Hyponatremia during a Severe Pneumococcal Meningitis with Renal Salt Wasting: A Cerebral Salt Wasting Syndrome?

doi:10.4236/ojneph.2011.11001

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Open Journal of Nephrology, 2011, 1, 1-4

doi:10.4236/ojneph.2011.11001 Published Online September 2011 (http://www.SciRP.org/journal/ojneph)

Hyponatremia during a Severe Pneumococcal Meningitis

with Renal Salt Wasting: A Cerebral Salt Wasting

Syndrome?

—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

E-mail: [email protected]

Received September 11, 2011; revised September 19, 2011; accepted September 26, 2011

Abstract

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.

J. P. DELABRE ET AL.

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

Clinical

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

Biological

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

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

Infusions

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

J. P. DELABRE ET AL.

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-

der.

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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