Introduction
The results of non-invasive tests (e.g. ultrasound) can be highly variable, often providing ambiguous results. Although other parameters can be reviewed, calculation of overall accuracy, sensitivity, and specificity as well as positive and negative predictive values are useful to the clinician who is managing the patient.
To calculate these statistics, ultrasound results must be compared to the established gold standards, usually angiography, surgery, or autopsy findings. The simplest statistic compares the outcome of each test as either positive or negative. A true-positive result indicates that both tests are positive. A true-negative result indicates that both tests are negative. A false-positive result means that the gold standard is negative, indicating the absence of disease, while the non-invasive study is positive, indicating the presence of disease. A false-negative result occurs when the non-invasive test indicates the absence of disease, but the gold standard is positive. True-positive and true-negative results can be used to calculate sensitivity and specificity. Sensitivity is the ability of a test to correctly diagnose disease. It can be calculated by dividing the number of true-positive tests by the total number of positive results obtained by the gold standard.
Specificity is the ability to diagnose the absence of disease and is calculated by dividing the true negative by the total number of negative results obtained by the gold standard. The positive predictive value (PPV) or likelihood means that disease is present and negative predictive value (NPV) means that disease is not present. Overall accuracy can be calculated by dividing the number of true negatives and true positives by the total number of tests performed. These results are not very specific and can be highly variable, based on the incidence of disease in the patient population. Because the patient population referred to the ultrasound lab is diverse, high levels of sensitivity and specificity help to make the diagnosis optimal.
Extracranial Ultrasound in Acute Stroke
The most important diagnostic question in ultrasonography is which extra- and intracranial vessel(s) is/are stenotic or occluded and can it/they be responsible for the clinical symptoms. Note that clinically silent stenotic processes might also influence the cerebral circulation.
Because of the interactions between extra- and intracranial hemodynamics, both extracranial and intracranial ultrasound techniques should be performed in acute stroke. Similarly, clinically silent stenoses should be detected by careful investigation of anterior, posterior, or ipsi- and contralateral vasculature.
Doppler ultrasonography is the primary non-invasive test for evaluating carotid stenosis.
Carotid ultrasonography consists of two steps: imaging and spectral analysis. Images are produced with the brightness-mode (B-mode) technique and sometimes color flow information is superimposed on the grayscale image. By convention, the color of the pulsating artery is red. The echogenicity of an object on the image determines its brightness. An object that rebounds very little of the pulse is hypoechoic. An object that reflects much of the signal, such as calcified plaque, is hyperechoic. Plaques with irregular surface and/or heterogeneous echogenicity are more likely to embolize. Soft plaques present a higher embolic risk than hard plaques. The sonographic characteristics of symptomatic and asymptomatic carotid plaques are different.
Recently, a meta-analysis (more than 1 000 articles and 6 000 plaques) demonstrated that plaque neovascularity (OR = 19.7), complexity (OR = 5.12), plaque ulceration (OR = 3.58) and echolucency (OR = 3.99), and intraplaque motion (OR = 1.57) are associated with ischemic symptoms. Heterogeneous echotexture and surface irregularity without ulceration had no significant correlation with symptom status. The authors conclude that sonographic evaluation of carotid artery stenosis should focus on the detection of these plaque characteristics in addition to quantifying the degree of stenosis [1].
The degree of stenosis is better measured on the basis of the waveform and spectral analysis of the CCA and its major branches, especially the ICA. Spectral (velocity) analysis is essential to identify stenosis or occlusion. An important general rule for ultrasound is the greater the degree of stenosis, the higher the velocity. Power Doppler provides color imaging that is independent of direction or velocity of flow and gives an angiographic-like picture of an artery.
Blood flow can be laminar, disturbed, or turbulent. When no stenosis is present, blood flow is laminar. Flow of blood is even, with the fastest flow in the middle and the slowest at the edges of the vessel. When a small degree of stenosis is present, the blood flow becomes disturbed and loses its laminar quality. Even in normal conditions, such flow can be seen around the carotid bulb. With even greater stenosis, the flow can become turbulent [2].
