• Michael N Diringer.
• Neurocritical Care Division, Department of Neurology, Washington University, Campus Box 8111, 660 S Euclid Ave, St Louis, MO, 63110, USA. diringerm@wustl.edu.
• Acta Neurochir. Suppl. 2016 Jan 1; 121: 3-6.

AbstractFor almost a century, it has been known that hypertonic solutions shrink cerebral tissue. Early attempts used hypertonic solutions of ions (sodium, magnesium) and sugars (glucose, dextrose, sucrose), concentrated albumin, and, later, urea. These early attempts were largely abandoned because the effect was short lived and often followed by a period of rebound edema. This was a result, to a great extent, of the osmotic agent either being metabolized or crossing the cell membrane.Renewed interest in osmotic therapy came in the 1960s, with the introduction of intracranial pressure monitoring in head injury and the use of mannitol as an osmotic agent. In the 1990s, use of hypertonic saline was reintroduced as an alternative to address concerns about mannitol. More recently, administration of hypertonic saline has transitioned from boluses to continuous infusions. The rationale for and data supporting the use of continuous infusions are presented.

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