@entity17166 -induced @entity772 to protect against XXXX and increased intracranial pressure.

@entity1 @entity4485 @entity12807 @entity64 @entity2806 @entity63 @entity542 @entity1372 @entity772 @entity17166 @entity51 @entity439 @entity1167
The use of barbiturates to induce @entity772 as a means of extending the period of reversible @entity2806 is reviewed. @entity17166 use in @entity1 who had had @entity64 or were undergoing @entity439 surgery was initially encouraging. In uncontrolled feasibility trials in @entity1 with @entity1167 or in deep @entity772 , 40 @entity1 received 10 mg/kg thiopental @entity1372 by i.v. push followed by 20 mg/kg thiopental @entity1372 i.v. over the next 30 minutes; 60% of these @entity1 regained consciousness. In a subgroup of 22 @entity1 who had @entity63 normally associated with a 90% mortality rate, 14 recovered completely. In the largest clinical trial, 45 @entity1 with severe @entity542 and elevated intracranial pressure received 3--5 mg/kg @entity4485 over 10--20 minutes. A serum @entity17166 level of 2.5--4.0 mg/dl was maintained for 14 days, and 30% of these @entity1 recovered but with @entity51 . Other results in @entity64 and drowning victims were not as encouraging. It is concluded that @entity17166 therapy is beneficial in the lowering of intracranial pressure. Focal and global @entity2806 have been shown amenable to @entity17166 therapy in isolated cases. The prophylactic use of barbiturates in surgical procedures requiring focal @entity12807 appears to be beneficial. Controlled trials of the use of @entity17166 -induced @entity772 are clearly indicated.
