OPIOIDS, CEREBRAL BLOOD-FLOW, AND INTRACR ANIAL-PRESSURE

The effects of the opioids alfentanil (A), fentanyl (F), and sufentani l (S) on cerebral blood flow (CBF) and intracranial pressure (ICP) hav e been discussed in several recent publications. The purpose of this r eview is to describe the results of studies in animals, healthy volunt eers, and patients with and without intracranial dieseases. Clinical r elevance and mechanisms of the reported ICP and CBF increases are anal ysed. Methods. Approximately 70 original articles and abstracts were r etrieved by a systematic literature search using the key word list at the end of this abstract. The cited studies came from computerised dat abase systems like Silver Platter and DIMDI, the SNACC reference list, and the bibliographies of pertinent articles and books. These studies were classified into three groups: significant increase of ICP and/or CBF; no significant or clinically relevant alterations; and significa nt decreases of ICP and/or CBF. Results. The numerical relationship wa s 6:7:3 for A, 7:16:9 for F, and 5:11:8 for S. Increases of previously normal or only slightly elevated ICP were registered in some studies in connection with a decrease in mean arterial pressure (MAP). On the other hand, in patients with brain injury and elevated ICP opioids did not further increase ICP despite MAP decreases. In studies monitoring ICP and/or CBF continuously, transient and moderate increases of ques tionable clinical relevance became apparent a few minutes after bolus injection of opioids. Alterations of systemic and cerebral haemodynami cs observed after bolus application were not registered during continu ous infusion of A and S. Discussion and conclusions. The cerebral effe cts of opioids are dependent on several factors, e.g., age, species, v entilation, anaesthesia before and during measurements, systemic haemo dynamics, and underlying diseases. The probable mechanism of ICP incre ase during decreasing MAP is cerebral vasodilatation due to maintained autoregulation. With increasing severity of the cerebral lesion autor egulation is often disturbed. Therefore, ICP often remains unaltered d espite MAP decreases. However, the resulting decrease in cerebral perf usion pressure makes such patients more susceptible to develop ischaem ic neurological deficits. Induction of somatic rigidity or (with high doses) convulsions, exceeding the upper limit of autoregulation, hista mine release, cerebral vasodilatation, increased cerebral oxygen consu mption, or carbon dioxide accumulation during spontaneous breathing we re discussed as mechanisms for transient ICP/CBF increases. It is conc luded that opioids are often beneficial and not generally contraindica ted for patients with cerebral diseases and compromised intracranial c ompliance. However, since negative side effects cannot be excluded, op ioid effects and side effects should be monitored (MAP, ICP, cerebrove nous oxygen saturation, transcranial Doppler sonography) in patients a t risk. It has to be stressed that opioids should be administered only to patients with stable haemodynamic situations and preferably in wel l-titrated, continuous infusions.