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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Acknowledgments
- •Contents
- •Contributors
- •1.2 How Is Critical Care Humanized?
- •References
- •2.1 Introduction
- •1.2.2 Communication
- •1.2.5 Post-ICU Syndrome
- •1.2.6 Humanized Infrastructure
- •1.2.7 End-of-Life Care
- •2.2 Which Patients Should Undergo ICP Monitoring?
- •2.5.2.3 CSF Drainage
- •2.5.2.4 Osmotherapy
- •2.5.2.5 Ventilation
- •2.5.2.6 CPP Augmentation
- •2.5.2.7 Metabolic Suppression
- •2.5.2.8 Pharmacologic Suppression
- •2.5.2.9 Temperature Modulation
- •2.5.2.10 Decompressive Craniectomy
- •2.7.1.1 Pressure Reactivity Index (PRx)
- •2.7.1.2 Multimodality Monitoring
- •2.8 Conclusion
- •Algorithm
- •References
- •3.1 Introduction
- •3.2 Intracerebral Hemorrhage (ICH)
- •3.3 ICH: Presenting Symptoms
- •3.5.1 Blood Hypertension
- •3.5.2 Other Risk Factors
- •3.6 ICH: Pathophysiology
- •3.7 ICH: Initial Management
- •3.7.1 Airway: Intubation
- •3.7.3 ICH: Imaging
- •3.7.4 ICH: Grading Scales
- •3.7.5 Fluid Management
- •3.7.6 Follow-Up Imaging
- •3.7.7 Blood Pressure Management
- •3.7.9 ICP Monitoring
- •3.7.10 Surgical Considerations
- •3.7.13 ICH: Venous Thromboembolism Prophylaxis
- •3.7.14 ICH: Seizure Management
- •3.8 ICH: Medical Complications
- •3.8.1 Glycemic Management
- •3.8.3 Disposition
- •3.9 Conclusion
- •Algorithm
- •Appendix: Direct Oral Anticoagulant Reversal
- •Reversal Strategies
- •References
- •4.1 Introduction
- •4.2.1 Hemodynamic Management
- •4.2.2 Hormonal Replacement Therapy
- •4.2.3 Respiratory Management
- •4.3 Cardiopulmonary Resuscitation (CPR)
- •4.4 Conclusion
- •Algorithm
- •References
- •5.1 Introduction
- •5.2.1 Vasoactive Agents
- •5.2.1.1 Vasodilators (Table 5.1)
- •Calcium Channel Blockers
- •Nimodipine
- •Nicardipine
- •Other Vasodilators
- •Magnesium
- •3-Hydroxy-3-Methyl-Glutaryl-CoA (HMG-CoA) Reductase Inhibitors (Statins)
- •Nitroprusside
- •Endothelin-1 Antagonists
- •Hydralazine
- •Phosphodiesterase Inhibitors
- •Papaverine
- •Norepinephrine
- •Epinephrine
- •Dopamine (DA)
- •Phenylephrine
- •Vasopressin
- •Neuromonitoring
- •5.2.2.1 Benzodiazepines
- •5.2.2.2 Barbiturates
- •5.2.2.3 Opioids
- •5.2.2.4 Anticonvulsant Medications
- •5.2.2.5 Other Sedatives/Anesthetics
- •5.2.3 Hemodynamic Agents
- •5.4 Conclusion
- •Algorithm
- •References
- •6.1 Introduction
- •6.2.3 Ultrasound Behaviour at Acoustic Boundaries
- •6.3 Pulse-Echo Principles (B-Mode Techniques)
- •6.4 Transducers
- •6.5 Artefacts
- •6.6 Doppler Principles
- •6.6.1 Pulsed Wave Doppler
- •6.6.2 Duplex Scanning
- •6.6.3 Colour Flow Imaging (CFI)
- •6.7.2 Flow Changes
- •6.7.3 Cerebrovascular Resistance
- •6.8 Transcranial Colour-Coded Duplex Sonography (TCCS)
- •6.9 Ultrasound Safety
- •6.10 Conclusion
