Intensive Care Med (2010) 36:304–311
DOI 10.1007/s00134-009-1692-0
Georg-Christian Funk
Gregor Lindner
Wilfred Druml
Barbara Metnitz
Christoph Schwarz
Peter Bauer
Philipp G. H. Metnitz
Received: 3 April 2009
Accepted: 23 September 2009
Published online: 22 October 2009
! Copyright jointly hold by Springer and
ESICM 2009
On behalf of the ASDI Study Group.
G.-C. Funk and G. Lindner contributed
equally to this study.
Electronic supplementary material
The online version of this article
(doi:10.1007/s00134-009-1692-0) contains ther the presence of disorders of
supplementary material, which is available sodium balance on ICU admission is
to authorized users.
G.-C. Funk ())
Department of Respiratory and Critical Care critically ill patients. Methods: We
Medicine, Otto Wagner Spital,
Vienna, Austria
e-mail: georg-christian.funk@wienkav.at
G. Lindner ()) ! P. G. H. Metnitz
Department of Anesthesiology and General period of 10 years (1998–2007).
Intensive Care Medicine, Medical
University of Vienna, Währingergürtel
18-20, 1090 Vienna, Austria
e-mail: lindner.gregor@gmail.com
Tel.: ?43-1-404004109
Fax: ?43-1-404004104
W. Druml
Department of Nephrology and Dialysis,
Medical University of Vienna,
Vienna, Austria
ORIGINAL
Incidence and prognosis of dysnatremias
present on ICU admission
B. Metnitz ! P. Bauer
Department of Medical Statistics, Medical
University of Vienna, Vienna, Austria
C. Schwarz
Third Medical Department, Krankenhaus
der Elisabethinen, Linz, Austria
Abstract Purpose: Dysnatremias
are common in patients admitted to
the intensive care unit (ICU). Whe-
independently associated with excess
mortality is unknown. We hypothe-
sized that dysnatremias at the time of
ICU admission are independent risk
factors for increased mortality in
conducted a retrospective study in 77
medical, surgical, and mixed ICUs in
Austria, with a database of 151,486
adults admitted consecutively over a
Results: Most patients (114,170,
75.4%) had normal sodium levels
(135 B Na B 145 mmol/L) on ICU
admission. The frequencies of bor-
derline (130 B Na \ 135 mmol/L),
mild (125 B Na \ 130 mmol/L), and Epidemiology
severe hyponatremia (Na \
125 mmol/L) were 13.8%, 2.7%, and
1.2%, respectively. The frequencies
of borderline
(145 \ Na B 150 mmol/L), mild
(150 \ Na B 155 mmol/L), and
severe hypernatremia (Na [ 155
mmol/L) were 5.1%, 1.2%, and 0.6%,
respectively. All types and grades of
dysnatremia were associated with
increased raw and risk-adjusted
hospital mortality ratios. Multiple
logistic regression analysis showed an
independent mortality risk rising with
increasing severity of both hypona-
tremia and hypernatremia. Odds
ratios and 95% confidence interval
(CI) for borderline, mild, and severe
hyponatremia were 1.32 (1.25–1.39),
1.89 (1.71–2.09), and 1.81
(1.56–2.10), respectively. Odds ratios
and 95% CI for borderline, mild, and
severe hypernatremia were 1.48
(1.36–1.61), 2.32 (1.98–2.73), and
3.64 (2.88–4.61), respectively.
Conclusions: Our results suggest
that both hypo- and hypernatremia
present on admission to the ICU are
independent risk factors for poor
prognosis.
Keywords Hyponatremia !
Hypernatremia ! Sodium ! Outcome !

