The impact of imaging on stroke treatment and clinical outcome - Karolinska Stroke Update Consensus Statement 2004

 

The following Consensus Statement was adopted by the 5th Karolinska Stroke Update meeting on November 15, 2004.

The consensus statement  was proposed by the chairpersons in the session, Professor Rüdiger von Kummer, Dresden, and Professor Wolf Dieter Heiss, Cologne, together with the Dr Patrik Michel, Lausanne, additional speaker in the session. The statement was then finally approved by the participants of the meeting, after listening to the different presentations.

The speakers in this session were Professor Rüdiger von Kummer, Dresden, Professor Wolf Dieter Heiss, Cologne and Dr Patrik Michel, Lausanne.

 

 

Consensus statement: The impact of imaging on stroke treatment and clinical outcome

To assess the accuracy and clinical effectiveness of an imaging test in stroke patients, one requires a prospective, blinded comparison of the imaging modality to a reference standard in a consecutive series of patients from a relevant clinical population. Effectiveness can be achieved on 6 different levels: 1. Availability and technical capacity of the imaging modality to detect stroke pathology and arterial dysfunction, 2. diagnostic accuracy, 3. diagnostic impact, 4. therapeutic impact; 5. impact on patient clinical outcomes, and 6. impact on health care costs. Efficacy on a lower level may not improve clinical outcomes and not reduce health care costs, but is a precondition for efficacy on a higher level.

In stroke, the following pathology is considered as relevant for the response to treatment and the patients’ prognosis:

  1. The ischemic nature of stroke by excluding brain hemorrhage and other diseases mimicking stroke.

  2. Cardio-vascular pathology.
  3. Volume of brain tissue at risk from hypoperfusion.
  4. Brain tissue volume of ischemic damage.

1.Computed tomography (CT) and magnetic resonance imaging (MRI) are now both widely available. It appears, however, that imaging the acute stroke patient is easier with CT than with MRI (grade B evidence). CT and MRI have the capacity to detect acute brain hemorrhage with similar accuracy (grade A evidence). MRI has in addition the capacity to detect hemoglobin in different stages of degeneration within the brain tissue and can thus differentiate between old and acute bleedings (grade C evidence). The accuracy of CT and MRI in detecting brain hemorrhages was never tested against a reference standard (pathology) in prospective trials. It is widely accepted (based on grade C evidence) that CT and MRI can both identify patients with ischemic stroke to allow reperfusion therapy. Large controlled randomised trials that had used CT to exclude brain hemorrhage showed a benefit from treatment with rt-PA. It was shown that CT scanning immediate after stroke  can increase quality adjusted life years and reduce health care costs (grade B evidence). A small phase 2-controlled-randomised trial that used echo planar MRI to exclude brain hemorrhage showed a benefit from treatment with desmoteplase. It is widely accepted that MRI is superior to CT in detecting other brain diseases that could mimic ischemic stroke (grade C evidence).

2. CT angiography (CTA) and MR angiography (MRA) can both detect stenoses and occlusions of extra- and intracranial brain supplying arteries and describe vessel wall pathology with high accuracy (grade B evidence). Digital subtraction angiography is still regarded as the reference standard, but is only required if intervention is an option. The assessment of arterial stenosis allow an estimate of the perfusion deficit and risk of stroke (grade B evidence). Regions with low contrast on CTA source images correlate with the final infarct volume (grade B evidence).

3. The brain tissue at risk to be damaged by hypoperfusion cannot be clearly differentiated from tissue experiencing benign oligemia that will survive independently of treatment effects. Perfusion imaging (PI) is feasible with CT and MRI in the acute clinical setting. CT using iodine or stable xenon as contrast agent has currently the capacity to display parameter images of time to contrast peak (TTP), mean transit time (MTT) of contrast, cerebral blood volume (CBV) and flow (CBF) in up to 4 sections through the brain. MRPI can display the same parameter images for the whole brain, however. These parameters, provide a rough estimate of tissue at risk from ischemia (grade B evidence). Compared with the standard reference positron emission tomography (PET), the accuracy of these perfusion parameters as assessed by CTPI or MRPI is not perfect, however (grade B evidence). PI may help to estimate the risk for stroke in patients with arterial stenosis or occlusions (grade C evidence). PET is a research tool, which can be used to calibrate data from other modalities. This is evident in a comparison of the mismatch between the extent of perfusion disturbance and of ischemic damage and increased oxygen extraction fraction, which both are considered surrogate markers of the ischemic penumbra. However, the correspondence is rather poor, and the mismatch volume does not reliably reflect misery perfusion as defined by PET. Brain regions with increased OE are considered to be at high risk of ischemic damage (grade B evidence). MRI, but not CT may have the capacity to identify brain regions with increased OE.

4. Irreversibly injured brain tissue cannot per definition benefit from reperfusion strategies. There is evidence (grade C) that such tissue may bleed when cerebral blood flow is restored. CT has the capacity to early detect ischemic edema that has a high prediction for ischemic damage with high specificity (grade B evidence). The assessment of decreased CBV with CTPI may show the ischemic damage as well (grade C evidence). Diffusion weighted imaging (DWI) has a lower specificity in defining ischemic damage early after stroke onset, but its sensitivity to detect ischemic brain tissue is higher than that of non-enhanced CT (grade B evidence). Patients with extended tissue hypoattenuation on CT beyond 3 hours (> 1/3 of the middle cerebral artery territory; < 8 points of ASPECTS) do not benefit from treatment with rt-PA (grade B evidence). Because the lesion on DWI may include the ischemic penumbra and because no randomised data regarding DWI-volume and thrombolysis exist, an upper lesion volume that should prevent from treatment with rt-PA cannot yet be defined. Patients with a small lesion on DWI, but extended perfusion deficit may benefit from reperfusion strategies even after the accepted time window of 3 hours (grade C evidence).