- •References
- •7.1 Introduction
- •Mesencephalic Plane
- •7.2.1.2 Diencephalic Plane (Thalamic Plane)
- •6.6.4 Power Doppler Imaging (PDI)
- •6.7 Transcranial Doppler Ultrasound (TCD)
- •6.7.1 Velocity Measurement
- •7.2.1.3 Ventricular Plane (Cella Media)
- •7.2.1.4 Upper Pons Plane
- •7.2.1.5 Lower Pons Plane
- •7.2.2 Transforaminal Window
- •7.3.1.2 Anterior Circulation
- •Carotid System
- •Anterior Cerebral Artery
- •Anterior Communicating Antery
- •7.3.1.3 Posterior Circulation
- •Vertebrobasilar System
- •Posterior Communicating Artery
- •Posterior Cerebral Arteries
- •7.5 Cerebral Circulation: Anatomical Variations
- •7.5.1.1 Anterior Circulation
- •Most Common Variations [28]
- •7.5.1.2 Posterior Circulation
- •Most Common Variants [28]
- •7.6.1.1 Deep Middle Cerebral Vein (DMCV)
- •7.6.1.2 Basal Vein (of Rosenthal)
- •7.6.1.3 Great Cerebral Vein (of Galen)
- •7.6.2.1 Sphenoparietal Sinus
- •7.6.2.2 Superior Petrosal Sinus
- •7.6.2.3 Inferior Petrosal Sinus
- •7.6.2.4 Cavernous Sinus
- •7.6.2.5 Transverse Sinus
- •7.6.2.6 Straight Sinus
- •7.7 Conclusion
- •Algorithm
- •References
- •8.1 Introduction
- •8.2 Cerebral Blood Flow Measures
- •8.3 Transcranial Doppler (TCD/TCCS)
- •8.4.1 Cerebral Autoregulation (CA)
- •8.4.2 CO2 Vasoreactivity
- •8.6.2 TCD/TCCS: Use After Traumatic Brain Injury (TBI)
- •8.7 Conclusion
- •References
- •9.1 Introduction
- •9.3 TCD Hemodynamic Parameters: Variations by Sex
- •9.4 TCD Hemodynamic Parameters: Variations by Age
- •9.5 TCD Hemodynamic Parameters: Variations by Laterally
- •9.7 TCD Normal Values: Latin American Population Sample
- •9.8 TCD Hemodynamic Parameters: Altitude
- •9.10 Conclusion
- •References
- •10.1 Introduction
- •10.2 TCD/TCCS: Acoustic Windows
- •10.2.1.1 Technique
- •10.2.2.1 Technique
- •10.2.3.1 Technique
- •10.2.4.1 Technique
- •10.2.5.1 Technique
- •10.4.1 Decompressive Craniectomy
- •10.4.2 Patient’s Position
- •10.5 TCD/TCCS: Contrast-Enhanced
- •10.6 Conclusion
- •Algorithm
- •References
- •11.1 Introduction
- •11.2 Basic Methods
- •11.2.1 Flow Velocities
- •11.2.2 Pulsatility Index (PI)
- •11.3 Advanced Methods
- •11.3.2 TAU (Cerebrovascular Time Constant)
- •11.3.4 Autoregulation
- •11.4.1 Traumatic Brain Injury
- •11.4.2 Aneurysmal Subarachnoid Hemorrhage
- •11.4.3 Stroke
- •11.4.4 Other Clinical Scenarios
- •11.5 Conclusion
- •Algorithm
- •References
- •12.1 Introduction
- •12.2 TCD: Spectral Wave
- •12.4 TCD: Clinical Utility
- •12.6 TCD: Technique
- •12.6.2 Transtemporal Acoustic Window
- •12.6.2.1 Anterior Circulation
- •Middle Cerebral Artery (MCA)
- •12.6.2.2 Posterior Circulation
- •Posterior Cerebral Artery (PCA)
- •12.6.3 Submandibular Acoustic Window
- •12.6.3.1 Internal Carotid Artery (ICA—Extracranial Portion)
- •12.6.4 Transoccipital Acoustic Window
