Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis
journal contributionposted on 22.10.2020, 13:43 by Usha K Misra, Jayantee Kalita, Tuberculous Meningitis International Research Consortium, Rob E Aarnoutse, Suzanne TB Anderson, Nathan C Bahr, Nguyen D Bang, David R Boulware, Tom Boyles, Lindsey HM te Brake, Satish Chandra, Felicia C Chow, Fiona V Cresswell, Reinout van Crevel, Angharad G Davis, Sofiati Dian, Joseph Donovan, Kelly E Dooley, Anthony Figaji, A Rizal Ganiem, Ravindra Kumar Garg, Diana M Gibb, Raph L Hamers, Nguyen TT Hiep, Darma Imran, Akhmad Imron, Sanjay K Jain, Sunil K Jain, Byramee Jeejeebhoy, Rashmi Kumar, Vinod Kumar, Arjan van Laarhoven, Rachel PJ Lai, Abi Manesh, Suzaan Marais, Vidya Mave, Graeme Meintjes, David B Meya, Manish Modi, Alvaro A Ordonez, Nguyen H Phu, Sunil Pradhan, Kameshwar Prasad, Alize M Proust, Lalita Ramakrishnan, Ursula Rohlwink, Rovina Ruslami, Johannes F Schoeman, James A Seddon, Kusum Sharma, Omar Siddiqi, Regan S Solomons, Nguyen TT Thuong, Guy E Thwaites, Ronald van Toorn, Elizabeth W Tucker, Sean A Wasserman, Robert J Wilkinson
© 2019 Misra UK et al. 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.