Code stroke CT (an approach)
A code stroke CT can be daunting to interpret as not only does it involve many sequences but it also includes CT perfusion with which many radiologists and clinicians alike are relatively unfamiliar. If that wasn’t challenging enough, there is usually the added pressure to make the diagnosis rapidly as treatment is time-critical. As such, having a standardized approach to these studies will not only reduce your stress and make you more resilient to interruptions but also allow you to make the correct diagnosis in a timely fashion.
As with all such articles, there is no single “correct” approach. What is presented below is merely “an approach” and the reader is invited to adapt it in light of local and personal preferences.
It should go without saying that identifying occlusive thromboembolism is the primary purpose of a stroke protocol CT. However, it is also important to recognize that many other diagnoses may have caused an acute stroke-like presentation and that many of these will be visible on CT.
The key findings that should be sought include:
- ischemic stroke findings
- non-ischemic stroke findings
Although all features of the three components of a code stroke (non-contrast CT of the brain, perfusion of the brain and CT angiography of the head and neck) need to eventually be looked at in detail, a strong argument can be made for having a systematic order that maximizes the efficiency with which key findings are identified.
Given the time-critical nature of assessing acute strokes, a two-pass approach can be useful and the first pass can be performed quickly, even at the CT workstation, prior to all reconstructions being available.
First pass review
First, quickly review the non-contrast CT scan for intracerebral hemorrhages (both parenchymal and extra-axial), and obvious established infarcts, tumors or other unexpected pathology. Take a few seconds to attempt to identify proximal hyperdense arteries (terminal internal carotid artery, proximal middle cerebral artery, basilar tip). This should only take 15-30 seconds.
Next move onto CT perfusion maps, starting with mean transit time (MTT). These will usually quickly identify large areas of brain with abnormal perfusion. If MTT is completely normal, it is unlikely that a sizable acute occlusive lesion is present.
If there is a region of prolongation, then review cerebral blood volume (CBV).
If the MTT region of abnormality is mostly infarct core, then you most likely will see a matched defect - in other words, an area of reduced CBV will conform to the area of MTT abnormality. This brain is unlikely to be able to be salvaged and clot lysis or retrieval is, therefore, less likely to be of benefit and may, in fact, be contraindicated.
If CBV is normal or elevated, in the context of acute neurological dysfunction, you are most likely looking at a sizable penumbra and this patient needs the most rapid management as they have the largest amount of salvageable tissue. Often, both core and penumbra will co-exist and therefore an attempt should be made to quantify each component as both are important for patient selection. For example “small core, large penumbra” or “large core, no appreciable penumbra”
It is worth noting that successful auto-regulation (for example due to long-standing carotid stenosis) or benign oligemia will also have prolonged MTT and normal or elevated CBV; however, they will usually be asymptomatic and thus not presenting as an acute stroke.
Cerebral blood flow (CBF) is also useful but as it is reduced in both penumbra and infarct core visually assessing it can be challenging and if relied upon to define core it will often lead to an overestimate of core and an underestimate of the penumbra. It is worth noting that some automated software solutions that calculate core and penumbra volume rely on CBF, but they used thresholds to distinguish between the two that are not readily visible to the harried naked eye.
Finally, review the intracranial portion of CT angiogram which should extend from the arch of the aorta to the vertex of this skull. Your search will be made much more targeted by the perfusion scans. If they were normal, it is unlikely that there is a sizable and treatable acute occlusion. Conversely, if you identified an area of abnormal perfusion, you will be able to identify the vessel involved due to the distribution.
By the end of this first pass, that should only take a total of a minute or two, you will in most instances have triaged patients accurately into one of four categories:
- no obvious abnormality and therefore unlikely to benefit from time-critical therapy
- obvious non-thromboembolic pathology (e.g. hemorrhage, tumor etc…)
- obvious thromboembolic stroke who are unlikely to benefit from clot retrieval or thrombolysis (e.g. established infarct with large infarct core and little if any penumbra)
- obvious thromboembolic stroke who are likely candidates for emergency therapy (e.g. large territory occlusive thromboembolism with small infarct core and large penumbra, or basilar tip thromboembolism)
Before going on to the second pass review you will likely need to/want to communicate your findings to relevant parties. Generally, it is worth letting the stroke team know regardless of the findings as even a message of “there is a large subdural hematoma” or “there is no obvious abnormality” has consequences for immediate management.
If your patient falls into the last category, an obvious acute thromboembolic stroke either with a large penumbra or of the basilar tip, then a few additional features that impact management should be sought before contacting the stroke team and/or neurointerventionalist. This will only take a few seconds.
- is the thromboembolism calcified?
- how long is the thromboembolism?
- how good are the collaterals?
- what is the arterial access like?
Calcific emboli are less likely to respond to thrombolysis and are more dangerous to retrieve. Depending on the demographics of the patient and clinical presentation (e.g. NIHSS) this may change treatment strategies.
