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Case Notes
History
36 year old male diabetic who was found down. Patient initially was unresponsive, and later exhibited a markedly depressed level of consciousness. Patient was uncooperative on presentation and aphasic.Exam
2 minute delayed post contrast head CTA with: analysis of pial collateralization, plus a comparative analysis of the CT density within the venocapillary pool (using the initial and delayed post contrast CTA’s), plus an analysis of venous egress. This part of the CTA is referred to as either the delayed post contrast CTA 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 CTA is used to detect distal pial collateralization and to assess the CT-density within the parenchymal venocapillary pool, which provides the best CTA evidence of ischemic injury.
Purposes
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. 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).
Purposes
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. 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
Non-Contrast Head CT1. Acute thrombus in Lt. intracranial primary and secondary stem components of the Lt. ICA
2. Early cytogenic edema in both Lt. ACA & MCA territories, likely stroke-age is in the 3-6 hour range.
CT Perfusion
1. CT perfusion was not obtained.
CTA of the Neck
1. There were no flow limiting stenoses in the lower and mid cervical major afferent arteries.
2. There is unexplained reduced lumen size of the upper Lt. cervical ICA likely secondary to downstream obstruction. However, the neck CTA did not include any of the intracranial/extradural parts of the left ICA.
CTA of the Head (using initial post contrast exam)
1. Likely source of the left ICA arterial obstruction is a dissection of the vertical intrapetrous ICA segment. There is no EC-IC collateralization.
2. There is complete thrombosis of both the intracranial/extradural and intradural Lt. ICA with no filling of the primary or secondary intracranial stem branches plus there is no distal pial artery filling from pial collaterals. In essence, there is no arterial circulation to the left ICA at all.
3. There is no filling of the left cortical or deep central veins. These same veins are all well seen on the normal right side. This is consistent with the venous collapse and advanced hemispheric dense ischemic core possibly to the level of acute sequestered infarction.
4. Cut-off of the opacified left P-com is indicative of incisural brain herniation on the left.
