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Journal Article
Neurological symptoms in hospitalised patients: do we assess hyponatraemia with sufficient care?
Acta Paediatrica 2014 January
AIM: To review the incidence of hyponatraemic encephalopathy in children treated in a tertiary care centre hospital, together with the clinical setting and clinical management of these cases.
METHODS: Retrospective descriptive study by chart review of patients admitted to hospital during 2000-2010. Patients older than 1 month were included who had severe hyponatraemia (sodium concentration <125 mmol/L) on admission or during their hospital stay and co-incidental neurological symptoms. Epidemiological, clinical, laboratory and therapeutic data were collected.
RESULTS: We analysed 41 cases of severe hypotonic hyponatraemia and neurological symptoms compatible with hyponatraemic encephalopathy. Boys accounted for 56.1% patients, and the median age was 1 year. Hyponatraemia was acquired in hospital by 61% of the patients, and 88% of those patients were receiving intravenous hypotonic fluids. The most frequent neurological symptom was seizures. The most common therapeutic strategy was sodium supplementation and antiepileptic drugs. Hypertonic fluids were only used in the initial treatment of 16 patients. There were two deaths related to hyponatraemic encephalopathy.
CONCLUSION: Hyponatraemia should always be considered a cause of neurological symptoms in hospitalised patients. Treatment should be prompt to prevent neurological sequelae and death. Current recommendations for fluid management in hospitalised children should be reviewed.
METHODS: Retrospective descriptive study by chart review of patients admitted to hospital during 2000-2010. Patients older than 1 month were included who had severe hyponatraemia (sodium concentration <125 mmol/L) on admission or during their hospital stay and co-incidental neurological symptoms. Epidemiological, clinical, laboratory and therapeutic data were collected.
RESULTS: We analysed 41 cases of severe hypotonic hyponatraemia and neurological symptoms compatible with hyponatraemic encephalopathy. Boys accounted for 56.1% patients, and the median age was 1 year. Hyponatraemia was acquired in hospital by 61% of the patients, and 88% of those patients were receiving intravenous hypotonic fluids. The most frequent neurological symptom was seizures. The most common therapeutic strategy was sodium supplementation and antiepileptic drugs. Hypertonic fluids were only used in the initial treatment of 16 patients. There were two deaths related to hyponatraemic encephalopathy.
CONCLUSION: Hyponatraemia should always be considered a cause of neurological symptoms in hospitalised patients. Treatment should be prompt to prevent neurological sequelae and death. Current recommendations for fluid management in hospitalised children should be reviewed.
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