Length of thromboembolism
The length of thromboembolism impacts the likelihood of successful thrombolysis, with longer clots less likely to be lyzed than short ones. Unfortunately, CT angiography can overestimate the length considerably as visualization of the distal end of the clot relies on backfilling of the vessel with contrast by collaterals (see below). Thus, assessing length based on artery hyperdensity on the thinnest images available windowed to accentuate the clot hyperdensity can be helpful.
Additionally, reviewing the raw perfusion images in some patients can clearly delineate the distal end of the occlusion, provided they have adequate collateral circulation. Perfusion scans are obtained over a relatively long period of time and thus give collaterals a better chance of opacifying the blood just distal to the clot.
The better the collateral arterial supply to the affected territory, the better the outcome will be. These patients will tend to be able to tolerate ischemia longer before their penumbra progresses to infarction. They are known as slow progressors. In contrast, poor collateral supply will result in rapid progression from penumbra to infarct core. Unfortunately, poor collaterals also increase the likelihood of treatment complications. Overall, therefore, poor collateral circulation is correlated with poor outcome.
There are numerous described grading scales for collateral supply but most boil down to assessing how well the vessels distal to the occlusion are opacified. If no opacification is seen, then collateral supply is poor. In contrast, if they are normal or even more pronounced than the normal contralateral territory, then collateral supply is good.
Successful endovascular clot retrieval relies on gaining access to the thromboembolism with a variety of catheters of various diameters and stiffness. Care must therefore be taken to examine the vessel that needs to be catheterized to access the clot from the aortic arch to the site of occlusion.
If, for example, the aortic arch anatomy is unfavorable (e.g. bovine origin of the left common carotid or highly tortuous vessels) accessing the cervical carotid or vertebral arteries may be more challenging, necessitate alternative choice of catheters or require a radial artery approach.
Alternatively, if a tandem lesion is present (i.e. occlusion or high-grade stenosis of the proximal internal carotid artery as well as ipsilateral thromboembolism to the terminal internal carotid or middle cerebral artery) then plans for treatment of both lesions with stents and/or balloons will be required.
It is worth being aware of carotid pseudo-occlusion that refers to apparent continuous cervical internal carotid artery occlusion actually resulting from a stagnant column of unopacified blood proximal to a terminal “T-junction” internal carotid artery occlusion. This can mimic a tandem lesion or cervical carotid dissection.
Second pass review
Satisfaction of search errors are particularly likely in situations where other abnormalities have already been identified and the patient has been taken for emergent treatment and an incidental aneurysm or tumor or abnormal soft tissues in the neck are easy to overlook if you know the patient is currently having a basilar tip thromboembolism retrieved.
As such, the second pass is a more leisurely and traditional approach to the entire study and need not have a specific approach in the setting of stroke compared to any other presentation. Rather, approach each component of the study independently (e.g. see CT head - an approach) paying particular attention to unexpected incidental findings that may be overlooked during the first pass.
Related Radiopaedia articles
Stroke and intracranial haemorrhage
stroke and intracranial hemorrhage
- code stroke CT (an approach)
- general discussions
- CT perfusion
- multiphase CT angiography
- fogging phenomenon
- calcified cerebral embolus
- DWI in acute stroke
- acute vs chronic ischemic stroke (CT)
- transient ischemic attack (TIA)
- intracranial atherosclerotic disease (ICAD)
- scoring and classification systems
- Alberta stroke program early CT score (ASPECTS)
- Canadian Neurological Scale
- NIH Stroke Scale
- Mathew Stroke Scale
- modified Rankin scale
- Orgogozo Stroke Scale
- Scandinavian Stroke Scale
- thrombolysis in cerebral infarction (TICI)
- TOAST classification
- collateral vessel scores
- by region
- hemispheric infarcts
- lacunar infarct
- thalamic infarct
- striatocapsular infarct
- cerebellar infarct
- midbrain infarct
- pontine infarct
- Brissaud-Sicard syndrome
- facial colliculus syndrome
- Gasperini syndrome: basilar artery or AICA
- inferior medial pontine syndrome (Foville syndrome): basilar artery
- lateral pontine syndrome (Marie-Foix syndrome): basilar artery or AICA
- locked-in syndrome: basilar artery
- Millard-Gubler syndrome: basilar artery
- Raymond syndrome: basilar artery
- medullary infarct
- acute spinal cord ischemia syndrome
- by vascular territory
- anterior circulation infarction
- posterior circulation infarction
- treatment options
- general discussions
- signs and formulas
- by region or type
- basal ganglia hemorrhage
- cerebellar hemorrhage
- cerebral contusions
- cerebral microhemorrhage
- hemorrhagic venous infarct
- hemorrhagic transformation of an ischemic infarct
- hypertensive intracranial hemorrhage
- intraventricular hemorrhage (IVH)
- jet hematoma
- lobar hemorrhage
- pontine hemorrhage
- extra-axial hemorrhage
- extradural versus subdural hemorrhage
- extradural hemorrhage (EDH)
- intralaminar dural hemorrhage
- subdural hemorrhage (SDH)
subarachnoid hemorrhage (SAH)
- vasospasm following SAH
- grading systems
- subpial hemorrhage
- intra-axial hemorrhage