Introduction
Dysnatremias (hyponatremia and hypernatremia) are
common findings on admission of patients to the intensive
care unit (ICU) [1–3] and can adversely affect various
physiologic functions and organ systems [4–7]. Limited
evidence suggests that dysnatremias on ICU admission
may be associated with adverse outcome [3].
The prevalence of hyponatremia on ICU admission is
between 13.7% and 15%, depending on the cutoff value
for normal sodium [2, 8]. In a retrospective analysis,
severe hyponatremia (Na \125 mmol/L) on ICU admis-
sion was suggested to be an independent predictor of
hospital mortality [2]. However, it was not determined
whether mild and borderline hyponatremia were also
associated with increased mortality.
Hypernatremia on ICU admission is found in 2–9% of
patients [1, 3]. Hypernatremia acquired during the ICU
stay is an independent risk factor for mortality in critically
ill patients [3]. Because the origin of hypernatremia is
often iatrogenic, hypernatremia acquired in the ICU has
been regarded as an indicator of the quality of ICU care
[1]. However, it is not known whether the presence of
hypernatremia on ICU admission is also independently
associated with excess mortality.
We hypothesized that dysnatremias on ICU admission
were independent risk factors for increased mortality in
critically ill patients. To test this hypothesis, we analyzed
a large prospective database of patients admitted to
Austrian medical, surgical, and mixed ICUs between
1998 and 2007.
Materials and methods
Database
Data were collected by the Austrian Center for Docu-
mentation and Quality Assurance in Intensive Care
Medicine (ASDI), a nonprofit organization that has
established an intensive care database and benchmarking
project [9, 10]. The prospectively collected data included
sociodemographic information, such as age, sex, and
comorbid conditions; causes of ICU admission according
to a predefined list of medical and surgical diagnoses
[11]; severity of illness, as measured by the Simplified
Acute Physiology Score (SAPS) II [12]; number and
severity of organ dysfunction, as measured by the
Logistic Organ Dysfunction system [13]; length of ICU
and hospital stay; and outcome data, including survival
status at ICU and hospital discharge. Data collectors
coded diagnoses on the basis of documentation in the
patients’ medical records. The study protocol was
approved by the institutional review board. Since no
additional interventions were performed and no individual
305
data were analyzed, the need for informed consent was
waived.
A total of 176,703 patients were admitted to the 77
ICUs during the 10-year study period. For patients who
were admitted more than once, only the first admission
was evaluated. Patients who were\18 years of age, those
with records that lacked an entry in the field ‘‘hospital
outcome,’’ those without a valid SAPS II score, and those
with missing sodium values were excluded, leaving
151,486 patients for analysis (Fig. 1).
Data quality was ascertained using prespecified
methods. Details are reported in the Electronic Supple-
mentary Material (ESM).
Sodium values on ICU admission
Data collectors entered into the database the most
abnormal (i.e., highest or lowest) serum sodium value
measured within 24 h after ICU admission. A range check
was applied to serum sodium during data entry, rejecting
values\50 mmol/L or[200 mmol/L. Values\80 mmol/L
or [180 mol/L required confirmation by the data
collector.
Since the association of serum sodium with hospital
mortality is not linear but U-shaped (Table 1), it was
treated as a categorical variable. Hyponatremia was cat-
egorized as borderline (130 B Na \ 135 mmol/L), mild
(125 B Na \ 130 mmol/L) or severe (\125 mmol/L).
Hypernatremia was also categorized as borderline
(145 \ Na B 150 mmol/L), mild (150 \ Na B 155
mmol/L), or severe ([155 mmol/L). Normal serum
sodium (135 B Na B 145 mmol/L) was used as the
reference category. Sodium-corrected SAPS II scores
were calculated as original SAPS II score minus the
allocated sodium points.
Statistical analysis
Statistical analysis was performed using SAS software,
version 9.1 (SAS Institute, Cary, NC). The chi-square test
and analysis of variance (ANOVA) were used when
appropriate. Unless otherwise specified, descriptive
results are expressed as median and first and third quar-
tiles. Observed-to-expected mortality ratios were
calculated by dividing the number of observed deaths per
group by the number of SAPS II-predicted deaths per
group. Confidence intervals (95%) were calculated
according to the formula described by Hosmer and
Lemeshow [14].
Logistic regression analysis was used to explore the
influence of sodium on mortality. Vital status at hospital
discharge (hospital mortality) was used as the dependent
variable. Details about the model are given in the ESM.
306
Fig. 1 Study flowchart. SAPS,
Simplified Acute Physiology
Score
Results
A total of 151,486 consecutively admitted ICU patients
were included in the cohort. Types of ICU admission were
medical and neurologic disorders in 72,352 patients
(48.0%), elective surgery in 48,566 (32.2%), and emer-
gency surgery in 29,925 (19.8%). ICU length of stay was 3
(2–7) days. Overall ICU mortality was 12.0%, and overall
hospital mortality was 17.6%. The majority of patients
(114,170, 75.4%) had normal sodium on ICU admission.
The frequencies of borderline, mild, and severe hypona-
tremia were 13.8%, 2.7%, and 1.2%, respectively. The
frequencies of borderline, mild, and severe hypernatremia
were 5.1%, 1.2%, and 0.6%, respectively. All types and
grades of dysnatremia were more common in patients who
died during hospitalization.
Raw and risk-adjusted hospital mortality increased with
increasing severity of hyponatremia and hypernatremia.
Unadjusted associations of dysnatremias with outcome,
demographic data, and clinical characteristics are shown in
Table 1 and Table E1. The univariate association of
dysnatremias with outcome was confirmed in the multi-
variate model adjusting for predefined confounders
(Table E2). Univariate and multivariate associations of
dysnatremias with hospital mortality are shown in Fig. 2.
Including age as a risk factor in the multivariate
logistic model showed an added effect over that of age
contained as an item in the SAPS II. However, the basic
 307