In normal hemodynamics, as vessel length increases so does resistance. With increasing radius, the resistance decreases significantly.
As vessel diameter (and area) decreases, blood velocity increases to maintain volume flow.
The extracranial ultrasound procedure starts with the CCA, internal carotid artery (ICA), and external carotid artery (ECA); at least two or three spectral analyses of each vessel should be obtained. Color imaging and power Doppler may be used, but may not necessarily provide additional information.
Note the carotid bifurcation, look for plaques, attempt to characterize the nature of the plaque, and color may be used at this point to identify flow within the artery and potential areas of high velocity.
CCA can be identified by pulsatile walls, smaller caliber than the jugular vein and systolic peak, and diastolic endpoints in between those of external and internal carotid arteries on spectral analysis. ECA has a smaller caliber, while ICA is often posterolateral to ECA and ECA may have a superior thyroid artery branch coming off. ECA has virtually no diastolic flow (i.e. high-resistance vessel) on spectral analysis. ECA shows positive “temporal tap” (i.e. undulations in waveform with tapping of the temporal artery). Perform spectral analysis and find the highest velocity or frequency. After assessment of the anterior circulation, the sonographer should assess the vertebral circulation. Usually, the C4–C6 segment is accessible. Vertebral arteries can be identified with a probe parallel to the carotid: angle the probe laterally and inferiorly. The vertebral body processes appear as hypoechoic transverse bars. The vertebral artery runs perpendicular to vertebral processes.
Use of color flow Doppler enables the more rapid identification of vessels (especially the vertebral artery) and often helps identify the area of highest velocity, reduces scan time, and may help in diagnosis of arterial occlusion [2].
Urgent CDU is useful in the quick assessment of patients suspected to have carotid dissection (unilateral neck/headache with or without focal neurological sign, e.g. Horner). The carotid ultrasound is an optimal choice for diagnosis because the symptoms may change time to time and the ultrasound investigation could be also performed every day. The main ultrasound findings are as follow: (1) an arterial luminal flap or false lumen; (2) bulbar and/or proximal ICA hematoma or low-echogenic thrombus; (3) bulb and origin of ICA with high-resistance flow pattern. In the vertebral artery the dissection results in circumscribed dilation of the vessel and non-specific signs (thrombus, high-resistance waveform, or absence of flow with no spectral Doppler waveform).
Doppler ultrasonography is the primary non-invasive test for evaluating carotid stenosis and dissection.
Symptomatic and asymptomatic carotid plaques and the degree of stenosis can be analyzed with ultrasonography by examining the echogenicity of the structures and the velocity of the blood flow.
Identification and Classification of ICA Stenosis
Mild stenoses (<50%) can be estimated by measurement of area and/or diameter in the cross-sectional and longitudinal image using the B- and color-mode of the ultrasound system. Area measurements in high-grade stenosis are difficult. Diagnosis of severe stenosis is based on hemodynamic parameters (measured by pre-, intra-, and post-stenotic Doppler spectrum analysis).
Investigation of flow direction in the ophthalmic artery is a simple, bedside, ancillary method in suspected ICA stenosis or occlusion [3]. In a case of hemodynamically significant ICA stenosis or occlusion (proximal to the origin of the ophthalmic artery) a reversed (extra → intracranial) flow could be detected using a simple continuous wave Doppler probe. If flow is detected in the ophthalmic artery by alternating compression of temporal, facial arteries (branches of external carotid artery) the source of collateral circulation could be identified.
Occlusion results in a complete absence of color flow signal in ICA, and the diagnosis can be confirmed by ultrasound contrast agents (Figure 5.2).
Figure 5.2 Duplex ultrasound reveals internal carotid occlusion. No flow signal could be detected in the occluded artery.
