Open Journal of Nephrology, 2011, 1, 1-4
doi:10.4236/ojneph.2011.11001 Published Online September 2011 (
Copyright © 2011 SciRes. OJNeph
Hyponatremia during a Severe Pneumococcal Meningitis
with Renal Salt Wasting: A Cerebral Salt Wasting
Diagnosing a Cerebral Salt Wasting Syndrome
Jean-Philippe Delabre, Stephane Pommet, Laurent Amigues, Olivier Jonquet, Kada Klouche
Department of Intensive Care Unit Lapeyronie University Hospital, Montpellier, France
Received September 11, 2011; revised September 19, 2011; accepted September 26, 2011
Background: The existence and prevalence of cerebral salt wasting and its differentiation from syndrome of
inappropriate antidiuretic hormone have been controversial. This controversy stems from overlapping clini-
cal and laboratory findings and an inability to assess the volume status of these patients. Objectives:To pre-
sent a case of a cerebral salt wasting syndrome secondary to a bacterial mengitis and to emphasize the diffi-
culty to assess the diagnosis. Case report: A 51-year-old male admitted to the ICU for a severe bacterial
meningitis who developed, four days later, hyponatremia associated with hypovolemia due to a renal salt
wasting. Clinical and biological parameters were collected; electrolytes balances and salt clearances were
calculated to best investigate this hydroelectrolytic disorder. Patient's volume status and improvement after
fluid and sodium replacement highly suggests the diagnosis of a cerebral salt wasting syndrome. Conclusion:
A thorough analysis of this case showed that occurrence of hyponatremia and renal salt wasting after brain
agression is not univocal underlying the fact that the diagnosis of cerebral salt wasting should be assessed
only after a careful examination of the different determinants of the hydroelectrolytical balance.
Keywords: Bacterial Meningitis, Cerebral Salt Wasting, Hyponatremia, Natriuresis
1. Introduction
Hyponatremia is a common electrolyte disturbance in
patients after central nervous system disease [1,2]. The
syndrome of inappropriate secretion of antidiuretic hor-
mone (SIADH) is the main attributed cause to this dis-
order [3]. In some few cases, however, hyponatremia
may be due to a renal salt wasting and diagnosed as a
cerebral salt wasting syndrome (CSWS). CSWS, first
described by Peters in 1950, is defined as the occurrence
of an elevated diuresis and natriuresis after a cerebral
injury, leading to hyponatremia and hypovolemia [4].
Despite substantial evidence in animal experiments, its
pathophysiology and pertinency remains a question of
debate in clinical settings [5]. We report herein the case
of a patient who developped hyponatremia with renal salt
wasting associated with hypovolemia following a severe
bacterial meningitis suggestive of CSWS. Since many
different mechanisms can lead to hyponatremia and a
diagnosis of CSWS is seldom univocal, we thoroughly
analyzed electrolytes balances, and salt clearances to
assess the diagnosis.
2. Case Report
A 51 year old male was admitted in our ICU with fever,
headache and drowsiness evolving since 24 hours. At
admission, the computed tomography (CT) scann was
normal. The lumbar puncture was purulent with 7000
leucocytes per mm3, 95% being polynuclears. Cefotaxi-
me and vancomycin in association with dexamethasone
were administered to the patient. At day 1, he required
mechanical ventilation because its consciousness dete-
riorated. Cerebro spinal flu id was positiv e with p enicillin -
sensitive streptococcus pneumoniae and antibiotherapy
was switched to amoxicillin. At day 5, the patient signi-
ficantly improved and was weaned of mechanical venti-
lation with a good neurological status.
From day 4, he developed a polyuria with daily diure-
sis between 4.4 and 5.7 liters which persisted four days
leading to a weight loss of 6.5 kg, clinical evidence of
hypovolemia, and an increase of blood urea nitrogen
(BUN) and hematocrit. In the same time, natremia de-
creased from 145 to 126 mmol/l and natriuresis increased
from 15 to 820 mmol/day. Clinico-biological disorders
are summarized on Tables 1 and 2. Cortisolemia was
normal at 8 am, phosphore excretion fraction was 18%
and chromatography of urinary aminoacids was normal.
Dehydration with inappropriate natriuresis evoked the
occurrence of a renal salt wasting. The association of this
tubulopathy with the cerebral agression was highly sug-
gestive of the diagnosis of CSWS. Rehydratation and salt
supplementation enabled, as shown in Table 2, correc-
tion of hypovolemia and hyponatremia, which increased
to 138 mmol/l at day 10.
3. Discussion
Hyponatremia is common in the setting of central ner-
vous system disease and is associated with significant
morbidity and mortality rates [6]. One third of patients in
the acute phase of subarachnoid haemorrhage and more
than one third of neurosurgical patients especially fol-
lowing transsphenoidal surgery suffer from this electro-
lyte disorder [6,7 ]. It is often attributed to SIADH. When
hyponatremia with increased urine Na+ concentration is
associated with a contracted extracellular fluid volume, it
may however be caused by renal salt wasting resulting
from a centrally mediated process and diagnosed as a
CSWS. The diagnosis of a CSWS requires the presence
of hyponatremia with hypovolemia associated with an
elevated natriuresis (sodium clearance > 200ml/day) af-
ter a cerebral injury in the exclusion of the curren t causes
of renal salt wasting: diuretics use, Bartter and Gitelman
syndrome, hypercalemia, renal failure, hypervolemia
correction, metabolic alkalosis and corticosteroid insuf-
ficiency. Increased secretion of natriuretic peptides like
brain natriuretic peptide (BNP) and atrial natriuretic pep-
tide (ANP) may be responsible for the excessive urinary
Na excre tion [8]. Disruption of kidney neural input may
also leads to renal salt wasting [9]. The precise mecha-
nism of CSWS remains however poorly under s tood.