\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
\0.0001
SAPS Simplified Acute Physiology Score, SD standard deviation. Comparisons between groups were made using analysis of variance (ANOVA) or the chi-square test
P

52 (40–66)
(n = 965)

5 (2–14)
62 ± 19

4 (3–4)
Severe

56.2
58.0

32.3

46.1

57.8
0.6

9.8
(n = 1,846)

46 (33–62)

6 (2–15)
62 ± 18

3 (2–4)
Mild

58.9
52.4
12.2
35.4

36.2

45.3
1.2
Hypernatremia

(n = 7,723)

37 (25–52)
Borderline

5 (2–12)
62 ± 19

3 (2–4)
57.8
52.9
18.0
29.1

21.1

28.5
5.1
Normal sodium

Fig. 2 Unadjusted (open circles) and adjusted (filled circles) risk

(n = 114,170)
Table 1 Unadjusted associations of dysnatremia with patients’ demographic, clinical, and outcome characteristics

of hospital mortality stratified by serum sodium on ICU admission.

27 (19–39)

CI, confidence interval

63 ± 17

2 (1–3)

3 (2–6)
75.4

58.7
47.1
34.0
18.9

14.6
9.7

relationship of sodium levels to adjusted mortality did not

(n = 20,842)

change. We performed a sensitivity analysis within sub-

32 (22–45)
Borderline

groups defined by age below and above the median in the

64 ± 16

2 (1–3)

4 (2–8)

model. In principle, the same pattern of dependence of

13.8

57.2
44.2
35.3
20.5

14.3

21.2

sodium levels was observed: In the lower age group the

U-shaped form of relationship was much more accentu-
ated; also, the odds ratio was 2.73 (2.26–3.30) for severe
(n = 4,076)

37 (27–53)

hyponatremia and 4.17 (3.03–5.74) for severe hyperna-

64 ± 16

3 (2–4)

4 (2–8)

tremia, compared with 1.43 (1.12–1.83) and 3.33 (2.34–

Mild

55.7
63.2
18.3
18.5

23.1

32.9
2.7

4.74), respectively, in the higher age group. We also

looked at the high-risk group of patients who had a
Hyponatremia

(n = 1,864)

sodium-corrected SAPS II score above the median (range

39 (28–53)

28–121). In this subgroup the risk pattern again showed

62 ± 16

3 (2–4)

4 (2–8)
Severe

the U-shaped form, with odds ratio of 1.77 (1.47–2.12) in

58.6
79.1

12.1

24.0

33.6
1.2

8.8

the severe hyponatremia group and up to 3.21 (2.46–4.19)

in the severe hypernatremia group. In the lower-risk
Sodium-corrected SAPS II score, median (quartiles)

group the range of the sodium-corrected SAPS II score

was too narrow to obtain reliable estimates for the risk
relationship.
Length of ICU stay, days, median (quartiles)
Number of organ failures, median (quartiles)

Interaction terms of hypo- and hypernatremia with the

Unscheduled surgical type of admission

sodium-corrected SAPS II score were significant in the

Scheduled surgical type of admission

logistic model, indicating that the effect of sodium-cor-

rected SAPS II score on mortality varied within the
Observed hospital mortality (%)

different types and grades of dysnatremia (Table E2).

Observed ICU mortality (%)

Specifically, the mortality risk associated with an increase

Medical type of admission
Age (years), mean ± SD

in the sodium-corrected SAPS II score decreased with

Patients affected (%)

increasing severity of both hypo- and hypernatremia.