Some sonographers characterize the degree of stenosis based on diameter or area reduction, but estimation of stenosis solely based on this criterion is not reliable. Commonly used methods are:
peak systolic velocities (PSV) and end diastolic velocities
ratios ICA/CCA maximal systolic flow velocity within the ICA stenosis
maximal systolic flow velocity within the non-affected CCA
ICA/ICA
maximal systolic flow velocity within the ICA stenosis
maximal systolic flow velocity of the non-affected ICA.
Most studies consider carotid stenosis of 60% or greater to be clinically important. In a case of a suspected stenosis not only the intrastenotic but also the flow from vessel segments proximal and distal to a stenosis have to be analyzed. If normal flow signals are present before and behind the suspected lesion significant stenosis can be excluded. The stenosis ranges vary from laboratory to laboratory. When possible, laboratories should perform their own correlations with angiographic measurements for quality control. A consensus statement of the Society of Radiologists in Ultrasound recommended the following criteria for estimating stenosis [4]:
Normal: ICA PSV <125 cm/s, no plaque or intimal thickening.
<50% stenosis: ICA PSV <125 cm/s and plaque or intimal thickening.
50–69% stenosis: ICA PSV is 125–230 cm/s and plaque is visible.
>70% stenosis to near occlusion: ICA PSV >230 cm/s and visible plaque and lumen narrowing.
Near occlusion: a markedly narrowed lumen on c-Doppler ultrasound.
Total occlusion: no detectable patent lumen is seen on grayscale ultrasound, and no flow is seen on spectral, power, and color Doppler ultrasound.
With stenosis over 90% (near occlusion), velocities may actually drop as mechanisms that maintain flow fail. Ratios may be particularly helpful in situations in which cardiovascular factors (e.g. poor ejection fraction) limit the increase in velocity [2].
<50% stenoses ICA/CCA: <2.0.
50–69% stenoses ICA/CCA: 2.0–4.0.
70% stenoses ICA/CCA: >4.0.
Doppler ultrasonography associated with stenosis might result in false-positive/negative results:
Ipsilateral CCA-to-ICA flow ratios may not be valid in the setting of contralateral ICA occlusion.
CCA waveforms may have a high-resistance configuration in ipsilateral ICA lesions.
ICA waveforms may have a high-resistance configuration in ipsilateral distal ICA lesions.
ICA waveforms may be dampened in ipsilateral CCA lesions.
Long-segment ICA stenosis may not have high end-diastolic velocity.
Velocities supersede imaging in grading stenosis.
Imaging can be used to downgrade stenosis in the setting of turbulence caused by kinking [5].
A consensus paper of Neurosonology Research Group of the World Federation of Neurology suggests the use of the NASCET method for measuring a stenosis (local diameter narrowing with the diameter distal to the bulb as denominator). Estimation of carotid stenosis should be primarily based on morphological information (B-mode, color flow, or B-flow imaging) in low to moderate degrees of stenosis. In addition to degree of narrowing, plaque thickness, plaque length, and residual lumen should also be reported. As for the statement the velocity measurements in a stenosis (PSV and carotid ratio) alone are not sufficient to differentiate a moderate from a severe (≥70% NASCET) stenosis. The reversed flow in the ophthalmic artery (from extracranial to intracranial direction) should also be investigated. The post-stenotic flow velocity distal to flow disturbances is an important diagnostic value, in which a reduction of velocities (comparison with the unaffected contralateral side or absolute reduction) allows additional grading within the category of severe stenosis. Hemodynamic criteria are appropriate for grading moderate to severe stenoses. Established collateral flow is the most powerful criterion, excluding a less than severe stenosis irrespective of PSV. Special care is recommended for converting Doppler frequencies into velocity by measuring the angle of incidence (Doppler angle). Measurements should be taken using the lowest possible angle of insonation and made in relation to the direction of the jet visualized by color velocity flow and not the vessel course [6].
