The child has had CNS symptoms including seizures or altered conscious stateįor emergency advice and paediatric or neonatal ICU transfers, call the Paediatric Infant Perinatal Emergency Retrieval (PIPER) Service: 1300 137 650.Children requiring care beyond the comfort of the local hospital.Management Investigations (recommended if Na Clinical assessment of the child’s current hydration status.History consistent with common causes for hyponatraemia.High rate fluid consumption post exercise.GI losses and rehydration with free water.Antiepileptics (valproate, carbamazepine, oxcarbazepine).Chemotherapy (cyclophosphamide, vincristine, platinum based agents).Pulmonary: pneumonia, bronchiolitis, mechanical ventilation.Administration of enteral hypotonic fluids (including dilute formula, Oral Rehydration Solutions, excessive water intake).IV fluid administration in excess of the child’s needs.Rapid correction of hyponatraemia can result in osmotic demyelination syndrome which manifests as irreversible neurologic features (dysarthria, confusion, obtundation and coma) which often present days after sodium correction. Hyponatraemia and rapid fluid shifts can result in cerebral oedema causing neurological symptoms.Ģ4 hours) may have more subtle features such as restlessness, weakness, fatigue or irritability (due to cerebral adaptation) Hyponatraemic seizures and/or altered conscious state are a medical emergency and can cause irreversible neurological damage.The rate of correction of hyponatraemia should not exceed 8 mmol/L in 24 hours as over rapid correction can cause osmotic demyelination syndrome.A child’s fluid status is key in determining the cause of hyponatraemia and dictating treatment.Prevention involves identifying children at risk (ie those with conditions associated with increased ADH secretion) and restricting their fluid to 1/2-2/3 maintenance of isotonic solution.In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.See also Hypernatraemia Intravenous Fluids Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality.
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