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ect the ICP and increase the risk of a cerebellar or temporal lobe herniation Nor do the neurologic signs that constitute the Glasgow Coma Scale re ect the pressure in the cranium The arguments for and against monitoring the ICP have been addressed earlier (page 532) Our impression is that in comatose patients, monitoring of the ICP, at a minimum, prevents errors in uid administration and re nes all the other details of management, including the appropriate use of osmotic diuretics and the correct level of hyperventilation In these respects, monitoring can be helpful However, there are few critical data to support the routine use of ICP monitoring; certainly the patient who is only drowsy or shows only minimal mass effect on CT scanning is not likely to be of bene t In the absence of data to help in making the decision regarding the insertion of these devices, as a practical guide we favor their use to warn of impending deterioration from brain edema or hemorrhage if the patient shows sustained drowsiness with inability to follow commands, has a Glasgow Coma Scale score of 8, and has evidence of mass effect on a CT scan The current generation of ICP monitors employs beroptic strain gauges that can be inserted directly into the cerebral cortex without apparent damage While the risk of infection is low, prolonged use may be complicated by bacterial meningitis The monitor is left in place for 3 to 5 days or less if the clinical state and ICP are stable for 24 to 48 h The rst step in lowering high ICP is to control the incidental factors that are known to raise the pressure, such as hypoxia, hypercarbia, hyperthermia, awkward head positions that compress the jugular veins, and high mean airway pressures (see the monograph by Ropper and colleagues) If the intracranial pressure exceeds 15 to 20 mmHg, several measures can be instituted, such as inducing hypocarbia by controlled ventilation (maintaining PCO2 at 28 to 33 mmHg) and hyperosmolar dehydration (025 to 10 g of 20% mannitol every 3 to 6 h or 075 to 1 mg/kg of furosemide, see below) to maintain serum sodium above 138 meq/L and an osmolality of 290 to 300 mosmol/L Even if ICP monitoring is not utilized, an attempt should be made to maintain this level of osmolality for the rst days if contusion and brain swelling are detected on the CT scan Elevations in osmolality due to excessive concentrations of diffusible solutes such as glucose are not useful in reducing intracranial volume because they do not provide a water gradient across the cerebral vasculature For this reason, the measurement of serum sodium is in some ways a more accurate re ection of free water depletion An initial sodium level of 136 to 141 meq/L is adequate Intravenous uids with free water should be avoided so as not to intensify cerebral edema This poses a particular danger in children who, because of inappropriate secretion of antidiuretic hormone, easily develop water intoxication With this exception, however, restriction of the overall volume of uid is less of a concern than effecting a reduction in free water Fluids such as 5% dextrose in water, 05% saline, and 5% dextrose in 05% saline are therefore avoided; lactated Ringer s solution is permissible; normal saline, with or without added dextrose, is ideal The effects of mannitol have been of great interest to neurosurgeons who treat head trauma, but the best plan for its use has never been established Among the randomized studies that provide clinical data, only the one by Cruz and colleagues has demonstrated a clear bene t and particularly in relation to acute subdural hematoma These authors administered mannitol in a bolus, 06 g/kg, to all patients immediately, and then, once a subdural hematoma was identi ed by CT scan, gave an additional similar second dose to those with reactive pupils and twice the original dose to those with unreactive pupils or anisocoria Bene ts were obtained. rdlc ean 13 EAN - 13 Client Report RDLC Generator | Using free sample for EAN ...
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