinguish CSW from
SIADH.
Diego Luis Carrillo-Pérez, MD
Department of Nephrology and Mineral Metabolism
Instituto Nacional de Ciencias Médicas y Nutrición Salvador
Zubirán, Mexico City, Mexico
E-mail: djiego51@gmail.com
Erwin Chiquete, MD, PhD
Department of Neurology and Psychiatry
Instituto Nacional de Ciencias Médicas y Nutrición Salvador
Zubirán, Mexico City, Mexico
Eduardo R. Argaiz, MD
Department of Nephrology and Mineral Metabolism
Instituto Nacional de Ciencias Médicas y Nutrición Salvador
Zubirán, Mexico City, Mexico
Eduardo Carrillo-Maravilla, MD
Department of Internal Medicine
Instituto Nacional de Ciencias Médicas y Nutrición Salvador
Zubirán, Mexico City, Mexico
http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2017.03.037
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References
1. Maesaka JK, Imbriano LJ, Ali NM, et al. Is it cerebral or
renal salt wasting? Kidney Int 2009;76:934-938.
2. Kalita J, Singh RK, Misra UK. Cerebral salt wasting is the
most common cause of hyponatremia in stroke. J Stroke
Cerebrovasc Dis 2017; pii: S1052-3057(16)30608-5.
doi:10.1016/j.jstrokecerebrovasdis.2016.12.011.
3. Chung HM, Kluge R, Schrier RW, et al. Clinical assessment
of extracellular fluid volume in hyponatremia. Am J Med
1987;83:905-908.
LETTER TO THE EDITOR
4. Musch W, Decaux G. Treating the syndrome of
inappropriate ADH secretion with isotonic saline. QJM
1998;91:749-753.
5. Maesaka JK, Imbriano L, Mattana J, et al. Differentiating
SIADH from cerebral/renal salt wasting: failure of the
volume approach and need for a new approach to
hyponatremia. J Clin Med 2014;3:1373-1385.
6. Sterns RH, Silver SM. Cerebral salt wasting versus
SIADH: what difference? J Am Soc Nephrol 2008;19:194-
196.