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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 1  |  Page : 190-193

Tuberculous Meningitis Presenting as Cerebral Salt Wasting Syndrome: A Review of Literature with Clinical Approach to Hyponatremia

Department of Anaesthesia, AIIMS, Saket Nagar, Bhopal, Madhya Pradesh, India

Date of Submission15-Nov-2016
Date of Decision02-Dec-2015
Date of Acceptance22-Mar-2017
Date of Web Publication24-Feb-2021

Correspondence Address:
Jyotsna Kubre
Department of Anaesthesia, AIIMS, Saket Nagar, Bhopal, Madhya Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.310074

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 » Abstract 

Hyponatremia in the neurocritical care patients is commonly encountered in the setting of either syndrome of inappropriate ADH secretion or cerebral salt wasting. However, differentiation of SIADH and CSW is paramount in view of their divergent treatment strategies.

Keywords: Cerebral salt wasting syndrome, FE urate, hyponatremia, tuberculous meningitis
Key Message: SIADH and CSWS lead to hyponatremia and mostly have overlapping features. However, volume status is the most important factor that clinches the diagnosis.

How to cite this article:
Kubre J, Goyal V, Saigal S, Sharma J P, Joshi R. Tuberculous Meningitis Presenting as Cerebral Salt Wasting Syndrome: A Review of Literature with Clinical Approach to Hyponatremia. Neurol India 2021;69:190-3

How to cite this URL:
Kubre J, Goyal V, Saigal S, Sharma J P, Joshi R. Tuberculous Meningitis Presenting as Cerebral Salt Wasting Syndrome: A Review of Literature with Clinical Approach to Hyponatremia. Neurol India [serial online] 2021 [cited 2021 May 6];69:190-3. Available from:

Hyponatremia is one of the most common electrolyte abnormalities occurring in critically ill patients and reported in approximately 30% of intensive care unit (ICU) admissions.[1] When hyponatremia is encountered in neurosurgical or neurologically ill patients, our differentials include syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting syndrome (CSWS). While CSW is considered to be rare, we feel that exceptions and misconceptions have fuelled this concept of rarity of CSW. We present a case of tubercular meningitis (TBM) who presented with hyponatremia, where our initial diagnosis was SIADH but which eventually turned out to be CSWS. Further, we have reviewed previous reports of TBM with CSWS and present clinical approach in managing hyponatremia.

 » Case Report Top

A 76-year-old gentleman presented to ICU with a history of on and off fever since 4 weeks, confusion since 3 weeks, and incoherent speech since 4 days. On examination, his Glasgow coma scale (GCS) score was E3V5M6, deep tendon reflexes were normal, his bilateral plantar were extensor, and limb ataxia and tremors were also present. On admission, his vitals were Pulse rate 96/min, Respiratory rate 28/min, Blood pressure 131/82 mmHg, Oxygen saturation 94% on room air. His hemogram was normal, serum Na+ was 122 mmol/l, serum osmolality was 240 mOsm/kg, serum potassium was 3.9 mmol/l, and serum uric acid was 5.2 mmol/L. His thyroid function and serum cortisol levels (random) were normal. His spot urine examination revealed urinary sodium at 108 mmol/l and potassium at 84 mmol/l. His Chest X-ray revealed right-sided infiltrates. Subsequently, magnetic resonance imaging (MRI) of the brain revealed multiple tuberculomas, and computed tomography (CT) chest showed bilateral mild pleural effusion and enlarged mediastinal lymph nodes. Antitubercular drugs were started on the same day, and the clinical picture was in favor of TBM.

His hyponatremia was initially attributed to SIADH and he was treated with water restriction. However, over the next 48 hours, his sodium levels did not show improvement and his sensorium deteriorated. We initiated hypertonic saline, but over the next 48 hours, his serum Na+ level did not show much improvement; on day 3 his serum Na+ was 124 and 24-hour urinary Na+ levels was 1487 mmol/l. As laboratory investigations showed increased urine osmolality along with polyuria (U.O >4 l) and urine sodium (1487 mmol/d), possibility of CWS was considered and we initiated him on oral salt supplementation and intravenous fluid replacement (two-third of last hour urine output). His serum sodium partially improved to 127 mmol/l but again fell reduced to 125 mmol/l; on day 8, we added tab. fludrocortisone 0.1 mg 3 times a day. Over the next 7 days, serum sodium improved to 134–135 mmol/l. His sensorium improved with this intervention.

 » Discussion Top

CSWS was first described by Peters et al.[2] in 1950 when they reported 3 patients with an intracranial process who exhibited renal salt wasting; however, the existence of CSW has remained uncertain after the identification of SIADH in 1957 by Schwartz et al.[3] For many years, CSW was considered either a variant or an element of SIADH or one that did not exist. However, now it is being recognized as a separate entity. Till now, there have been 4 cases reported in the literature of TBM associated with CSW in adult population, although it is widely reported in the pediatric population.[4],[5],[6],[7] As we know, TBM is common in the southeast Asian region (SEAR), hence, all 4 cases have been reported from SEAR. Two cases have been reported in the age group of 30–35 years and two in 70–75-year age group. Fifty percent males and 50% females have been affected. Two of the 4 cases had comorbid illness (1 had HIV and other SLE). In all cases, initially, diagnosis of SIADH was considered. In 2 of the 4 cases, tab. fludrocortisone was added.