A carotid occlusion is shown in Figure 5.3.
Figure 5.3 High-intensity microembolus signal is superposed onto the velocity spectrum of anterior cerebral artery.
Morphological measurements (B-mode images and color flow imaging) are the main criteria for low and moderate degrees of stenosis.
Most studies consider carotid stenosis of 60% or greater to be clinically important. This equals a peak systolic velocity over 125 cm/s. With stenosis over 90% (near occlusion), velocities may actually drop as mechanisms that maintain flow fail.
Ratios (maximal systolic flow velocity within the ICA stenosis/maximal systolic flow velocity within the non-affected CCA) may be helpful in situations in which cardiovascular factors (e.g. poor ejection fraction) limit the increase in velocity.
Velocity measurements in a stenosis (PSV and carotid ratio) alone are not sufficient to differentiate a moderate from a severe (≥70% NASCET) stenosis.
Additional criteria refer to the effect of a stenosis on pre-stenotic flow (common carotid artery), the extent of post-stenotic flow disturbances, and derived velocity criteria (diastolic peak velocity and the carotid ratio).
The AHA/ASA guideline also recommends that each laboratory should validate its own Doppler criteria for clinically relevant stenosis [7].
Extracranial Vertebral and Subclavian Arteries
The origin of the vertebral artery (VA) is one of the most common locations of atherosclerotic stenosis, but is difficult to investigate, especially its origin. Raised flow velocities and spectral broadening can be seen in over 50% of stenoses. A distal extracranial VA occlusion may cause a stump signal or a high pulsatile flow signal with almost absent end-diastolic flow component.
A high grade of subclavian stenosis (>50%) results in increased flow velocities and a turbulent flow. In high-grade subclavian stenosis an alternating flow, or even a retrograde flow, can be detected within the ipsilateral VA. The levels of evidence of the European Federation of Neurological Societies are shown in Table 5.1.
Table 5.1 Highlights of the guidelines of the European Federation of Neurological Societies
| Domains | Class and level |
|---|---|
| Ultrasonography is the non-invasive screening technique indicated for the study of vessels involved in causing symptoms of carotid stenosis | Class IV, GCPP |
| Transcranial Doppler (TCD) is useful for screening for intracranial stenosis and occlusion in patients with cerebrovascular disease | Class II, level B |
| Transcranial Doppler is very useful for monitoring arterial reperfusion after thrombolysis of acute MCA occlusions | Class II, level B |
| Clinical studies have suggested that continuous TCD monitoring in patients with acute MCA occlusion treated with intravenous thrombolysis may improve both early recanalization and clinical outcome | Class II, level A |
| The presence of embolic signals with carotid stenosis predicts early recurrent stroke risk | Class II, level A |
| Even in asymptomatic patients, TCD is the only imaging technique that allows detection of circulating emboli | Class II, level A |
| Asymptomatic embolization is common in acute stroke, particularly in patients with carotid artery disease. In this group the presence of embolic signals has been shown to predict the combined stroke and transient ischemic attack (TIA) risk and more recently the risk of stroke alone | Class II, level A |
Floating Thrombus
Free-floating thrombosis in the common or internal carotid arteries is one of the unusual diseases resulting in stroke. Around 150 patients have been reported in the literature. Only the real-time ultrasound can diagnose this disease due to its excellent time resolution. The CT or MR angiography shows only a static vessel stenosis (misdiagnosis), while the ultrasound detects the high-risk, pulse-synchron movement of the thrombus. This status is characterized by an elongated thrombus attached partially to the arterial wall which can move according to blood flow caused by the cardiac cycle. The floating thrombus needs emergent intervention. Both conservative and surgical approaches have proved successful in the literature, but none of them is clearly superior to the other [9].
Ultrasound Diagnosis of Intracranial Stenosis and Occlusion
Intracranial disease corresponds to approximately 8–10% of acute ischemic stroke, depending on gender and race. Diagnosis is frequently reached through arteriography.