Due to the extremely large sample size and the
resulting small variability of the estimated mortality not
Characteristic

surprisingly the application of a goodness-of-fit test

Males (%)

indicated a rather poor fit of the regression model (chi-

square 505.12, p \ 0.0001). However, there was good
agreement between observed and estimated mortality in
308

the low- to moderate-risk patients. Noticeable deviations Hyponatremia is often the consequence of chronic
between observed and estimated mortality occurred only organ dysfunctions such as heart failure or liver cirrhosis
in high-risk patients, with a maximum deviation of 3.6 [4]. Therefore hyponatremia on ICU admission may often
percent points for patients in the highest-risk decile. be a surrogate for severe underlying comorbidity and
hence be associated with increased mortality. However,
this effect was addressed in the present analysis by mul-
tivariable adjustment for comorbidities, main diagnosis
Discussion responsible for ICU admission, and the severity of illness.
The results suggest that hyponatremia itself carries a risk
This is the largest study available on the association of increased mortality. The increased prevalence of
between dysnatremias and the outcome in critical illness. hyponatremia in patients with comorbid cirrhosis and
It demonstrates that both hyponatremia and hypernatre- heart failure indicates that the confounding effects of
mia, when present at ICU admission, are independent these comorbidities were sufficiently covered.
prognostic factors for risk-adjusted hospital mortality in Apart from chronic heart and liver disease, hyponatre-
critically ill patients. Even borderline dysnatremias were mia may be the consequence of diuretic use, the syndrome
associated with increased hospital mortality, independent of inappropriate antidiuretic hormone (ADH) secretion,
of the severity of the underlying disease. adrenal insufficiency, and cerebral or renal salt wasting
Hyponatremia is the most common electrolyte disor- [23]. These conditions are potential confounders of the
der and can be found in 30–40% of hospitalized patients, association between hyponatremia and outcome, but should
depending on the cutoff value of normal serum sodium at least partly manifest in an increased SAPS II score,
[15]. Recently, the presence of hyponatremia on hospital which in turn was adjusted for in the multivariable model.
admission was reported to be independently associated Beyond the statistical adjustment for underlying
with an increase in the need for intensive care and thus an problems it is quite plausible that hyponatremia itself has
increase in costs and mortality [16]. Much less is known an unfavorable effect on prognosis, since both acute and
about hyponatremia when present on admission of criti- chronic hyponatremia have dismal consequences for the
cally ill patients to the ICU. In a retrospective analysis brain; for example, in cirrhosis, hyponatremia is definitely
Bennani et al. found the prevalence of hyponatremia, a surrogate for the severity of liver disease, however, in
defined as a serum sodium level \130 mmol/L, on addition it is believed to contribute to hepatic encepha-
admission to the ICU to be 14% compared with our lopathy [24].
finding of about 4% [2]. A multivariate analysis showed In addition to the direct cerebral consequences of
that severe hyponatremia (Na \125 mmol/L) on ICU hyponatremia its association with outcome may also be
admission was independently associated with an increase explained by inadequate treatment. Correction rates of up
in mortality [2]. This finding was confirmed in our study. to 12 mmol/L per day are recommended to be safe [4],
In addition, our study is the first to demonstrate that even but they are based on retrospective data only and have not
small decreases in serum sodium are independently been tested in prospective trials. Osmotic demyelination
associated with adverse outcome in critically ill patients. may even occur at correction rates below 12 mmol/L per
Studies on hypernatremia have traditionally focused on day, depending on the individual time of development of
electrolyte disturbance as a geriatric disease [17–20]. More hyponatremia. Hyponatremia should only be treated
recently, hypernatremia was shown to be a problem in acutely if it is documented to have started no longer than
critically ill patients as well. Hypernatremia acquired dur- 48 h before [25]. However, the previous duration of
ing the ICU stay was identified as an independent risk factor hyponatremia detected on ICU admission is mostly
for mortality [3, 21, 22]. In contrast, patients with hyper- unknown, suggesting that too rapid correction may not be
natremia on admission to the ICU were reported to have a a rare problem.
comparatively low mortality, but these subjects were At the other end of the spectrum, the association
mostly elderly patients with hypertonic volume depletion between hypernatremia and outcome may also be due to
[1]. Until now, no multivariate methods adjusting for dis- both the underlying diseases and the direct unfavorable
ease severity had been performed to assess the influence of effects of hyperosmolality. Hypernatremia on ICU
hypernatremia at the time of ICU admission on patient admission clearly indicates that the patient has some sort
outcome. Our study shows for the first time that hyperna- of neurological impairment preventing adequate water
tremia on ICU admission is independently associated with uptake. Severe hypernatremia may be a marker of
prognosis. Notably, even small elevations in serum sodium advanced underlying neurological impairment, and
levels, which are often neglected, are reflected in a sub- intensive care physicians or surrogate decision-makers
stantial increase in mortality risk. In our study the increased might be more likely to limit or withdraw care if the
mortality risk associated with severe hypernatremia was dementia or other neurological disease were advanced.
not only restricted to older patients but was even higher in However, such major neurological impairment should be
younger patients. covered by the Glasgow Coma scale which, as a part of

