Ischemic Microvascular Failure in Severe Head Injury

Abstract

It is becoming increasingly evident that cerebral dysfunction and outcome after severe (i.e., Glasgow Coma Scale — GCS ≤ 8) head injury (SHI) are related, as a rule, not only to the initial structural injury to the brain, but also to a variety of secondary pathophysiological mechanisms, the common denominator of which is ischemia. The ischemic insult apparently initiates several known (and probably many others yet unknown) metabolic/biochemical cascades that are often interacting, and may also, in themselves additionally contribute to the ischemic insult. Many pathways of the injurious pattern had been described and recently reviewed (1–3). Accordingly, reports of improved animal outcome have often appeared which were related to employment of various specific antagonists/competitors/inhibitors to either block, blunt or treat steps in these injurious pathways. The reports from the laboratories leave little doubt as to the relevance of these cascades to the clinical equivalent following SHI in man. Several recent reports have now come from studies in humans that tend to reinforce the evidence from the laboratory. The use of pharmacological agents to prevent, or treat the results of these cascades in humans must still be viewed as experimental at the time these lines are being written. It is not the intention of this presentation to review the extensive research that we and many others had published on the chain of very important events associated with the secondary ischemic injury following SHI.