A guideline paper summarized the existing clinical conditions and standards for which a variety of TCD tests and monitoring are performed in clinical practice.
TCD has been shown to provide diagnostic and prognostic information that determines patient management decisions in multiple cerebrovascular conditions and periprocedural/surgical monitoring [10, 11].
The consensus confirms the importance of standardized investigation and emphasizes the following aspects:
1. The examiner should follow the course of blood flow in each major branch of the circle of Willis.
2. Identify spectral waveforms at least at two key points per artery.
3. MCA signals should be stored as proximal, mid, and distal.
4. VA signals may be stored at 40–50 and 60–70 mm.
5. BA signals can be stored as proximal, mid, and distal given the length and variability of velocities in these segments.
6. Measure the highest velocity signals at each key point.
General characteristics of the investigation are as follows [12–15]:
About 15% of patients cannot be examined by TCCD because of the insufficient acoustic window. Identification rates decline with advancing age.
The mean velocity analysis is not enough to identify intracranial vessel abnormalities. It must be combined with other parameters such as asymmetry, segmental elevations, spectral analysis and knowledge of extracranial circulation.
Either flow velocities (frequency-based TCCD) or the integrated power of the reflected signal (power TCCD) can be coded. The power TCCD does not display information on the flow direction.
Flow velocities are determined by spectral Doppler sonography using the color Doppler image as a guide to the correct positioning of the Doppler sample volume.
The angle correction should only be applied to velocity measurements when the sample volume can be located in a straight vessel segment of at least 2 cm length.
Flow velocities in the arterial as well as in the venous system are higher in women than in men, and decrease with age, whereas the pulsatility index increases.
Intracranial stenosis: local increase in the peak systolic flow velocities, post-stenotic flow disturbances with low frequency, and high-intensity Doppler signals.
The intracranial vessel is occluded if the color signal is absent in one segment, while other vessels and parenchymal structures can be correctly visualized.
The use of contrast material increases the sensitivity and specificity and only 4% of examinations are inconclusive because of insufficient bone windows.
After application of echo-contrast enhancing agents (ECE) the diagnostic confidence of TCCD for intracranial vessel occlusion is similar to that of magnetic resonance angiography.
In an acute stroke study the ability of duplex ultrasound to diagnose main stem arterial occlusions within the anterior circulation was between 50% and 60% of studied vessels in unenhanced TCCS but reached 80–90% after intravenous contrast administration.The diagnostic strength of contrast-enhanced TCCD can be the highly specific identification of a normal intracranial arterial status. Therefore, if an experienced sonographer detects no abnormalities by using TCCD in a patient with sufficient bone windows, no more imaging is needed.
A correctly performed TCD investigation also provides valuable information about the vascular status of the ICA. The presence of collaterals and delayed flow acceleration on TCD usually indicates a hemodynamically significant lesion (>80% ICA stenosis or occlusion).
The investigation should start on the presumably non-affected side (roadmap! clinical symptoms).
The sonographer looks for a focal velocity rise in a circumscribed vessel segment, and differences between the affected and non-affected sides, extending more than 30 cm/s.
If a pathological finding is present, the proximal and distal vessel segments should also be evaluated.
Occlusions are characterized by missing color and Doppler flow signals at the site of the occlusion or reduced flow signals in vessel segments proximal to the occlusion.
MCA Stenosis
Stenoses of the M1-MCA can be graded according to flow velocity, turbulence, and asymmetry into mild, moderate, and high-grade stenoses and all detectable MCA segments should be insonated [13–14].
MCA Occlusion
Depending on the location of the occlusion, the Doppler spectrum may be completely absent or reduced. If there is a proximal M1-MCA occlusion no flow signal is seen. In occlusions of the middle part of the MCA, a small orthograde flow with increased pulsatility may be present. In distal M1-MCA occlusion a reduced flow velocity is present with variable pulsatility depending on the presence of a temporal branch.
