Carotid Doppler Imaging

Welcome to the Carotid Doppler Imaging presentation. The goal of this presentation is to review cerebrovascular anatomy, hemodynamics, and diagnostic criteria used for categorizing ICA (Internal Carotid  Artery) stenosis and other pathologic conditions affecting the cerebrovascular system.   Presentation created by: Christine E. McDonald, RDMS Siemens Medical Solutions Laminar Flow (aka parabolic flow) Blood tends to be slower near the vessel wall due to friction and energy loss Highest velocities are detected center stream ICA LAMINAR FLOW PLUG FLOW ECA LAMINAR FLOW FLOW SEPARATION CCA Plug Flow Occurs at the entrance of a tube or vessel.  As blood flows through the vessel, it’s velocity causes drag against vessel walls producing flow laminae Flow Separation/Disturbance Blood cells are less uniform and orderly, producing spectral broadening Flow Dynamics Exam Components Normal Waveforms Anatomy of a Critical Stenosis Duplex Stenosis Criteria Proximal/Distal Obstruction Carotid Pathology Subclavian/Innominate Pathology Protocols and Pitfalls Summary Color Doppler is Qualitative Vessel tortuosity and branching produce normal disturbed or altered flow Color Changes: As vessels bend, zones of increased frequency shifts are displayed as brighter shades, causing aliasing Skewed Velocity/Frequency Shift Pulsed (Spectral) Doppler Quantitative When the ultrasound beam is at right angles to the vessel (90°), the Doppler shift is theoretically zero Angle Correct for Velocity and Tortuosity Gray scale assessing anatomy and plaque morphology Color Doppler for vessel identification, cursor placement and flow patterns Pulsed Doppler for quantification Color Spectral Heterogeneous Classifying plaque can be subjective: Homogeneous Heterogeneous Focal Calcified Heterogeneous/Irregular is the predominant type in symptomatic patients with greater than 70% stenosis. Clin Rad (1997) 52, 643-653 Plaque Ulceration Predisposes the development of thrombus Criteria for diagnosis includes sharply marginated crater and flow detected within DX: 2x2 mm crater; filled with color.   Sonography detection of ulcerations remains controversial.  With sensitivities ranging from <30% to more than 90%. Clin Rad (1997) 52, 643-653 Color indicates flow presence, direction, and mean velocity Away Toward Laminar Aliasing Velocity Range: 60-100 cm/sec ICA-low resistance ECA-high resistance CCA-combined ICA/ECA Vertebral- similar to CCA with velocity range 20-40 cm/sec Seminars in Roentgenology Jan, 1992 Normal Waveforms: ICA CCA ECA Hemodynamics of a Stenosis: Velocity flow remains normal until lumen diameter is reduced by 50% (Spectral Broadening) Flow velocity increases proportionally as the severity of the lumen decreases Moderate (50-70%) a pressure gradient exists throughout diastole Diastolic Velocities Severe (70-90%) increased pressure gradient Peak Systolic & End Diastolic Velocities with Post stenotic Turbulence Hemodynamically Significant Stenosis: Greater than 70% diameter or 90% cross-sectional area reduction When the severity of the stenosis increases beyond a certain point, velocity increases to maintain flow volume.  This phenomenon produces a “Jet” of high velocity indicated by spectral Doppler (increased peak systolic and end diastolic velocities) Exhibits Post stenotic Turbulence “PST” (indirect sign of >70%) Peak Systolic Velocity 250 cm/sec or greater “JET” flow & End Diastolic Velocity greater than 100 cm/sec Quantifying Carotid Stenosis Stenosis Measurement/Parameters: Peak Systolic Velocity (PSV) Best documented parameter Limitation: Cardiac Output/Blood pressure End Diastolic Velocity (EDV) Highly accurate for greater than 80% stenosis Systolic Velocity Ratio (ICPSV/CCPSV) Compensates for patient Hemodynamic Variables ICA/CCA Ratio: Important to use in situations where the ICA PSV may not be by itself, representative of the extent of ICA disease due to: Tandem ICA stenosis Elevated CCA velocities or stenosis