CSWS and SIADH have quite common features, both present with hyponatremia, urinary Na+ >40 meq/l, and hyperuricemia with increased fractional excretion of urate (FE urate).[8] SIADH is commonly reported in patients with TBM. In our case, SIADH was suspected and we tried to restrict fluid, but there was no effect on serum sodium levels. Pathophysiology of two hyponatremias differ; in SIADH it is basically ADH excess which leads to volume retention, which in turn leads to increase glomerular filtration rate (GFR) and acts as a stimulus for kidneys to release atrial natriuretic factor (ANF), and hence, there is hyponatremia with increase excretion of urinary Na+. CSW is a type of hypovolemic hyponatremia which is associated with increased urinary Na+. As we know, stimulus for it is release of brain or B-type natriuretic peptide which leads to increased release of water and Na+ and hence increased urinary Na+.[9]

Only thing which differentiates the two is volume status and calculation of FE urate. CSW is basically a type of hypovolemic hyponatremia and SIADH is euvolemic hyponatremia; however the caveat is we do not have any accurate and effective methods of measuring volume status, with CVP, IVC status, and clinical status of the patient (urine color, tongue moistness) being rough markers. We tried restricting fluids and hypertonic saline was added, which also led to increase loss of Na+ with no improvement in Na+ levels. We ultimately put in a CVP line as his CVP was quite low (1–2 mmHg); we started fluid resuscitation, but as more and more fluids were given, it led to increased diuresis and more Na+ loss in urine. There was transient benefit but it was not sustained. In view of natriuresis and hypovolemia, diagnosis of CSW was confirmed. We initiated tab. fludrocortisone for the same, and within 4 days of starting fludrocortisone, his Na+ levels improved (130 mmol/l), as can be seen in the [Table 1], this in turn led to marked improvement in serum Na levels.
Table 1: Serial Na+ levels

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As we struggled with management of our patient, we suggest a clinical algorithm for management of these patients so that cause of hyponatremia can be diagnosed early and prompt and appropriate management could be initiated early [Figure 1] and [Figure 2]. As CSWS and SIADH have quite common features, we suggest a fluid challenge of 2 l normal saline over 24 hours,[10] could be tried to see what happens to serum Na+ levels; if it worsens it is SIADH and if it improves it is CSWS. One drawback in our case is that we did not calculate FE urate [(urine uric acid × serum creatinine/urine creatinine × serum uric acid) × 100], normal is <10%. If this would have been calculated, it would have helped us in early diagnosing and managing such a case. This is emphasized in [Figure 1].
Figure 1: Diagnostic approach to patient with hyponatremia

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Figure 2: Bedside management of hyponatremia

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 » Conclusion Top

We feel that hyponatremia is a common condition encountered in the ICU and that too in neurological patients. Early identification of the cause of hyponatremia is of immense importance. As differentiation of CSWS from SIADH is of great value because of different treatment options, therefore possibility of CSWS should always be kept in one of the differentials, especially in neurological patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of Interest

There are no conflicts of interest.

 » References Top

DeVita MV, Gardenswartz MH, Konecky A, Zabetakis PM. Incidence and etiology of hyponatremia in an intensive care unit. Clinical Nephrol 1990;34:163-6.  Back to cited text no. 1
Peters JP, Welt LG, Sims EA, Orloff J, Neeham J. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians 1950;63:57-64.  Back to cited text no. 2
Schwartz WB, Bennett W, Curelop S, Bartter FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. Am J Med 1957;23:529-42.  Back to cited text no. 3
Loo KL, Ramachandran R, Abdullah BJ, Chow SK, Goh EM, Yeap SS. Cerebral infarction and cerebral salt wasting syndrome in a patient with tuberculous meningoencephalitis. South-East Asian J Trop Med Public Health 2003;34:636-40.  Back to cited text no. 4
Jabbar A, Farrukh SN, Khan R. Cerebral salt wasting syndrome in tuberculous meningitis. J Pak Med Assoc 2010;60:964-5.  Back to cited text no. 5
Ravishankar B, Mangala, Prakash GK, Shetty KJ, Ballal HS. J Assoc Physicians India 2006;54:403-4.  Back to cited text no. 6
Ti LK, Kang SC, Cheong KF. Acute hyponatraemia secondary to cerebral salt wasting syndrome in a patient with tuberculous meningitis. Anaesth Intensive Care 1998;26:420-3.  Back to cited text no. 7
Maesaka JK, Imbriano L, Mattana J, Gallagher D, Bade N. Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia. J Clin Med 2014;3:1373-85.  Back to cited text no. 8
Berendes E, Walter M, Cullen P, Prien T, Van Aken H, Horsthemke J, et al. Secretion of brain natriuretic peptide in patients with aneurismal subarachnoid haemorrhage. Lancet 1997;349:245-9.  Back to cited text no. 9
Fenske W, Störk S, Koschker AC, Blechschmidt A, Lorenz D, Wortmann S, et al. Value of Fractional Uric Acid Excretion in Differential Diagnosis of Hyponatremic Patients on Diuretics. J Clin Endocrinol Metab 2008;93:2991-7.  Back to cited text no. 10


  [Figure 1], [Figure 2]

  [Table 1]


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