Fluid resuscitation using hypertonic saline results in volume expansion and less total infusion volume. It is a lifesaving therapy in many acute clinical conditions. This may be of interest in oedematous patients with intravascular volume depletion. When such strategies are employed, renal effects may differ markedly according to prior intravascular volume status. In hyper-volumetric states with depleted intravascular volume, hypertonic sodium therapy of 5% NaCl and 8.4% NaCo3 turns it into hypervolaemia with massive diuretic effect. Hypertonic saline induced changes in serum osmolality and sodium return to baseline within a limited period. Sparse evidence indicates that resuscitation with hypertonic saline results in less perioperative complications, ICU days and mortality in selected patients. In conclusion, the use of hypertonic saline may have beneficial features in selected critically ill patients when carefully chosen. Hypertonic sodium therapy of 5% NaCl and 8.4% NaCo3 has proved lifesaving in treating the TUR syndrome, hyponatraemia and ARDS. Further clinical studies assessing relevant clinical outcomes are warranted.

Clinicians use hypertonic fluids to increase intravascular fluid volume and restore blood pressure. Hypertonic saline can be utilized in the treatment of hyponatremia. Hypertonic saline and mannitol are both indicated to reduce intracranial pressure. 

Hypertonic saline is a crystalloid intravenous fluid composed of NaCl dissolved in water with a higher sodium concentration than normal blood serum. Both 3% and 5% hypertonic saline (HS) is currently FDA-approved for use in hyponatremia and increased intracranial pressure (ICP). Patients with hyponatremia with severe features should have their serum sodium gradually corrected with boluses of hypertonic saline. Patients should have their serum sodium monitored at regular intervals and can receive multiple boluses a day.[1]

In patients with severe hyponatremia, serum sodium should undergo correction by 4 to 6 mEq/L per day, which can be achieved with 100 mL boluses of 3% HS at 10-minute intervals up to three total boluses. Some authorities recommend up to  8 mEq/L per day.[9] Less severe hyponatremia can achieve control with enough hypertonic saline to manage symptoms.[10] Due to the insufficient number of patients over age 65 in various trials, hypertonic fluids should start at the lowest ends of the dosing scale in the geriatric population. Pediatric traumatic brain injury generally receives treatment with a 6.5 to 10 mL/kg bolus of hypertonic saline.[11] Administration via a peripheral intravenous catheter is acceptable if no other access is available, but central venous access is the preferred route.

Hypertonic sodium therapy (HST) of 5%NaCl and 8.4%NaCo3 has proved lifesaving for treating the acute severe cases of the TUR syndrome, acute dilutional hyponatraemia and the acute respiratory distress syndrome (ARDS).

This HST was used successfully in treating the TUR syndrome, acute dilutional hyponatraemia of <120>

The treatment was given in bolus therapy of 200 ml alternating both fluids given over a period of 10 minutes and repeated after rechecking serum sodium monitored by clinical improvement and urine output [15]. More than 4 L of urine was excreted by the end of one hour period of treatment matching a remarkable clinical recovery from shock and coma. The effect of hypertonic sodium infusion on serum sodium and osmolality are shown in (Figure 1).

Figure: shows mean changes in measured serum osmolality (OsmM) and calculated osmolality (OsmC) in patients with the TURP syndrome comparing those infused with 5% hypertonic sodium (solid lines) and those treated conservatively (slashed lines). OsmC was calculated from the formula 2xNa+urea+glucose in mmol/l of serum concentration48 thus reflecting changes in serum sodium concentration. The vertical dotted line represents the start of operation (Time B) followed by C, C1, C2 (end of treatment) and D, respectively.

Fluid resuscitation using hypertonic saline results in volume expansion and less total infusion volume. This may be of interest in oedematous patients with intravascular volume depletion. When such strategies are employed, renal effects may differ markedly according to prior intravascular volume status. Hypertonic saline induced changes in serum osmolality and electrolytes return to baseline within a limited period. Sparse evidence indicates that resuscitation with hypertonic saline results in less perioperative complications, ICU days and mortality in selected patients. In conclusion, the use of hypertonic saline may have beneficial features in selected critically ill patients when carefully chosen. Further clinical studies assessing relevant clinical outcomes are warranted.

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