Contralateral high-grade ICA stenosis Discrepancy between visual assessment of plaque and ICA PSV is significantly altered Cardiac output states (high or low) Diameter reduction % Peak Systolic Velocity End Diastolic Velocity Spectral Characteristics 0 < 125 cm/s   Normal spectral window 1 - 15 < 125 cm/s   Spectral broadening in systolic deceleration 16 - 49 < 125 cm/s   Spectral broadening throughout systole 50 - 79 > 125 cm/s < 140 cm/s Extensive spectral broadening 80 - 99 > 125 cm/s > 140 cm/s Extensive spectral broadening Occluded Absent Signals Dampened signal in CCA IC:CC ratio > 4.0 = > 70% stenosis (Sensitivity: 91%; PPV = 87%; NPV = 94%) The Society of Radiologists in Ultrasound: Vascular ultrasound experts representing different specialties all practicing in the field Come up with a set of consensus panel recommendations for assessing carotid stenosis Normal  < 50 % 1- 15 % subcategory 16-49 % subcategory 50 – 69 % > 70 % > 80 % subcategory String sign or near occlusion Occluded ICAVL-   Intersocietal Commission for the Accreditation of Vascular Laboratories  http://icavl.org/icavl/main/icavl_standards.htm 1cm past - PST 2cm past - minimal flow disturbance 3cm past - normal laminar flow   Laminar Flow Mild Disturbance Critical Disturbance Post Stenotic Turbulence Critical Disturbance Spectral Broadening with Forward and Reverse Components (Post Stenotic Turbulence) Color indicating hemodynamic stenosis Tissue vibration caused by severe obstruction  (Mosaic pattern). Post-stenotic turbulence useful for detecting >70% decreased diameter. Forward & reverse flow components. Transverse Dot Flow Power Jet String Sign Power Doppler Ipsilateral High Resistance ICA Ipsilateral High Resistance CCA With severe blockage, CCA waveforms proximal to the obstruction are high-resistance similar to the ECA   Detection of  ICA occlusion: Absent flow by spectral & color imaging Thrombus completely filling the lumen Reverse flow in segment proximal to ICA or CCA High Resistance waveforms in ipsilateral CCA/Proximal ICA Internalization of ECA Increased velocities in contralateral CCA No evidence of stenosis Pattern of CCA varies due to secondary collateralization If there is collateralization from the External Carotid Artery to the intracranial vessels, the CCA waveform maybe normal ICA Occlusion Ipsilateral Internalized ECA  Ipsilateral High Resistance CCA Stump Flow High Resistance CCA Color Void/Low Flow Internalization ECA Common Carotid Artery Occlusion: Clinical features similar to ICA occlusion Incidence 1-5% of cases (rare) Left side predilection (89%) Type (1) Associated with ipsilateral ICA occlusion Type (2) Isolated CCA occlusion better surgical outcome Arteriosclerosis is the major cause of CCAO occlusion Other causes include: Takayasu disease, fibromuscular dysplasia, CCA dissection, cardiac embolism, trauma, and idiopathic occlusion. ECA supplies ICA via carotid bifurcation ECA flow is reversed Ipsilateral Intracranial ICA not fully compensated by Vertebrobasilar circulation Contralateral ICA Ipsilateral ICA flow is antegrade/damped Absent CCA Flow by Color & Spectral ECA/ICA Reverse Flow Directions Antegrade/Damped ICA Flow Reverse Flow in ECA by Color/Spectral Note: Spectral Doppler rules over color when quantifying and confirming flow direction.   Cardiac Function or Localized Obstruction? Tardus-Parvus/Monophasic Waveforms: Right ECA Right CCA/ICA Paragangliomas: Rare tumors, 1 in 30,000 in general population Malignant potential 2-10% of cases Palpable, painless slow growing neck mass Other signs; pain, headache, hypertension, Horner’s syndrome Highly vascular located between the ICA & ECA Blood supply via the ECA Splaying of ICA/ECA Solid well-circumscribed hypoechoic mass ECA circulation supplies the tumor Pitfalls: Lymph Nodes, Hematoma, False Aneurysm   Low Resistance Ipsilateral ECA   Spontaneous dissection (Hypertension, Marfan’s) commonly occurs in the ICA also involves the CCA Trauma causes