However, there are few critical data to support the routine use of ICP monitoring. Certainly in the patient who is only drowsy or shows only minimal mass effect on CT, it is usually not necessary. Guidelines given by the American Association of Neurological Surgeons and allied groups have been that monitoring is appropriate if Glasgow Coma Scale is between 3 and 8 and there are abnormalities on CT scan, or if there is no abnormality on the CT but the patient has any two of age over 40, posturing, or has systolic blood pressure below 90 mm Hg. They set a desirable level of ICP of below 20 mm Hg and this has reinforced the role of ICP monitoring in head trauma management.
A reassessment of the effectiveness of ICP monitoring in a randomized trial reached the contrary conclusion that the information gained offers no advantage over clinical observation and imaging with CT scan. This trial was carried out by Chesnut and colleagues (called BEST:TRIP) in developing countries and defined raised ICP at a level that has been criticized as too low (20 mm Hg). Nevertheless, the study demonstrated that the use of a clinical approach to management of raised ICP is as feasible as a program based on direct ICP measurement. This does not negate the desirability of keeping ICP controlled at some arbitrary level; it merely questions the need for direct monitoring as a guide to management. Two trials of decompressive craniectomy (called DECRA and RESCUEicp) detailed below, used persistently raised ICP as an index for surgical treatment and in that context, ICP monitoring, of course, becomes a necessary.
As a practical matter, we use ICP monitoring in our unit to warn of impending deterioration from brain edema or hemorrhage if the patient cannot be effectively examined or shows poor responsiveness with evidence of mass effect on a CT scan. Although the risk of infection with a ventricular catheter is low, less than 3 percent, prolonged use may be complicated by bacterial meningitis. The catheter may be left in place for 3 to 5 days, or fewer if the clinical state and ICP are stable for 24 to 48 h. The current generation of ICP monitors employs fiberoptic strain gauges that can be inserted directly into the cerebral cortex without apparent damage.
General measures The first step in lowering elevated ICP is to control the incidental factors that are known to raise pressure, such as hypoxia, hypercarbia, particularly hyperthermia, awkward head positions that compress the jugular veins, and high mean airway pressures from positive pressure ventilation (see the monograph by Ropper and colleagues [2004] and Chap. 29 for further details). The avoidance of hyponatremia and serum hypoosmolarity that would allow water to enter the brain and increase its volume is accomplished by infusing only isoosmolar or hyperosmolar solutions such as normal saline. Elevations in serum osmolality as a consequence of excessive concentrations of diffusible solutes such as glucose are not useful in reducing intracranial volume because they do not create gradient for water and solutes across the cerebral vasculature. Consequently, fluids such as 5 percent dextrose in water, 0.5 normal saline, and 5 percent dextrose in 0.5 normal saline are avoided; lactated Ringer solution is permissible; normal saline, with or without added dextrose, is ideal. In a post hoc study of a cohort of severely injured patients, resuscitation with albumin was found to have a detrimental effect compared to saline (SAFE Investigators).
Hyperosmolar therapy The basis for this class of treatments is the creation of a gradient of water concentration from the brain to the blood that reduces brain volume. Mannitol, glycerol, and urea are effective in lowering ICP by producing serum hyperosmolarity initially and then causing a diuresis that sustains this state and secondarily causes hypernatremia and hypovolemia. Hyperosmolar saline, in contrast, raises serum sodium directly and expands intravascular volume.