the SAPS II score, is adjusted for in the multivariable
regression. On the other hand this may not be true for
mild dementia with preserved major neurological func-
tions but already impaired thirst and water uptake. While
we do not have information about the prevalence of mild
cognitive impairment on ICU admission, it may represent
an important confounder of the relationship between
hypernatremia and mortality.
Hypernatremia acquired in the ICU is an iatrogenic
problem caused by the excess administration of hypertonic
solutions and inadequate water substitution [26, 27]. This is
probably also true for noncritically ill hospitalized patients.
Hence when hypernatremic hospitalized patients are
admitted to the ICU their hypernatremia may often not only
be related to the underlying disease but also to malpractice.
Hypernatremia has multiple adverse effects on physi-
ologic functions, which may explain its association with
increased mortality. Hypernatremia aggravates peripheral
insulin resistance [7], impairs hepatic gluconeogenesis and
lactate clearance [6, 28], and decreases left ventricular
contractility [29]. Additionally, hypernatremia is associ-
ated with various neuromuscular manifestations, such as
muscle weakness and cramps [30]. Neurologic impairment
is the most severe consequence of hypernatremia and may
prolong the need for mechanical ventilation and delay
weaning [5]. Finally too rapid correction of chronic
hypernatremia can cause cerebral edema [5].
While there is no proven beneficial effect on func-
tional outcome, iatrogenic hypernatremia can be used for
the treatment of intracranial hypertension [31]. In our data
hypernatremia was more common in patients with trauma.
However, whether this is due to traumatic brain damage
with subsequent diabetes insipidus or due to a therapeutic
intervention cannot be differentiated based on our data.
Some diagnoses are associated on the one hand with
dysnatremias and on the other hand with poor prognosis
itself, e.g., diabetes insipidus after severe head trauma, or
the syndrome of inappropriate ADH secretion after
complicated neurosurgery for subarachnoid hemorrhage.
The severity of these states was not taken into account by
either the main diagnoses or the comorbidities, since
‘‘trauma,’’ ‘‘neurologic disease’’ or ‘‘neurosurgery’’ were
associated with good prognosis in a majority of patients.
Therefore, logistic regression does not exclude the pos-
sibility that dysnatremias are markers of disease severity
rather than an additional factor for bad prognosis.
Overall, the association of dysnatremias with increased
mortality is likely to be a combination of the effects of
underlying organ dysfunction and the harmful conse-
quences of the dysnatremias itself. While dysnatremias
have various unfavorable physiological consequences,
cerebral dysfunction is the most severe one. Dysnatremias
and their inadequate treatment impair cerebral function
and consecutively both hyponatremia and hypernatremia
are risk factors for ICU-acquired delirium [32]. Delirium
in turn contributes to increased morbidity and mortality in
309
the ICU [33, 34] and could therefore at least partly explain
the association of dysnatremias with outcome.
The prognostic importance of hypernatremia may be
underestimated by the SAPS II, a scoring system used
worldwide to assess the severity of disease. SAPS II
assigns more points to hyponatremia than to hypernatre-
mia. This is in contrast to our finding that increases in
serum sodium are associated with a higher mortality risk
than similar decreases in serum sodium.
The mortality associated with the severity of the
underlying disease (measured by sodium-corrected SAP-
S II score) depends on the presence and severity of both
hypo- and hypernatremia. The more abnormal the serum
sodium, the lower the effect of an increase in the sodium-
corrected SAPS II score. Individual risk can be estimated
from the respective odds ratios (Table E2); e.g., a patient
with severe hyponatremia (serum sodium \125 mmol/L)
on ICU admission has a 1.81-fold greater risk of dying if
the comparable sodium-corrected SAPS II score is at the
mean value of the cohort (32.6). A patient with the same
sodium but with a sodium-corrected SAPS II score of
42.6 (i.e., a 10-point increase) has an increased mortality
risk of 1.81 9 1.82 = 3.29.
There are some limitations to the current study. First,
we obtained serum sodium values on ICU admission but
not during the ICU stay. Therefore, dysnatremias acquired
during treatment in the ICU are not discussed in this
paper. Second, the participating ICUs may have used
different methods to measure serum sodium. However,
since the cohort was very large, and the contributing ICU
was included as a covariable in the multivariate logistic
model, the main results of the study should be unaffected
by such differences.
The results of this observational study cannot prove
causality but can be used for generating hypotheses. We
speculate that avoidance and appropriate treatment of
dysnatremias may improve prognosis. This hypothesis
should be clarified in a prospective interventional trial
randomizing patients with dysnatremia on ICU admission
to either normalization of serum sodium according to a
treatment algorithm (treatment group) or usual care
(control group). Additionally, future research may pro-
vide deeper insight into the effects of hypo- and
hyperosmolarity on cellular functions and organ systems,
even on a molecular level. Serum osmolarity is regulated
within a very narrow range in healthy humans, suggesting
that it may be critical to avoid disturbances of serum
sodium if possible, or at least adequately treat them [35].
Conclusions
Both hyponatremia and hypernatremia present on ICU
admission may be independent risk factors for poor
prognosis. This applies even to borderline and mild types
310

