Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis.

Jayantee Kalita,Usha K. Misra

doi:10.12688/wellcomeopenres.15502.2

Jayantee Kalita, Usha K. Misra

Open Access

https://doi.org/10.12688/wellcomeopenres.15502.2

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Abstract

Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.

Highlights

Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome
Hyponatremia in a patient may be due to a number of causes such as poor intake of sodium, drugs, vomiting, diarrhea, liver, kidney or heart failure, endocrine disorders, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW)
An increase in ADH in the presence of normal or low serum osmolality is regarded as inappropriate, which results in continued absorption of water by the kidney resulting in hyponatremia and natriuresis

Summary

28 Nov 2019

Any reports and responses or comments on the article can be found at the end of the article. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) The underlying mechanism of SIADH is inappropriate release of ADH or arginine vasopressin resulting in low serum osmolality and water absorption This leads to expansion of extra-cellular volume and dilutional hypotonic hyponatremia despite normal renal sodium handling. Diagnosis of cause of hyponatremia in TBM In a patient with hyponatremia, assessment of volume status is the most important step that differentiates SIADH from CSW (Table 3). FC results in earlier normalization of serum sodium and fewer infarctions in deep white matter in patients with TBM-related CSW. This results in excretion of water (aquaresis) leading to increased urinary output and decreased urinary tonicity Both conivaptan and tolvaptan have been studied in patients with SIADH55–57 and are both effective in increasing serum sodium.

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