CT perfusion in subarachnoid hemorrhage: pieces of a complicated puzzle

Abstract

Subarachnoid hemorrhage (SAH) accounts for 5% of all strokes and is caused by a ruptured intracranial aneurysm in 85% of the cases. After aneurysmal SAH (aSAH) many complications can occur. A common neurological complication is delayed cerebral ischemia (DCI), which can present as focal neurological impairment, a decrease in the level of consciousness, or both. DCI can be reversible or progress to cerebral infarction, which is related to poorer outcome. A common non-neurological complication is temporary cardiac dysfunction, which is related to worse outcome. The pathophysiological mechanism of this relationship is unknown. The prognosis after aSAH is relatively poor with a case-fatality rate of 35%. Many patients who survive have cognitive impairment, but the cause of cognitive impairments after aSAH is poorly understood. A rare subtype of SAH is non-aneurysmal perimesencephalic hemorrhage (PMH). The cause of PMH is still unknown but is suggested to be of venous instead of arterial origin. In contrast to patients with aSAH, patients with PMH have an uneventful clinical course and good prognosis.

CT perfusion (CTP) is a readily accessible and relatively quick method to visualize cerebral perfusion. The aim of this thesis was to explore the clinical application of CT perfusion (CTP) in patients with aSAH, with a focus on DCI. In addition, we explored the relationship between cardiac dysfunction and cerebral perfusion, the etiology of cognitive impairment after aSAH, and the etiology of perimesencephalic hemorrhage. We found that CTP on admission cannot be used reliably to predict DCI. Although significant differences in CTP measures were identified between patients with and without DCI at time of clinical deterioration, the clinical applicability is limited since no threshold values with good test characteristics exist to distinguish between DCI and non-DCI. We also found that DCI patients with a perfusion deficit on CTP more often developed an infarction on follow-up imaging compared to DCI patients without a perfusion deficit. Regarding cardiac dysfunction, we found a relationship between cardiac dysfunction and cerebral hypoperfusion on admission. Further studies are needed to investigate if this association implies causality. Regarding cognitive impairment, no relationship was found between cerebral perfusion within 24 hours after ictus and cognitive outcome 3 months after aSAH. Finally, we found that patients with PMH have a significantly higher cerebral blood flow (CBF) on admission compared to patients with aSAH. A plausible explanation for this finding is that the source of bleeding of aSAH is of arterial origin (which results in a sharp increase in intracranial pressure (ICP) and decrease in CBF), while PMH is of venous origin with a less pronounced increase in ICP and decrease in CBF.