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LETTERS TO EDITOR
Year : 2018  |  Volume : 66  |  Issue : 5  |  Page : 1515-1516

Hyponatremia in tuberculosis: Focus on brain instead of adrenals


1 Department of Internal Medicine, People Tree Hospitals, Bengaluru, Karnataka, India
2 Department of Neurology, People Tree Hospitals, Bengaluru, Karnataka, India
3 Department of Intensive Care Unit and Critical Care, People Tree Hospitals, Bengaluru, Karnataka, India
4 Department of Endocrinology, People Tree Hospitals, Bengaluru, Karnataka, India

Date of Web Publication17-Sep-2018

Correspondence Address:
Dr. D M Mahesh
Department of Endocrinology, People Tree Hospitals, Bengaluru - - 560 022, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.241340

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How to cite this article:
Chaya B E, Rajesh K N, Mohan K, Mahesh D M. Hyponatremia in tuberculosis: Focus on brain instead of adrenals. Neurol India 2018;66:1515-6

How to cite this URL:
Chaya B E, Rajesh K N, Mohan K, Mahesh D M. Hyponatremia in tuberculosis: Focus on brain instead of adrenals. Neurol India [serial online] 2018 [cited 2018 Oct 23];66:1515-6. Available from: http://www.neurologyindia.com/text.asp?2018/66/5/1515/241340




Sir,

Hyponatremia is one of the most common electrolyte abnormalities observed in acute neurological disorders. The differential diagnoses for hyponatremia in central nervous system (CNS) disorders are syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt wasting syndrome (CSWS). Clinical manifestations of these two conditions may be similar, but their pathogenesis and management protocols are different.

We report the case of a 41-year old man who presented with fever for 7 days, diffuse headache, and generalized seizure. His physical examination revealed neck stiffness with right hemiparesis. Contrast-enhanced computed tomography (CECT) of the brain was normal. Cerebrospinal fluid (CSF) analysis and other biochemical parameters are summarized in [Table 1]. In view of CSF lymphocytosis, tuberculous meningitis was considered and he was empirically started on anti-tuberculous therapy (ATT) with intravenous (iv) dexamethasone. In the hospital, his sensorium deteriorated and serum sodium reduced to 106 mEq/L, with a low serum osmolality (221 mOsm/kg), a low spot urinary sodium (128 mEq/L; indicative of natriuresis), and a high urine osmolality (476 mOsm/kg). In view of euvolemic hyponatremia, SIADH was considered and managed with tolvaptan (a selective arginine vasopressin (AVP) V2 receptor blocker used to induce free water diuresis in the treatment of euvolemic or hypervolemic hyponatremia in a dose of 15 mg) and 3% saline iv infusion. On day 3, the hyponatremia persisted (112 mEq/L) with a high fractional uric acid excretion (41.79%). In view of the persisting polyuria (urine output: 4.5 L/day) with hypotension (BP: 100/60 mmHg], he was diagnosed to have CSWS and started on fludrocortisone 0.2 mg/day with 3% saline (1 ml/kg/h). Despite sodium correction with 3% saline (2 ml/kg/h), sodium levels were persistently low (<125 mEq/L); hence, on a daily basis, the fludrocortisone dose was increased to 1.2 mg by day 17, when the serum sodium was 132 mEq/L [Figure 1]. Subsequently, urine output reduced to < 3 L/day and he was weaned off iv saline. Brain natriuretic peptide levels were not assessed due to cost constraints. The fludrocortisone dose was tapered gradually over 2 weeks and stopped. On the follow-up visit at 4 weeks, his serum sodium and urine output had normalized. He was continued on ATT and had a complete recovery.
Table 1: Cerebrospinal fluid (CSF) analysis

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Figure 1: Fluid balance, urine, and serum sodium concentration before and after fludrocortisone administration

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CSWS leads to severe hyponatremia with excessive natriuresis and volume depletion in the presence of acute intracranial diseases, and responds to volume and salt replacement. The exact underlying pathophysiology is unclear, but exaggerated natriuresis is attributed to increased release of brain natriuretic peptides and ouabain-like factors by the injured brain.[1] The net effect is polyuria and decrease in the effective circulating volume, leading to hypotension and hyponatraemia. The critical point for distinguishing CSWS from SIADH is the presence of hypovolemia and a negative salt balance.[2] Documenting elevated levels of brain natriuretic peptide (BNP) aids in the definitive diagnosis of CSWS.[2],[3],[4]

Replacement of urinary salt and water losses using 0.9% or 3% sodium chloride is the cornerstone of CSWS treatment.[2],[3],[4],[5],[6] In addition, fludrocortisone has been used in doses of 0.1–1 mg/day to treat CSWS.[2],[3],[4],[5],[6] In our patient, the maximum dose of fludrocortisone used was 1.2 mg/day. This high requirement was likely due to the concomitant use of rifampicin. Rifampicin has been known to be capable of affecting metabolism of various medications such as phenytoin, glucocorticoids, and mineralocorticoids.[6],[7] The patients may require doubling or tripling the dose of adrenal steroids to achieve an optimal therapeutic response. Mineralocorticoid supplementation seems to be a safe and effective treatment for CSWS. Once the underlying pathology is corrected, CSWS is usually a transient condition that resolves within 3–4 weeks.[2],[5] Hence, a long-term therapy is usually not needed.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Berendes E, Walter M, Cullen P, Prien T, Van Aken H, Horsthemke J, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid hemorrhage. Lancet 1997;349:245-9.  Back to cited text no. 1
    
2.
Nagotkar L, Shanbag P, Dasarwar N. Cerebral salt wasting syndrome following neurosurgical intervention in tuberculous meningitis. Indian Pediatr 2008;45:598-601.  Back to cited text no. 2
    
3.
Tobin G, Chacko AG, Simon R. Evaluation of NT-ProBNP as a marker of the volume status of neurosurgical patients developing hyponatremia and natriuresis: A pilot study. Neurol India 2018;66:1383-88.  Back to cited text no. 3
  [Full text]  
4.
Maesaka JK, Imbriano L, Mattana J, Gallagher D, Bade N, Sharif S. 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. 4
    
5.
Taplin CE, Cowell CT, Silink M, Ambler GR. Fludrocortisone therapy in cerebral salt wasting. Pediatrics 2006;118:e1904-8.  Back to cited text no. 5
    
6.
Momi J, Tang CM, Abcar AC, Kujubu DA, Sim JJ. Hyponatremia-what is cerebral salt wasting? Perm J 2010;14:62-5.  Back to cited text no. 6
    
7.
Kyriazopoulou V, Parparousi O, Vagenakis AG. Rifampicin-induced adrenal crisis in addisonian patients receiving corticosteroid replacement therapy. J Clin Endocrinol Metab 1984;59:1204-6.  Back to cited text no. 7
    


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