Cerebral hemodynamic effects of pentobarbital coma in head-injured patients

The purpose of this study was to examine the changes in cerebral hemodynami cs of head-injured patients undergoing barbiturate treatment of refractory intracranial hypertension. Cerebral blood flow (CBF) and metabolism variabl es were measured in 67 severely head-injured patients at the following time s: before the loading dose of pentobarbital; after the loading dose of pent obarbital (average pentobarbital level 28.1 +/- 8.3 mu g/mL); and 3 days la ter, when the peak pentobarbital level averaged 42.5 +/- 17.2 mu g/mL. Intr acranial pressure (ICP) and mean arterial blood pressure (MAP) were decreas ed by the loading dose of pentobarbital by an average of 12 and 9 mm Hg, re spectively. Cerebral perfusion pressure (CPP) was unchanged when the entire group was analyzed together. CBF, cerebral oxygen consumption (CMRo(2)), a nd arteriovenous oxygen difference (AVDo(2)) were significantly decreased a fter the loading dose of pentobarbital, by 20%, 31%, and 11%, respectively. The average cerebrovascular resistance (CVR) was increased by 20%. The cha nge in CMRo(2) with the loading dose of pentobarbital was closely related t o the pretreatment value (n = 67, r(2) = 0.65, p <.001). Thirty (45%) of th e patients had a "good ICP response," with a reduction in ICP from 34 +/- 9 to 15 +/- 5 mm Hg after the initial loading dose of pentobarbital. Twenty- seven (40%) of the patients had a "partial ICP response," with ICP decreasi ng but still remaining above 20 mm Hg after the loading dose of pentobarbit al. In the remaining 10 patients, ICP did not change or even increased afte r pentobarbital. In the 30 patients with a good ICP response, pretreatment CMRo(2) and AVDo(2) were greater before administration of pentobarbital, an d CMRo(2) and AVDo(2) decreased more with the loading dose of pentobarbital , than in the patients with partial or no ICP response. The outcome was sig nificantly better in the patients with a good or partial ICP response to pe ntobarbital, with 21% of these patients having a good recovery or moderate disability at 3 months after injury, compared with 100% persistent vegetati ve state or death in the nonresponders. In summary, barbiturate coma can be a useful treatment modality for acutely reducing ICP in selected patients. Patients with overwhelmingly severe injuries are not likely to benefit, pa rtly because their CMRo(2) is already markedly reduced by the injury and pa rtly because their outcome is already predetermined by the injury. Patients with systemic hypotension are not likely to have a good response because h ypotension limits the amount of barbiturates that can be given.