Distal MCA occlusion, e.g. of a relevant M2-MCA branch or more than one M2 branch, will result in a reduced flow with low velocities and a marked bilateral asymmetry.
Stenosis and Occlusion in Posterior Circulation
Again the typical clinical symptoms of vertebrobasilar insufficiency should orient the sonographer. Alteration of flow velocities and turbulence, at least 30 cm/s flow velocity difference between the right and left sides, may also be useful. A proximal PCA occlusion can be diagnosed by absent flow signal. Vertebral stenoses can be diagnosed by flow velocity, profile disturbances, and pre- and post-stenotic flow patterns. Velocity values for mild and severe stenosis are given in Table 5.2. Flow signals in VA occlusion strongly depend on the site of the occlusion, mainly on their relation to the origin of the PICA (proximal or distal). Occlusions distal to the PICA origin will result in mild to moderate flow alterations of the extracranial VA, mainly depending on its diameter and its former relevance in the posterior circulation [14].
Table 5.2 Ultrasound grading of intracranial stenosis
| Stenosis | <50% | 50–80% | ≥80% |
|---|---|---|---|
| Middle cerebral artery | ≥155 cm/s | ≥220 | distal M1/M2-MCA post-stenotic fp A1-ACA and/or P1/P2-PCA↑ |
| Anterior cerebral artery | ≥120 | ≥155 | A2-ACA post-stenotic fp ipsilateral M1-MCA and/or contralat. A1↑ |
| Posterior cerebral artery | ≥100 | ≥145 | distal PCA post-stenotic fp ipsilateral M1-MCA↑ |
| Basilar artery | ≥100 | ≥140 | distal BA/PCA post-stenotic fp VA/proximal BA pre-stenotic fp |
| Vertebral artery | ≥90 | ≥120 | distal VA/BA post-stenotic fp VA extracranial pre-stenotic fp |
Fp: flow pattern, ↑ increased velocity as collateral sign.
Basilar Artery Stenosis and Occlusion
Transforaminal and transtemporal insonation allows the investigation of the total length of the basilar artery. The most distal segment of the basilar artery may be better insonated transtemporally, but the visualization of the distal part of the basilar artery appears to be difficult even using echo-enhancing agents.
Occlusions are difficult to assess and diagnostic certainty depends on the site of the occlusion. A proximal BA occlusion will always result in pre-stenotic flow alterations of both extracranial vertebral arteries [14]. Therefore, apparently normal VA and proximal BA velocities are not sufficient to exclude top of the basilar occlusion.
However, as this cannot exclude the presence of, for example, a fragmented thrombus, ultrasound should always be used together with other diagnostic tools such as CTA, MRA, or DSA in presumed BA pathology.
With transcranial color-coded duplex sonography (TCCD), using low frequencies to penetrate the skull, most intracranial stenoses and occlusions can be detected by combining velocity analysis with other parameters. With the use of echo-contrast enhancing agents (ECE), the sensitivity and specificity can be increased and the diagnostic confidence of contras enhanced TCCD for intracranial vessel occlusion can reach that of magnetic resonance angiography.
Fast-Track Neurovascular Ultrasound Examination
A practical algorithm has been published for urgent bedside neurovascular ultrasound examination with carotid/vertebral duplex and transcranial Doppler in patients with acute stroke [16].
Using such a protocol, urgent TCD studies can be completed and interpreted quickly at the bedside. The expanded fast-track protocol for combined carotid and transcranial ultrasound testing in acute cerebral ischemia is shown in Box 5.1. Below, we highlight the most important details of the algorithm.
Box 5.1 Fast-Track Neurovascular Ultrasound Examination
Use portable devices with bright display overcoming room light. Stand behind patient headrest. Start with TCD because acute occlusion responsible for the neurological deficit is likely to be located intracranially. Extracranial carotid/vertebral duplex may reveal an additional lesion often responsible for intracranial flow disturbance. Fast-track insonation steps follow clinical localization of patient symptoms.