of hypo- and hypernatremia. The effect of early treatment
of dysnatremias in ICU patients should be clarified in a
prospective interventional trial.
Acknowledgments We thank the members of the ASDI study
group and the respective study coordinators in each intensive care
unit:
Hubert Artmann, Kardinal Schwarzenberg’sches Krankenhaus,
Schwarzach/Pongau; Andreas Bacher, AKH Wien Universitätsk-
liniken, Wien; Thomas Bauer, LK Krems; Florin-Voicu Botha,
Landes-Nervenklinik Linz Wagner-Jauregg, Linz; Georg Dezsenyi,
LK Waldviertel Horn; Kurt Dörre, LK Waldviertel Waidhofen a.d.
Thaya; Günther Edelmann, KA Rudolfstiftung, Wien; Ingrid Eder,
UKH Linz; Felix Ernst, LK Weinviertel Mistelbach; Ulrike Fas-
ching, A.ö. LKH Steyr; Fritz Firlinger, A.ö. KH der Barmherzigen
Brüder Linz; Herbert Fresacher, KH Hietzing m.Neurolog.Zentrum
Rosenhügel, Wien; Norbert Fritsch, A.ö. LKH Enns; Alexander
Geppert, Wilhelminenspital der Stadt Wien; Peter Grausenburger,
LK Krems; Burkhart Gustorff, Wilhelminenspital der Stadt Wien;
Georg Halvax, A.ö. KH der Barmherzigen Brüder St.Veit; Bern-
hard Hartenthaler, A.ö. LKH Vöcklabruck; Gottfried Heinz, AKH
Wien Universitätskliniken, Wien; Ursula Hiermanseder, A.ö. LKH
Schärding; Michael Hiesmayr, AKH Wien Universitätskliniken,
Wien; Michael Hill, A.ö. KH der Barmherzigen Brüder Eisenstadt;
Martin Holzleithner, A.ö. LKH Gmunden; Kurt Hudabiunigg, UKH
Graz; Wolfgang Hufnagl, KH der Barmherzigen Brüder Salzburg;
Thomas Janous, LK Waldviertel Zwettl; Sylvester Klaunzer, UKH
Salzburg; Walter Klimscha, Donauspital SMZ Ost, Wien; Ilse
Köfler, A.ö. LKH Bad Ischl; Gerhard Koinig, LK Thermenregion
Neunkirchen; Claus Krenn, AKH Wien; Universitätskliniken,
Wien; Dietmar Krucher, LK St. Pölten; Karl Lampl, LK Voralpen
Lilienfeld; Peter Liebhart, LK Waldviertel Horn; Dieter Linemayr,
LK Mödling; Siegfried Lister, Hartmannspital, Wien; Gottfried
Locker, AKH Wien Universitätskliniken, Wien; Christian Madl,
AKH Wien Universitätskliniken, Wien; Heinz Malle, UKH Kla-
genfurt; Walter Mauritz, UKH Lorenz Böhler, Wien; Alfred
Meguscher, KH Hietzing m.Neurolog.Zentrum Rosenhügel, Wien;
Gerfried Naderer, LK Weinviertel Hollabrunn; Petrus Novotny, KH
Hietzing m.Neurolog.Zentrum Rosenhügel, Wien; Brigitte Pichler,
LK Weinviertel Mistelbach; Walter Plöchl, AKH Wien Universi-
tätskliniken, Wien; Georg Pötzl, Neurologisches Krankenhaus
Rosenhügel, Wien; Thomas Publig, KH Hietzing m.Neuro-
log.Zentrum Rosenhügel, Wien; Richard Rabitsch, A.ö. LKH
Rohrbach; Johanna Rech, A.ö. KH der Barmherzigen Brüder Linz;
Wolfgang Regal, Kaiser-Franz-Josef-Spital Wien; Michael Rosner,
Kaiser-Franz-Josef-Spital Wien; Günter Sagmüller, UKH Meidling;
Stefan Schatzl, KH Hietzing m.Neurolog.Zentrum Rosenhügel,
Wien; Ingrid Schindler, Sozialmedizinisches Zentrum Floridsdorf,
Wien; Oswald Schuberth, A.ö. LKH Kirchdorf; Reinhard Schuster,
Donauspital SMZ Ost, Wien; Franz Schwameis, LK Thermenre-
gion Baden; Christian Spiess, AKH Wien Universitätskliniken,
Wien; Gabriele Sprinzl, LK Donauregion Tulln; Franz Sterrer, Aö
LKH Vöcklabruck; Franz Tichelmann, SMZ Baumgartner Höhe,
Otto-Wagner-Spital, Wien; Helmut Trimmel, LK Wr. Neustadt;
Roman Ullrich, AKH Wien Universitätskliniken, Wien; Andreas
Valentin, KA Rudolfstiftung, Wien; Herbert Vesely, Hanusch
Krankenhaus, Wien; Ernst Weilguny, A.ö. LKH Freistadt; Christian
Weinstabl, AKH Wien; Universitätskliniken, Wien; Franz Wim-
mer, Kardinal Schwarzenberg’sches Krankenhaus, Schwarzach/
Pongau; Peter Zanon, Zentrales Krankenhaus Bozen; Michael
Zeilinger, Sozialmedizinisches Zentrum Floridsdorf, Wien.
Conflicts of interest The authors have no actual or potential
conflicts of interest. There was no financial support for the reali-
zation of this study. The authors have full control of all primary
data and agree to allow the journal to review their data if requested.

