Hyperacute Arterial Stroke: CT Venocapillary Pool

History

Acute change in neurologic status; rule out stroke.

Exam

Post contrast (2 minute delayed) head CT
The delayed post contrast head CT is used primarily to analyze the parenchymal CT density within the venocapillary pool using the initial and delayed post contrast CTA’s, while comparing CT density in affected versus unaffected areas of the brain. Reduced CT density indicates reduced transcapillary blood flow. The post contrast head CT can also be used to evaluate the effectiveness of the pial collateralization and of the state of venous egress. This part of the CTA is referred to as either the delayed post contrast CT, or the 2nd pass CTA, since it is performed after the 2nd contrast bolus. It has the benefit of recirculation effects, and twice the contrast load, as the initial post contrast head CTA. The delayed post contrast CT provides the best CTA evidence of focal persistent oligemia. When there is no rise in the CT density in the affected area, then completed stroke will have occurred.

Directive:
This imaging step is a comparative analysis. There are two sequences: a 1st pass CTA performed after the 1st IV contrast injection (labelled initial perfusion in the print section of the images) and a 2nd pass CTA performed after the 2nd IV contrast injection (labelled delayed perfusion in the print section of the images). First evaluate the CT parenchymal contrast density on the initial perfusion exam, comparing gray matter vs. white matter differentiation and also compare differences between non-affected vs. affected areas of brain. Then evaluate the delayed perfusion in the same way and compare any suspicious areas with the initial perfusion sequence in order to detect any failure of parenchymal density to return to normal (i.e. areas of persistent oligemia).

Purpose

1. To identify any, and all, sites of intracranial afferent block (either occlusion or combination of tandem stenosis and an incomplete circle of Willis).

2. To determine whether the observed pial collateral gap observed on the CTA head finally reaches the proximal thrombus on the delayed post contrast CTA head (considered fair collateral). However, this tissue may still be at risk for ischemic injury.

3. If the a pial collateral gap remains on the delayed post contrast head CTA, then tissue within the gap will likely be in the dense ischemic core and become a completed stroke (ischemic cascade plus glutamate cascade leading to liquefactive necrosis or sequestered infarct or both).

4. Given there is observably reasonable pial collateral, it does NOT ensure that there is perfusion of the underlying tissue. To assess whether the existing pial collateral actually perfuses the underlying brain parenchyma, a comparative analysis is made between the CT contrast density within the venocapillary pool in the affected region on the initial post contrast CTA with the CT density on the delayed post contrast CTA, and that is compared to unaffected comparable region on the contra lateral side. At-risk tissue (ischemic penumbra) will exhibit a partial rise in CT density between the 1st and the 2nd post contrast CTA, but it will not reach normal range compared to unaffected brain. Tissue that shows little or no rise in CT density in the venocapillary pool will be within the dense ischemic core. The areas of significantly reduced & absent parenchymal contrast CT density are at higher risk of hemorrhagic conversion upon reperfusion (spontaneous or therapeutic). Note: analysis of the CT density in the venocapillary pool and CT perfusion are both approximations of tissue actual perfusion based on changes in concentration of the contrast media in tissue over time. Thus, an initial short-term high depth-duration oligemic event can occur, initiating the ischemic cascade. But the afferent block can quickly clear, which means tissue injury can be initiated, but the antegrade blood flow is restored. In this circumstance, tissue injury will have occurred, but the restroration of pial blood flow will appear as normal or near normal on both the CT perfusion and the CT density within the venocapillary pool. Thus, both the CTA and CT perfusion may underestimate tissue injury, which is why the stroke protocol MR is of value, since actual tissue injury will always show up, in some fashion, on MR diffusion sequences.

5. Given there is an ICA stenosis/occlusion, is there effective EC-IC collateral.

6. In the context of restricted intradural afferent arterial blood flow obstruction (in the absence of a primary stem occlusion), has regional hypoperfusion produced oligemia in the expected anastomotic border zones producing a watershed stroke pattern.

7. In the context of an ICA thrombosis, tandem stenoses, incomplete portions of circle of Willis, or a combination of these, is there a shift in the location of the anastomotic border zones such that oligemia produces an end-of the-line watershed stroke pattern in an unexpected position. Low flow ischemia within the end-of the-line portion of a shifted watershed can account strokes that involve tissue not primarily affected by the thrombus.

8. To evaluate the state of venous egress, at least for the major veins (note: SWI is the most effective of assessing flow in the deep parenchymal medullary veins).

Prior Study

CT Head

CT Perfusion

CTA Head

Findings

Pial Collateral Analysis

Does the pial collateral reach the distal end of the arterial thrombus on the 1st pass initial post contrast head CT (good if yes). [Yes/No]

Does the pial collateral reach the distal end of the arterial thrombus on the 2nd pass delayed post contrast head CT (fair if yes). [Yes/No]

There is an incomplete circle of Willis contributing to delayed collateral filling (increases probability of stroke w/ intercurrent hypotension). [Yes/No]

There is a gap between the site of the thrombus versus the available pial collateral on the 1st pass initial post contrast head CT. [Yes/No]

There is a gap between the site of the thrombus versus the available pial collateral on the 2nd pass delayed post contrast head CT. [Yes/No]

Given the prior two answers, did the pial collateral-to-thrombus distance improve between the 1st & 2nd pass post contrast head CT. [Yes/No]

Venocapillary Pool (CT density) Analysis

The 1st pass initial post contrast head CT demonstrates reasonable (fair or good) retrograde pial collateral, and the CT density within the parenchymal CT density within the venocapillary pool appears reasonably normal, as well. [Yes/No]

The 1st pass initial post contrast head CT’s demonstrate reasonable but incomplete retrograde pial collateral, but the CT density within the parenchymal CT density within the venocapillary pool appears absent or nearly absent (compared to the contralateral side). [Yes/No]

The 2nd pass delayed post contrast head CT demonstrates reasonable retrograde pial collateral, but, the CT density within venocapillary pool within the stroke-zone appears exaggerated, compared to the contralateral side, reflecting vasodilatation indicating post ischemic dysautoregulation. [Yes/No]

The 2nd pass delayed post contrast head CT demonstrates reasonable (fair) retrograde pial collateral, and the CT density within the venocapillary pool now appears normal on the delayed CT, as well indicating the pial collateral effectively supplies the underlying brain. [Yes/No]

The 2nd pass delayed post contrast head CT demonstrates fair retrograde pial collateral but the CT density within venocapillary pool, although present, appears significantly reduced from expected normal. [Yes/No]

There is oligemic brain on the initial and delayed post contrast CTA’s is smaller when compared to the CT perfusion, because of functional pial collateral. [Yes/No]

There is oligemia in perforating artery territories with reduced or absent venocapillary pool CT density evident on both the initial & delayed post contrast CT head indicating perforating artery stroke. [Yes/No]

There is oligemia in brain with a “usual watershed distribution” with both incomplete retrograde pial collateral and reduced or absent venocapillary pool CT density evident on both the initial & delayed post contrast CT head. [Yes/No]

There is oligemia in brain with a shifted end-of the-line watershed distribution with both retrograde pial collateral but reduced or absent venocapillary pool CT density evident in the region of the shifted watershed zone. [Yes/No]

Repeat analysis of the venous egress on the delayed post contrast head CTA reveals persistent evidence of reduced opacification or absence of cortical veins deep central veins or of the dural sinuses. [Yes/No]