a rent in the intima separating the arterial layers (membrane) results; Ischemic Stroke Arterial dissection produces a false lumen which may have a blind end causing stenosis and or occlusion Echogenic Membrane Lanzer; Vascular Diagnostics 1994 Patent True and False Lumen “To and Fro” Signal “To and Fro” Signal CCA ICA Dissection Pseudo-Occlusion   High Resistance Ipsilateral ICA   High Resistance Ipsilateral CCA   Occurs with a high-grade stenosis or occlusion of the proximal subclavian or Innominate arteries Diversion of blood from the high-pressure vertebrobasilar circulation to the low-pressure upper extremity circulation  via “Retrograde” vertebral artery flow Brachial systolic pressure >15-20 mm Hg indicates obstruction Abnormal Vertebral Waveforms Complete Bunny/Pre-steal Incomplete Tardus-Parvus Left Subclavian Steal Right Subclavian Steal AJR:174:March 2000, Doppler Sonography of Subclavian Steal Physiology Right Vertebral Right Subclavian Stenosis Left Vertebral Complete steal resulting from Innominate stenosis Innominate Stenosis Right Subclavian Right Vertebral Primary means of treating patients with symptomatic high-grade stenosis Diseased intima “shelled” out & artery wall closed/sutured Vein patch or synthetic material (polytetrafluoroethylene, or PTFE) used to enlarge site of stenotic narrowing Duplex sonography to confirm patency, presence of flaps, & stenosis due to neointimal hyperplasia 3,6,12 Month follow-up exams Post endarterectomy flow disturbances: Spectral broadening due to exposure of rough sub intimal layer Stenosis/occlusion caused by intimal flap/retained plaque & neointimal hyperplasia ICA often exhibits an “Externalized” waveform 2 years post-surgery when most (70%) of re-stenosis occur Re-stenosis within the first 3 years results from progression of neointimal hyperplasia Indirect Signs of Stenosis/Obstruction Obscured Jet by Calcification Post stenotic Waveform Indicates >70% Diameter Reduction Tardus-Parvus Proximal Disease CCA High Resistance Distal Disease CCA Aortic valve disease, cardiac arrhythmias, and hypertension produce aberrant waveforms commonly encountered in the cerebrovascular exam   Cardiac Arrhythmia False High Velocity Increased flow from contralateral disease Poor visualization, bad angle Post endarterectomy Typically without vein patch The cosine of the Doppler angle changes rapidly for angles more than 60 degrees.  Above 60 degrees, small changes in the Doppler angle result in a large error in estimating velocity Pseudo spectral broadening by increasing the sample gate, sampling near the vessel wall, and increasing Doppler gain.   Not really occluded Use power Doppler to demonstrate flow through calcifications, in large patients, and to confirm trickle flow and or occlusion False Positive/False Negative High-resistance waveforms with elevated systolic peaks in the absence of carotid obstruction is seen with hypertension, tachycardia, and diminished arterial compliance.  Symmetry of waveforms is the key to diagnosing cardiac disease, and the key to avoiding false-positive diagnoses of distal carotid obstruction Collateralization While the ECA typically lies anterior and medial to the ICA, variations in anatomic configuration of the neck vasculature, particularly vessel tortuosity, can complicate acquisition of spectral Doppler Changes in resistivity in the cerebral circulation and some types of cardiac co-morbidity can alter the spectral waveform appearance ECA – “temporal tapping”. Transmitted oscillation from tapping the temporal artery just anterior to the pinna of the ear are seen during diastole Carotid duplex ultrasound, when performed in accordance with strict technical standards, equals or exceeds catheter angiography in detecting a ≥70% ICA stenosis.   Understanding normal and abnormal hemodynamics, instrumentation, spectral waveform patterns, and validating diagnostic criteria is paramount in providing the utmost standard of care to our patients.