Hyponatremia in children with tuberculous meningitis: A hospital-based cohort study

结核性脑膜炎患儿低钠血症:一项基于医院的队列研究

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Abstract

BACKGROUND: Hyponatremia has long been recognized as a potentially serious metabolic consequence of tuberculous meningitis (TBM) occurring in 35-65% of children with the disease. The syndrome of inappropriate antidiuretic hormone (SIADH) secretion has for long been believed to be responsible for the majority of cases of hyponatremia in TBM. Cerebral salt wasting syndrome (CSWS) is being increasingly reported as a cause of hyponatremia in some of these children. AIM: This study was done to determine the frequency and causes of hyponatremia in children with TBM. METHODS: Children with newly diagnosed TBM admitted over a 2-year period (January 2009 to December 2010) were included. All patients received anti-tubercular therapy, mannitol for cerebral edema, and steroids. Patients were monitored for body weight, urine output, signs of dehydration, serum electrolytes, blood urea nitrogen, serum creatinine, and urinary sodium. Hyponatremia was diagnosed if the serum sodium was <135 mEq/L. CSWS was diagnosed if there was evidence of excessive urine output, volume depletion, and natriuresis in the presence of hyponatremia. The outcome in terms of survival or death was recorded. RESULTS: Twenty-nine of 75 children (38.7%) with TBM developed hyponatremia during their hospital stay. In 19 patients, hyponatremia subsided after the discontinuation of mannitol. Ten patients with persistent hyponatremia had CSWS. There were no patients with SIADH. CONCLUSIONS: CSWS is an important cause of hyponatremia in children with newly diagnosed TBM. In our patients, it was more commonly seen than SIADH.

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