Table 1. Biological and clinical data measured at 8:00 am. (MAP: mean arterial pressure, BUN: blood urea nitrogen, [Na]p:
plasmatic sodium, Osm plasm : plasmatic osmolality. ND: not determinated).
D1 D2 D3 D4 D5 D6 D7 D8 D9
Weight (kg) 68 70 72.2 73.5 71.5 68 67 66 66
MAP (mmHg) 105 100 110 95 105 100 80 100 98
BUN (mmol/l) 6 12 15
Hematocrit (%) 42 52
[Na]p (mmol/l) 135 143 141 145 140 140 126 132 133
Protidemia (g/l) 70 60 57 60 62 64 77 76 69
Osm plasm (mosm/l) 268
Table 2. Data measured and calculated on 24 hours period. ([Na]u + [K]u: sum of the kaliuresis and natriuresis concentra-
tions, Dexa: Dexamethasone).
D1 - D2 D2 - D3D3 - D4D4 - D5 D5 - D6 D6 - D7 D7 - D8 D8 - D9
Urine output (ml/d) 1400 1800 1250 4400 4700 5300 5700 3100
[Na]u + [K]u (mmol/d) 26.6 ND 176 792 855 1118 707 484
Infused volume (ml/d) 5820 5000 3320 3100 2050 3500 4750 3227
Na+ and K+ infused (m mol/day) 726 588 202 146 165 182 290 199
Sodium clearance (ml/d) 110 ND 926 5002 5740 6688 3901 2480
Isonatric balance (ml) +4388 ND +163 –3976 –4323 –6054 –2760 –1873
Associated treatments Dexa Dexa Dexa furosem ide
Intubation Extubation
Copyright © 2011 SciRes. OJNeph
Copyright © 2011 SciRes. OJNeph
CSWS is yet unrecognized and its incidence is varia-
bly estimated among authors [1-3,10]. In the study of
Sherlock, hyponatremia after subarachnoid haemorrhage
was induced by a CSWS in 6.5% of cases and by SIADH
in 69% of cases [10]. A few observations of CSWS after
infectious meningitis have been published and they were
mainly tuberculous or viral origin [11-13]. Yet, at the
best of our knowledge, only two cases of bacterial me-
ningitis with a CSWS has been reported [14,15]. This
report adds a new observation of a CSWS after bacterial
meningitis, but also underlines the difficulty to assess
this diagnosis particularly in ICU settings. Indeed, our
patient developed at day 7 of a severe pneumococcal me-
ningitis a clinical disorder associating dehydration, hy-
ponatremia and renal salt wasting. Significant weight
loss, increase of BUN and hematocrit support the fact
that he was hypovolemic. Moreover, the occurrence of
polyuria and correction of the disorder by saline infusion
ruled out the diagnosis of SIADH. Main etiologies of
tubulopathy have been also ruled out (calcemia, kaliemia,
acido-basic status, cortisolemia and renal function were
normals) but multiple factors that may play a role must
be taken into acco unt to secure the diagnosis. Firstly, the
patient exhibited three days before occurrence of hypo-
natremia (at day 4), an opposite situation associating
hypernatremia and hypervolemia as a result of a net gain
of isonatric volume (infusion of isotonic saline) and the
occurrence of a low clearance of sodium (Table 2). De-
creased urinary Na excretion was secondary to the asso-
ciation of corticotherapy and positive pressure ventila-
tion. Secondarly, natriuresis and diuresis increased after
day 4 leading to an increase of Na clearance and a dra-
matic decrease of isonatric balance to day 8 as displayed
in Table 2. This results probably from the occurrence of
a CSWS but also, for a part, from positive pression ven-
tilation interruption, and discontinuation of dexametha-
sone (Table 2). Unless integrating all these elements, it
seems therefore somewhat difficult to assess definitively
the diagnosis of CSWS and this should be a general rule
in hyponatremia diagnosis in similar circumstances.
Nonetheless, rehydration and salt loading, that is thera-
peutic management of CSWS, best corrected the disor-
4. Conclusions
The case of our patient is an illustration of the problem in
diagnosing a CSWS: the appearance of a renal salt wast-
ing syndrome with hypovolemia and hyponatremia after
a cerebral injury is insufficient to claim the presence of a
CSWS. In fact, such patients generally benefit from se-
veral treatments affecting the hydroelectrolytical balance:
isotonic saline, positive pressure ventilation, corticoste-
roid s and man nitol. Even af ter ex cluding major cause s of
tubulopath y, the presence of a CSWS should be assessed
only afte r a careful examinati on of the different determi-
nants of the hydroelectrolytical balance, and considering
cessation of treatments.
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