Cerebral blood flow changes in acute subarachnoid hemorrhage

Abstract

Delayed vasospasm and secondary injury due to ischemia occur frequently in the setting of subarachnoid hemorrhage (SAH), and these changes have been well characterized within the last decades. Considerable effort has also been put into the development of therapeutic strategies and appropriate monitoring modalities. However, although in particular acute injury is known to contribute significantly to overall outcome in SAH, these immediate alterations still remain largely neglected in current research. Few studies exist to date which mainly describe rapid alterations in perfusion and metabolism. As the main characteristic of the very first minutes and hours after SAH, an immediate phase of CPP-independent hypoperfusion has been observed repeatedly both experimentally and clinically, and it has mostly been attributed to the development of acute vasospasm. Endothelin and nitric oxide, prime suspect in the pathogenesis of chronic vasospasm, may play a pivotal role in this early scenario, possibly being promoted by the drastic ICP increase and extravasation of blood compounds. The much disputed concept of inflammation in chronic vasospasm may not be applicable this early after the ictus, but mechanisms of cellular and structural changes causing microvascular platelet aggregation and immediate disruption of the basal lamina, however, are thought to contribute significantly to the imminent cascade of disturbances in perfusion and metabolism. This review is intended to summarize current insights and illustrate recent efforts to better understand alterations in cerebral perfusion in these very first minutes and hours after SAH which--at some point--may also be amenable to early therapeutic intervention.

Microglia inflict delayed brain injury after subarachnoid hemorrhage

“…In the early phase of SAH, brain injury has been discussed to take place via apoptotic pathways, induced by the sudden rise of intracranial pressure and the subsequent impairment of the cerebral perfusion. Several downstream pathways of this concept have been described within the past years [16,27,29,47,56,60,61,71,73].…”

“…Direct brain injury in the early phase starts with the onset of the bleeding and is mediated mainly through physical stress. A rise in intracranial pressure (ICP) leads to a decrease in cerebral perfusion, which can induce hypoxia [40,61]. Furthermore, blood elicits a deleterious effect on the brain parenchyma, leading to a swelling of the brain within the first days after SAH.…”

Blood–brain barrier permeability change and regulation mechanism after subarachnoid hemorrhage

“…Rapidly increased intracranial pressure after SAH leads to significantly decreased regional cerebral blood flow (rCBF) and metabolic changes (Doczi 1985;Schubert and Thome 2008). Acute brain injury following SAH is a key factor related to the poor prognosis (Broderick et al 1994).…”

Risk Profile of Patients with Poor-Grade Aneurysmal Subarachnoid Hemorrhage Using Early Perfusion Computed Tomography

“…A more pronounced initial decrease in CBF has also been found in patients with a higher Hunt and Hess grade (5,12,19). Acute hypoperfusion is caused by various cellular and structural changes, but the theory that acute vasospasms are a major factor has gained widespread acceptance (20). A retrospective analysis of a large multicenter trial has also shown angiographically that acute vasospasms within the first 48 hours occur in 10% of patients admitted for SAH treatment (2,16,22).…”

“…This early and profound change in perfusion is thought to reflect the impact of the primary injury and vulnerability to secondary insults (20). Also, the initial severity of the hemorrhage and CBF reduction during the early SAH period are the major determinants of imminent morbidity and mortality (3,17).…”