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 ce rebral artery flow velocity (MCAV), ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP), were continuously recorded bef ore (T-0), at the end (T-1), and 30 min after (T-2) a 10-min intraveno us (IV) infusion of 2.5 mu g/kg clonidine. The cerebral arteriovenous oxygen content difference (AVDO(2)) and Paco(2) were sequentially obta ined. ICP, Paco(2), AVDO(2), and MCAV did not change after clonidine a dministration. In contrast, MAP and CPP decreased (P < 0.05 and P < 0. 05, respectively, at T-1 and T-2). Three subjects displayed a transien t increase in ICP (> 10 mm Hg) at T-1; this increase was concomitant w ith the decrease in MAP. Clonidine administered as an IV 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.