References
1. Polderman KH, Schreuder WO, Strack
van Schijndel RJ, Thijs LG (1999)
Hypernatremia in the intensive care
unit: an indicator of quality of care?
Crit Care Med 27:1105–1108
2. Bennani SL, Abouqal R, Zeggwagh
AA, Madani N, Abidi K, Zekraoui A,
Kerkeb O (2003) Incidence, causes and 7.
prognostic factors of hyponatremia in
intensive care. Rev Med Interne
24:224–229
3. Lindner G, Funk GC, Schwarz C,
Kneidinger N, Kaider A, Schneeweiss
B, Kramer L, Druml W (2007)
Hypernatremia in the critically ill is an
independent risk factor for mortality.
Am J Kidney Dis 50:952–957
4. Adrogue HJ, Madias NE (2000)
Hyponatremia. N Engl J Med
342:1581–1589
5. Adrogue HJ, Madias NE (2000)
Hypernatremia. N Engl J Med
342:1493–1499
6. Lenz K, Gossinger H, Laggner A,
Druml W, Grimm G, Schneeweiss B
(1986) Influence of hypernatremic-
hyperosmolar state on hemodynamics
of patients with normal and depressed
myocardial function. Crit Care Med
14:913–914
Bratusch-Marrain PR, DeFronzo RA
(1983) Impairment of insulin-mediated
glucose metabolism by hyperosmolality
in man. Diabetes 32:1028–1034
8. DeVita MV, Gardenswartz MH,
Konecky A, Zabetakis PM (1990)
Incidence and etiology of hyponatremia
in an intensive care unit. Clin Nephrol
34:163–166
9. Metnitz PG, Vesely H, Valentin A,
Popow C, Hiesmayr M, Lenz K, Krenn
CG, Steltzer H (1999) Evaluation of an
interdisciplinary data set for national
intensive care unit assessment. Crit
Care Med 27:1486–1491
10. ASDI (2008). Available at:
http://www.asdi.at
11. Metnitz PG, Steltzer H, Popow C,
Valentin A, Neumark J, Sagmuller G,
Schwameis F, Urschitz M, Muhlbacher
F, Hiesmayr M, Lenz K (1997)
Definition and evaluation of a
documentation standard for intensive
care medicine: the ASDI (Working
Group for Standardization of a
documentation system for Intensive
care medicine) pilot project. Wien Klin
Wochenschr 109:132–138
12. Le Gall JR, Lemeshow S, Saulnier F
(1993) A new Simplified Acute
Physiology Score (SAPS II) based on a
European/North American multicenter
study. JAMA 270:2957–2963
13. Le Gall JR, Klar J, Lemeshow S, Saulnier
F, Alberti C, Artigas A, Teres D (1996)
The logistic organ dysfunction system. A
new way to assess organ dysfunction in
the intensive care unit. ICU Scoring
Group. JAMA 276:802–810
14. Hosmer DW, Lemeshow S (1995)
Confidence interval estimates of an
index of quality performance based on
logistic regression models. Stat Med
14:2161–2172

