Changes in cerebral hemodynamics after a single dose of clonidine in severely head-injured patients

alpha 2-Adrenergic agonists induce cerebral vasoconstriction, reduce intracranial pressure (ICP) in experimental animals and may be useful in the hemodynamic management of head-injured patients. We studied the effects of the alpha 2 agonist clonidine on the cerebral circulation in 12 head-injured patients (Glasgow Coma Scale score < 8). Middle cerebral artery flow velocity (MCAV), ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP), were continuously recorded before (T0), at the end (T1), and 30 min after (T2) a 10-min intravenous (i.v.) infusion of 2.5 micrograms/kg clonidine. The cerebral arteriovenous oxygen content difference (AVDO2) and Paco2 were sequentially obtained. ICP, Paco2, AVDO2, and MCAV did not change after clonidine administration. In contrast, MAP and CPP decreased (P < 0.05 and P < 0.05, respectively, at T1 and T2). Three subjects displayed a transient increase in ICP (> 10 mm Hg) at T1; this increase was concomitant with the decrease in MAP. Clonidine administered as an i.v. infusion may induce a critical but transient increase in ICP in some severely head-injured patients. This effect may result from cerebral autoregulatory vasodilation and increased cerebral blood volume as a response to the hypotensive effects of clonidine.