Although mannitol remains the mainstay of hyperosmolar therapy, Hypertonic Saline Infusion is an alternative to mannitol.
The main theoretical justification for using Hypertonic Saline Infusion stems from the fact that an intact BBB is less permeable to saline than to mannitol.
In clinical reports of intracranial hypertension from various causes, HS has been shown to effectively lower ICP in cases refractory to mannitol.
Hypertonic Saline Infusion administered in bolus form demonstrates the same biphasic response as mannitol and is generally considered to act like mannitol; first rheologically, then osmotically.
Hypertonic Saline Infusion solutions are also used for small volume resuscitation in patients with haemorrhagic shock. Since head injury often occurs in the setting of multiple trauma accompanied by haemorrhage, and hyperosmolality is known to reduce brain volume, small-volume resuscitation is particularly favoured ii these patients.
In TBI with haemorrhagic shock, the aggressive volume expansion must be balanced by the concern to avoid cerebral oedema with resultant increase in ICP, which has been demonstrated with large-volume isotonic fluid administration.
Laboratory and clinical data in adult and paediatric models also suggest that hypertonic solutions improve mean arterial pressure with smaller fluid volumes and without the concomitant rise in ICP.
Vassar et al have performed four randomized controlled studies in trauma patients wherein they found better haemodynamic parameters in the groups resuscitated with hypertonic saline. A metaanalysis using these studies88 to evaluate the effect of HS on patients with TBI and hypotension found significantly better survival outcome in patients receiving HS.
The dangers of using Hypertonic Saline Infusion in the treatment of cerebral oedema are somewhat hypothetical and are extrapolated from known toxicities of normal saline administration and mannitol.
Central pontine myelinolysis is an unusual but well-known complication of over-rapid correction of hyponatraemia. There has been no reported case of central pontine myelinolysis in any patient treated with Hypertonic Saline Infusion for cerebral oedema.
The metabolic effects of Hypertonic Saline Infusion are purely related to a heavy salt load to which the kidney responds by retaining bicarbonate and excreting potassium and calcium. The resultant hypokalaemia and hypocalcaemia can effectively be treated with routine repletion.
Supplementation of Hypertonic Saline Infusion with acetate is a simple way to counteract associated metabolic acidosis. Volume overload is another common side effect of all hyperosmolar solutions and is potentially problematic among patients with cardiopulmonary disease. For patients in whom volume expansion must be maintained (e.g., SAH), Hypertonic Saline Infusion provides an elegant solution to both issues of ICP treatment and prophylaxis/treatment of vasospasm.
Rebound oedema is another understudied but recognized clinical entity that can occur with any hyperosmolar agent. Prolonged hyperosmolar therapy results in equalization of the osmotic gradient across BBB. When hyperosmolar therapy is discontinued after such equilibrium has occurred, a reverse gradient is established, drawing water into the brain.
The extent to which this actually occurs is unknown and is of concern in patients with extensive BBB destruction. Qureshi et al suggested limiting continuous Hypertonic Saline Infusion to 24 to 48 hours to prevent this phenomenon.
Ogden et al from their experience have proposed that it may be even more critical to wean Hypertonic Saline Infusion slowly over a period of 24 to 48 hours as this allows the kidneys to adjust to a lower sodium load.