BACKGROUND: Acute hyponatremia is a medical emergency that confers high mortality, attributed primarily to cerebral edema. Expert guidelines advocate the use of intravenous boluses of hypertonic saline rather than traditional continuous infusion to achieve a faster initial rise in plasma sodium (pNa) concentration. However, there is a limited evidence base for this recommended policy change. METHODS: We prospectively assessed the clinical and biochemical outcomes in patients treated for symptomatic hyponatremia caused by syndrome of inappropriate antidiuresis in response to intravenous bolus treatment with 3% saline (100 mL, repeated up to two more times) and compared the outcomes to retrospective data from patients treated with continuous intravenous infusion of low-dose (20 mL/h) 3% saline. RESULTS: Twenty-two patients were treated with bolus infusion and 28 with continuous infusion. Three percent saline bolus caused more rapid elevation of pNa at 6 hours [median (range) 6 (2 to11) vs 3 (1 to 4) mmol/L, P < 0.0001], with a concomitant improvement in Glasgow Coma Scale (GCS) [median (range) 3 (1 to 6) vs 1 (-2 to 2), P < 0.0001] at 6 hours. Median pNa concentration was similar at 24 hours in the two treatment groups. The administration of a third saline bolus was associated with greater need for dextrose/dDAVP to prevent overcorrection (OR 24; P = 0.006). There were no cases of osmotic demyelination in either group. CONCLUSION: Three percent saline bolus produces faster initial elevation of pNa than continuous infusion with quicker restoration of GCS, and without osmotic demyelination. Frequent electrolyte monitoring, and judicious intervention with dDAVP is required to prevent overcorrection with bolus therapy.
BACKGROUND: Acute hyponatremia is a medical emergency that confers high mortality, attributed primarily to cerebral edema. Expert guidelines advocate the use of intravenous boluses of hypertonicsaline rather than traditional continuous infusion to achieve a faster initial rise in plasma sodium (pNa) concentration. However, there is a limited evidence base for this recommended policy change. METHODS: We prospectively assessed the clinical and biochemical outcomes in patients treated for symptomatic hyponatremia caused by syndrome of inappropriate antidiuresis in response to intravenous bolus treatment with 3% saline (100 mL, repeated up to two more times) and compared the outcomes to retrospective data from patients treated with continuous intravenous infusion of low-dose (20 mL/h) 3% saline. RESULTS: Twenty-two patients were treated with bolus infusion and 28 with continuous infusion. Three percent saline bolus caused more rapid elevation of pNa at 6 hours [median (range) 6 (2 to11) vs 3 (1 to 4) mmol/L, P < 0.0001], with a concomitant improvement in Glasgow Coma Scale (GCS) [median (range) 3 (1 to 6) vs 1 (-2 to 2), P < 0.0001] at 6 hours. Median pNa concentration was similar at 24 hours in the two treatment groups. The administration of a third saline bolus was associated with greater need for dextrose/dDAVP to prevent overcorrection (OR 24; P = 0.006). There were no cases of osmotic demyelination in either group. CONCLUSION: Three percent saline bolus produces faster initial elevation of pNa than continuous infusion with quicker restoration of GCS, and without osmotic demyelination. Frequent electrolyte monitoring, and judicious intervention with dDAVP is required to prevent overcorrection with bolus therapy.
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