15. Sedlacek M, Schoolwerth AC,
Remillard BD (2006) Electrolyte
disturbances in the intensive care unit.
Semin Dial 19:496–501
16. Zilberberg MD, Exuzides A, Spalding J,
Foreman A, Jones AG, Colby C, Shorr
AF (2008) Epidemiology, clinical and
economic outcomes of admission
hyponatremia among hospitalized
patients. Curr Med Res Opin
24:1601–1608
17. Snyder NA, Feigal DW, Arieff AI
(1987) Hypernatremia in elderly
patients. A heterogeneous, morbid, and
iatrogenic entity. Ann Intern Med
107:309–319
18. Himmelstein DU, Jones AA,
Woolhandler S (1983) Hypernatremic
dehydration in nursing home patients:
an indicator of neglect. J Am Geriatr
Soc 31:466–471
19. Mahowald JM, Himmelstein DU (1981)
Hypernatremia in the elderly: relation
to infection and mortality. J Am Geriatr
Soc 29:177–180
20. Beck LH, Lavizzo-Mourey R (1987)
Geriatric hypernatremia [corrected].
Ann Intern Med 107:768–769
21. Hoorn EJ, Betjes MG, Weigel J, Zietse
R (2008) Hypernatraemia in critically
ill patients: too little water and too
much salt. Nephrol Dial Transplant
23(5):1562–1568
22. Stelfox HT, Ahmed SB, Khandwala F,
Zygun D, Shahpori R, Laupland K
(2008) The epidemiology of intensive
care unit acquired hyponatremia and
hypernatremia in medical-surgical
intensive care units. Crit Care 12:R162
23. Brimioulle S, Orellana-Jimenez C,
Aminian A, Vincent JL (2008)
Hyponatremia in neurological patients:
cerebral salt wasting versus
inappropriate antidiuretic hormone
secretion. Intensive Care Med
34:125–131
24. Gines P, Guevara M (2008)
Hyponatremia in cirrhosis:
pathogenesis, clinical significance, and
management. Hepatology
48:1002–1010
25. Halperin ML, Goldstein MB (1998)
Fluid, electrolyte and acid-base
physiology: a problem-based approach.
WB Saunders Co., Philadelphia
26. Hoorn EJ, Betjes MG, Weigel J, Zietse
R (2008) Hypernatraemia in critically
ill patients: too little water and too
much salt. Nephrol Dial Transplant
23:1562–1568
27. Lindner G, Kneidinger N, Holzinger U,
Druml W, Schwarz C (2009) Tonicity
balance in patients with hypernatremia
acquired in the intensive care unit. Am J
Kidney Dis 54:674–679
28. Druml W, Kleinberger G, Lenz K,
Laggner A, Schneeweiss B (1986)
Fructose-induced hyperlactemia in
hyperosmolar syndromes. Klin
Wochenschr 64:615–618
311
29. Kozeny GA, Murdock DK, Euler DE,
Hano JE, Scanlon PJ, Bansal VK,
Vertuno LL (1985) In vivo effects of
acute changes in osmolality and sodium
concentration on myocardial
contractility. Am Heart J 109:290–296
30. Knochel JP (1982) Neuromuscular
manifestations of electrolyte disorders.
Am J Med 72:521–535
31. Himmelseher S (2007) Hypertonic
saline solutions for treatment of
intracranial hypertension. Curr Opin
Anaesthesiol 20:414–426
32. Aldemir M, Ozen S, Kara IH, Sir A,
Bac B (2001) Predisposing factors for
delirium in the surgical intensive care
unit. Crit Care 5:265–270
33. Ely EW, Shintani A, Truman B, Speroff
T, Gordon SM, Harrell FE Jr, Inouye
SK, Bernard GR, Dittus RS (2004)
Delirium as a predictor of mortality in
mechanically ventilated patients in the
intensive care unit. JAMA
291:1753–1762
34. Lin SM, Liu CY, Wang CH, Lin HC,
Huang CD, Huang PY, Fang YF, Shieh
MH, Kuo HP (2004) The impact of
delirium on the survival of
mechanically ventilated patients. Crit
Care Med 32:2254–2259
35. Sterns RH (1999) Hypernatremia in the
intensive care unit: instant quality—just
add water. Crit Care Med
27:1041–1042