Online Letters to the Editor
monitoring or collect data on where the samples are taken.
Furthermore, monitoring the native cardiac output relative
to ECMO flow and the degree of ischemia prior to reperfu-
sion will be important to address the important hypotheses
raised by Winiszewski et al (1).
The authors have disclosed that they do not have any poten-
tial conflicts of interest.
Laveena Munshi, MD MSc, Eddy Fan, MD PhD,
Interdepartmental Division of Critical Care Medicine,
University Health Network/Sinai Health System, University of
Toronto, Toronto, ON, Canada
REFERENCES
1. Winiszewski H, Piton G, Perrotti A, et al: Hyperoxemia and Veno-
Arterial Extracorporeal Membrane Oxygenation: Do Not Forget the
Gut. Crit Care Med 2018; 46:e98–e99
2. Munshi L, Kiss A, Cypel M, et al: Oxygen thresholds and mortality dur-
ing extracorporeal life support in adult patients. Crit Care Med 2017;
45:1997–2005
DOI: 10.1097/CCM.0000000000002786
Hyponatremic Encephalopathy
To the Editor:
W
e have read with interest the article published in a
recent issue of Critical Care Medicine by Achinger et
al (1) about hyponatremic encephalopathy, which has
been first described by Arieff (2). Given that a respiratory arrest
can occur within the first hour following seizures, it is crucial to
initiate without delay a treatment able to lower intracranial pres-
sure and brain edema. We would like to underline several dis-
crepancies between the author’s recommendations and European
guidelines, which recommend to 150 mL NaCl 3% over 20 min-
utes, to be repeated every 20 minutes until a serum sodium (S Na)
increase of 5 mmol/L has been achieved. Such a gradient is needed
to significantly lower intracranial pressure and even rapidly reverse
transtentorial herniation in patients presenting brain herniation
not linked to hyponatremia (3). It is mandatory to check S Na after
each NaCl 3% infusion. An apparent lack of efficacy of this early
treatment could be linked to ongoing water reabsorption from the
gut, notably in case of “water intoxication” (primary polydipsia).
Some authors have proposed to look after a ventricular collapse
on brain tomodensitometry to assess the reality of brain edema.
Nevertheless, waiting for a brain tomodensitometry can result in
a loss of time so that it is preferable to promptly initiate NaCl 3%
infusions. Anyway, European guidelines also recommend limiting
the increase in S Na to a total of 10 mmol/L during the first 24
hours and an additional 8 mmol/L during every 24 hours until
the S Na concentration reaches 130 mmol/L. These goals differ for
the ones recommended by the author (increase of S Na by 15–20
mmol over 48 hr). The uncertainty of the degree of brain adap-
tation to its hypotonicity remains an issue. The same European
guidelines also suggest to consider to start an infusion of 10 mL/kg
body weight of electrolyte-free water (e.g., glucosesolutions) over
1 hour under strict monitoring of urine output and fluid balance
and also to discuss if it is appropriate to add IV desmopressin 2
e100 www.ccmjournal.org January 2018 • Volume 46 • Number 1
Copyright © 2017 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
µg, such S Na relowering could minimize brain damage due to an
overcorrection.
Another therapeutic option is to give urea (e.g., 30g through
gastric tube), which can result (in < 1 hr) in an osmotic gradi-
ent sufficient to significantly lower intracranial pressure and
to increase S Na afterwards (4). The advantages of urea in this
setting are to avoid fluid overload (and hence lung edema) and
also to prevent osmotic demyelinating syndrome (5). A further
prospective trial is needed to compare the classical treatment
of hyponatremic encephalopathy based on NaCl 3% with an
alternative treatment with urea.
The authors have disclosed that they do not have any poten-
tial conflicts of interest.
Guy Decaux, PhD, Fabrice Gankam, PhD, Frédéric
Vandergheynst, PhD, Departement of Internal Medicine,
University Hospital Erasme, Brussels, Belgium
REFERENCES
1. Achinger SG, Ayus JC: Treatment of Hyponatremic Encephalopathy
in the Critically Ill. Crit Care Med 2017; 45:1762–1771
2. Arieff AI: Hyponatremia, convulsions, respiratory arrest, and perma-
nent brain damage after elective surgery in healthy women. N Engl J
Med 1986; 314:1529–1535
3. Koenig MA, Bryan M, Lewin JL 3rd, et al: Reversal of transtentorial
herniation with hypertonic saline. Neurology 2008; 70:1023–1029
4. Annoni F, Fontana V, Brimioulle S, et al: Early effects of enteral urea on
intracranial pressure in patients with acute brain injury and hyponatre-
mia. J Neurosurg Anesthesiol 2017; 29:400–405
5. Soupart A, Schroëder B, Decaux G: Treatment of hyponatraemia by
urea decreases risks of brain complications in rats. Brain osmolyte
contents analysis. Nephrol Dial Transplant 2007; 22:1856–1863
DOI: 10.1097/CCM.0000000000002775
The authors reply:
W
e thank Decaux et al (1) for their interest in our
article (2), recently published in Critical Care Medi-
cine. We are happy that they endorse our approach
of active therapy for hyponatremic encephalopathy with the
use of hypertonic saline. However, we take exception when
they suggest that our approach differs from recent European
guidelines (3). It is important to note that we were the first to
introduce the concept of the use of intermittent boluses for
the treatment of hyponatremic encephalopathy in marathon
runners (4) with hyponatremia. We have continued to advance
this concept since that time (5). It is this original research upon
which the European guidelines are now based. There is no dis-
crepancy in the approach other than 150 mL of 3% saline as a
bolus rather than 100 mL as we have advocated. Please refer to
Figure 4 of our article (2) as our approach to hyponatremic
encephalopathy is detailed there.
Furthermore, we are a bit confused when Decaux el al
(1) suggest that 10 mL/kg of free water be given during the
treatment of hyponatremic encephalopathy as this would be
counterproductive. Likely, they are referring to actively relow-
ering the sodium if an overcorrection has occurred, in which
case we would agree with such. We also present in our article
(2) a detailed description of the use of desmopressin for the