The role of hypertonic saline in exercise-induced hyponatremia

Clinical Journal of Sport Medicine, 2008

tonicity of extracellular fluids during or after endurance exercise which results in a blood sodium concentration <135 mmol/L. Both excessive fluid intake and a concurrent decrease in urine formation contribute to this rapid-onset, predominantly dilutional, decrease in serum sodium, which can result in life-threatening pulmonary and cerebral oedema. Marathon runners with hypotonic encephalopathy related to EAH, including two cases with fatal cerebral oedema, demonstrated non-osmotic secretion of arginine vasopressin and fulfilled the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The pathophysiology of SIADH as the proximate cause of EAH accounts for otherwise puzzling clinical observations such as cases occurring after only moderate fluid intake or presenting hours after races. This formulation provides a framework for enhancing prevention by monitoring weight changes during races to detect positive fluid balance before the onset of mental status changes. Most importantly, SIADH supports a strategy for use of oral and intravenous hypertonic solutions, including 3% sodium chloride, for the emergent treatment of moderate and life-threatening symptoms of hypotonic encephalopathy, respectively.

The American Journal of Medicine, 1982

Severe hyponatremia with hypoosmolality carries a high morbidity and mortality and constitutes a life-threatening emergency. We report seven cases of severe hyponatremia (serum sodium concentration 99.7 f 3.0 meq/lfter) (mean f SEM) wfth hypoosmolality (212 f 8 mOsm/kg water) that presented with severe neurologic complications. Serum sodium concentration was corrected in 13.3 f 2.2 hours to mildly hyponatremic levels (serum sodium concentration 128.3 f 1.8 meqiliter). The rate of correction of serum sodium concentration was 2.4 f 0.5 meq/llter/hr. This was achieved by the intravenous administration of 3 percent hypertonic saline solution (887 f 43 meq sodium chloride) and furosemide or by hemodlalysis where indicated. No complications occurred from treatment and all of our patients recovered without neurologic sequelae. Early diagnosis and rapid correction of serum sodium concentration appear to reduce the significant morbidity and mortality of severe hyponatremia. Leslie KO, Robertson AS, Norenberg MD: Central pontine 2. Covey CM, Arieff Al: Disorders of sodium and water metab-myelinolysis: an osmotic gradient pathogenesis (abstract). olism and their effects on the central nervous system. In:

Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine, 2018

To determine whether oral administration of 3% hypertonic saline (HTS) is as efficacious as intravenous (IV) 3% saline in reversing symptoms of mild-to-moderate symptomatic exercise-associated hyponatremia (EAH) in athletes during and after a long-distance triathlon. Noninferiority, open-label, parallel-group, randomized control trial to IV or oral HTS. We used permuted block randomization with sealed envelopes, containing the word either &quot;oral&quot; or &quot;IV.&quot; Annual long-distance triathlon (3.8-km swim, 180-km bike, and 42-km run) at Mont-Tremblant, Quebec, Canada. Twenty race finishers with mild to moderately symptomatic EAH. Age, sex, race finish time, and 9 clinical symptoms. Time from treatment to discharge. We successfully randomized 20 participants to receive either an oral (n = 11) or IV (n = 9) bolus of HTS. We performed venipuncture to measure serum sodium (Na) at presentation to the medical clinic and at time of symptom resolution after the intervention. The...

Virtually all investigators now agree that self-induced water intoxication, symptomatic hospital-acquired hyponatremia, and hyponatremia associated with intracranial pathology are true emergencies that demand prompt and definitive intervention with hypertonic saline. A 4-to 6-mmol/L increase in serum sodium concentration is adequate in the most seriously ill patients and this is best achieved with bolus infusions of 3% saline. Virtually all investigators now agree that overcorrection of hyponatremia (which we define as 10 mmol/L in 24 hours, 18 mmol/L in 48 hours, and 20 mmol/L in 72 hours) risks iatrogenic brain damage. Appropriate therapy should keep the patient safe from serious complications of hyponatremia while staying well clear of correction rates that risk iatrogenic injury. Accordingly, we suggest therapeutic goals of 6 to 8 mmol/L in 24 hours, 12 to 14 mmol/L in 48 hours, and 14 to 16 mmol/L in 72 hours. Inadvertent overcorrection owing to a water diuresis may complicate any form of therapy, including the newly available vasopressin antagonists. Frequent monitoring of the serum sodium concentration and urine output are mandatory. Administration of desmopressin to terminate an unwanted water diuresis is an effective strategy to avoid or reverse overcorrection. Semin Nephrol 29:282-299

Journal of the American Heart Association, 2013

Fin indicates final (postinfusion) serum sodium concentration.

Critical Care Medicine, 2009

Objective: To evaluate potential side effects of continuous hypertonic 3% saline (CHS) as maintenance fluid in patients with brain injury.

Wilderness & Environmental Medicine, 2013

Journal of Science and Medicine in Sport, 2013

Objectives: To determine more conclusively whether intravenous (IV) administration of 3% saline is more efficacious than oral administration in reversing below normal blood sodium concentrations in runners with biochemical hyponatremia. Design: Randomized controlled trial. Methods: 26 hyponatremic race finishers participating in the 161-km Western States Endurance Run were randomized to receive either an oral (n = 11) or IV (n = 15) 100 mL bolus of 3% saline. Blood sodium concentration (Na + ), plasma protein (to assess %plasma volume change), arginine vasopressin (AVP), blood urea nitrogen (BUN) and urine (Na + ) were measured before and 60 min following the 3% saline intervention. Results: No significant differences were noted with respect to pre-to post-intervention blood [Na + ] change between intervention groups, although blood [Na + ] increased over time in both intervention groups (+2 mmol/L; p < 0.0001). Subjects receiving the IV bolus had a greater mean (±SD) plasma volume increase (+8.6 ± 4.5% versus 1.4% ± 5.7%; p < 0.01) without significant change in [AVP] (−0.2 ± 2.6 versus 0.0 ± 0.5 pg/mL; p = 0.49). 69% of subjects completing the intervention trial were able to produce urine at race finish with a mean (±SD) pre-intervention urine [Na + ] of 15.2 ± 8.5 mmol/L (range 0-35; NS between groups). [BUN] of the entire cohort pre-intervention was 30.7 ± 10.5 mg/dL (range 13-50). Conclusions: No group difference was noted in the primary outcome measure of change in blood [Na + ] over 60 min of observation following a 100 mL bolus of either oral or IV 3% saline. Administration of an oral hypertonic saline solution can be efficacious in reversing low blood sodium levels in runners with mild EAH.

Kidney international. Supplement

Severe hyponatremia may be chronic (days) or acute (hours), symptomatic or asymptomatic. Severe chronic symptomatic hyponatremia (serum sodium concentration &lt; 110 to 115 mM/liter) occurs most commonly in the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The treatment of this hyponatremia is a challenge to practicing physicians, in part because an overly rapid correction of hyponatremia may cause brain damage. The latter sometimes takes the form of central pontine myelinolysis (CPM). On the basis of available clinical and experimental literature, the rate of correction of this symptomatic hyponatremia should be no more than 0.5 mM per liter per hour, and the initial treatment should be halted once a mildly hyponatremic range of the serum sodium concentration has been reached (approximately 125 to 130 mM/liter). In contrast, severe chronic asymptomatic hyponatremia may be treated sufficiently by a fluid restriction. On the other hand, severe symptomatic acute hy...

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