A. Clinical diagnosis of cerebral ischemia in the anterior circulation
STEP 1: Transcranial Doppler
1. If time permits, begin insonation on the non-affected side to establish the temporal window, normal MCA waveform (M1 depth 45–65 mm, M2 30–45 mm), and velocity for comparison with the affected side.
2. If short on time, start on the affected side: first assess MCA at 50 mm. If no signals detected, increase the depth to 62 mm. If an anterograde flow signal is found, reduce the depth to trace the MCA stem or identify the worst residual flow signal. Search for possible flow diversion to the ACA, PCA, or M2 MCA.
Evaluate and compare waveform shapes and systolic flow acceleration.
3. Continue on the affected side (transorbital window). Check flow direction and pulsatility in the OA at depths 40–50 mm followed by ICA siphon at depths 55–65 mm.
4. If time permits or in patients with pure motor or sensory deficits, evaluate BA (depth 80–100 mm) and terminal VA (40–80 mm).
STEP 2: Carotid/vertebral duplex
1. Start on the affected side in transverse B-mode planes followed by color or power-mode sweep from proximal to distal carotid segments. Identify CCA and its bifurcation on B-mode and flow-carrying lumens.
2. Document if ICA (or CCA) has a lesion on B-mode and corresponding disturbances on flow images. In patients with concomitant chest pain, evaluate CCA as close to the origin as possible.
3. Perform angle-corrected spectral velocity measurements in the mid-to-distal CCA, ICA, and external carotid artery.
4. If time permits or in patients with pure motor or sensory deficits, examine cervical portion of the vertebral arteries (longitudinal B-mode, color or power mode, spectral Doppler) on the affected side.
5. If time permits, perform transverse and longitudinal scanning of the arteries on the non-affected side.
B. Clinical diagnosis of cerebral ischemia in the posterior circulation
STEP 1: Transcranial Doppler
1. Start suboccipital insonation at 75 mm (VA junction) and identify BA flow at 80–100 mm.
2 If abnormal signals present at 75–100 mm, find the terminal VA (40–80 mm) on the non-affected side for comparison and evaluate the terminal VA on the affected side at similar depths.
3. Continue with transtemporal examination to identify PCA (55–75 mm) and possible collateral flow through the posterior communicating artery (check both sides).
4. If time permits, evaluate both MCAs and ACAs (60–75 mm) for possible compensatory velocity increase as an indirect sign of basilar artery obstruction.
STEP 2: Vertebral/carotid duplex ultrasound
1. Start on the affected side by locating CCA using longitudinal B-mode plane, and turn transducer downward to visualize shadows from transverse processes of midcervical vertebrae.
2. Apply color or power modes and spectral Doppler to identify flow in intratransverse VA segments.
3. Follow VA course to its origin and obtain Doppler spectra. Perform similar examination on other side.
4. If time permits, perform bilateral duplex examination of the CCA, ICA, and external carotid artery as described above.
The choice of fast-track insonation steps is determined by the clinical localization of ischemic arterial territory. For example, if patients present with middle cerebral artery symptoms, the insonation begins with the non-affected side. This is followed by locating the MCA on the affected side, with insonation starting at the mid-M1-MCA depth range, usually 50–58 mm. The waveforms and systolic flow acceleration are compared to the non-affected side. If a normal MCA flow is found, the distal MCA segments are insonated (range 40–50 mm); this is followed by proximal MCA and ICA bifurcation assessment (range 60–70 mm) [16]. The non-invasive vascular ultrasound evaluation (NVUE) in patients with acute ischemic stroke has a high yield and accuracy in diagnosing lesions amenable to interventional treatment (LAIT). The ultrasound screening criteria for LAIT are shown in Table 5.3.
Table 5.3 Ultrasound screening criteria for lesions amenable for intervention
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