The effects of mannitol have been of great interest to those who treat head trauma, but the ideal plan for its use has never been established. If ICP exceeds a predetermined level, for example, 20 mm Hg as recommended by aforementioned guidelines for the treatment of traumatic brain injury, mannitol 20 percent, 0.25 to 1.0 g/kg is given every 3 to 6 h to maintain serum sodium above approximately 142 mEq/L and osmolarity of 290 to 315 mOsm/L. Even if ICP monitoring is not used, an attempt may be made to maintain this level of serum osmolality for the first days after injury if contusion and brain swelling are detected on the CT scan.
Mannitol in large amounts may cause renal failure, almost always reversible, though an uncertain mechanism perhaps having to do with renal blood flow. Limited evidence suggests that this complication occurs only with the use of more than 200 g of mannitol daily.
The relative merits of hypertonic saline and mannitol are frequently discussed and have been reviewed by one of us (Ropper, 2012). Several small series comparing the agents, referenced in the review, have shown too little difference to allow a choice between the two agents. Local experience and an overall assessment of the side effects of each typically dominate practice. Hypertonic saline (concentrations of 3 to 23 percent) has a comparable effect to mannitol in the treatment of raised ICP and has the advantage of avoiding severe dehydration because it increases osmolarity directly rather than through diuresis. The opposite also pertains, namely that patients with poor cardiac output may be subject to congestive heart failure with hypertonic saline in high volumes. Diuretics have been used to mitigate this effect. Either agent can produce a hyperglycemic, hyperosmolar state in diabetics, particularly in the elderly and in those receiving corticosteroids.
Hypertonic saline, 3 percent, can be used in boluses of 150 mL; a 7.5 percent solution, in 75 mL boluses; and 23 percent, in volumes of approximately 30 mL. All but the lowest concentration of saline require a central venous catheter to prevent sclerosis of veins. The same levels of sodium concentration as noted for mannitol are used as a reference to guide graduated increments of sodium administration, with serum sodium higher than about 156 mEq/L infrequently providing additional reductions in ICP.
Hypocarbia by hypervantilation Hypocarbia, induced by mechanical hyperventilation produces alkalosis of the CSF and cerebral vasoconstriction with a corresponding reduction in cerebral blood volume and ICP. It is effective for a limited period of time, as the pH of the spinal fluid equilibrates over hours by the elaboration of ammonium ions in the choroids plexus, allowing cerebral blood volume to return to its previous level. A single-step reduction in Pco2 typically lowers ICP for approximately 20 to 40 min. Attempts to prolong the effect of hypocarbia and the alkalosis by the intravenous administration of ammonium buffers have met with mixed success.
It has been suggested that hyperventilation may be harmful to some head-injured patients because of a reduction in cerebral blood flow, but the risk, if any, appears to be minimal, at least in adults. In children, reductions in cerebral blood flow have been demonstrated by Skippen and colleagues at even modest levels of hypocarbia and three-quarters show slight brain ischemia when Pco2 is below 25 mm Hg. For these reasons, hypocarbia is used in cases of head trauma mainly in acute circumstances and has been eschewed for chronic use. If the ICP continues to rise and brain swelling progresses despite these measures, the outlook for survival is poor. It should be mentioned that many patients, particularly children, hyperventilate spontaneously after head trauma.