- •12.6.4.1 Posterior Circulation
- •12.6.5 Transorbital Acoustic Window
- •12.6.6.2 Pulsatility Index
- •12.7.1 High-Velocity Pattern
- •12.7.2 Low-Velocity Pattern
- •12.7.3 High Resistance Pattern
- •12.7.4 Cerebral Circulatory Arrest Pattern
- •12.8 TCD: Other Clinical Uses
- •12.8.1.1 Cerebral Vascular Reactivity
- •12.9 TCD: Limitations
- •12.10 Conclusion
- •Algorithm
- •References
- •13.1 Introduction
- •13.2 Acoustic Windows
- •13.3 2D-Guided TCD Monitoring
- •13.6 Conclusion
- •Algorithm
- •References
- •14.1 Introduction
- •14.2 TCCS: Anatomical Aspects
- •14.3.1 Anterior Circulation
- •14.3.1.1 Carotid System
- •14.3.2 Posterior Circulation
- •14.3.2.1 Vertebro-Basilar System
- •14.5 TCCS: Examiner Considerations
- •14.6 TCCS: Acoustic Windows
- •14.7 TCCS: Examination Protocol
- •14.7.1.1 Considerations
- •Doppler: (Convention)
- •14.7.2 Transtemporal Acoustic Window Examination (Coronal Planes)
- •14.7.3 Transoccipital (Transnuchal/Transforaminal) Acoustic Window Examination
- •14.7.4 Submandibular Acoustic Window Examination
- •14.7.5 Transorbital Acoustic Window Examination
- •14.7.6 Frontal Bone Window Examination
- •14.8 TCCS Protocol: Clinical Applications
- •14.9 TCCS Protocol: Hemodynamic Parameters
- •14.10 TCCS Protocol: Limitations
- •14.10.1 Limitations
- •14.10.1.1 Acoustic Windows
- •Transtemporal Acoustic Window
- •Suboccipital Acoustic Window
- •14.10.1.2 Middle-Line Shift Measurement
- •14.11 Conclusion
- •Algorithm
- •References
- •15.1 Introduction
- •15.2 Clinical Applications
- •15.2.1 Intracranial Stenosis
- •15.2.2 Cerebral Vasospasm
- •15.2.3 Cerebral Veins
- •15.3 Conclusion
- •References
- •16.1 Introduction
- •16.3.1 Autoregulation Index (ARI)
- •16.3.2 Mean Flow Velocity Index (Mx)
- •16.5 Conclusion
- •References
- •17.1 Introduction
- •17.2.1 Cerebrovascular Resistance (CVR)
- •17.2.2 Cerebral Autoregulation
- •17.2.4 Carbon Dioxide Reactivity
- •17.3.2 Collateral Flow
- •17.3.3 Elastic Reservoir (“Windkessel Effect”)
- •17.4 TCD: Waveform Interpretation
- •17.4.1 TCD Waveforms
- •17.5.1 Aneurysmal Subarachnoid Hemorrhage
- •17.5.2 Increased ICP
- •17.6 Conclusion
- •References
- •18.1 Introduction
- •18.3.1 Subarachnoid Hemorrhage (SAH)
- •18.3.1.1 Cerebral Autoregulation (CA)
- •18.3.1.2 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.1.3 Cerebral Blood Flow
- •18.3.1.4 Electrophysiology
- •Seizure Detection
- •18.3.1.5 Cerebral Metabolism
- •18.3.2 Intracerebral Hemorrhage (ICH)
- •18.3.2.1 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.2.3 Electrophysiology
- •18.3.3 Traumatic Brain Injury (TBI)
- •18.3.3.2 Cerebral Autoregulation
- •18.3.3.3 Intraparenchymal Cerebral Oxygen Monitoring
- •18.3.3.4 Cerebral Blood Flow
- •18.3.3.5 Electrophysiology
- •18.3.3.6 Cerebral Metabolism
- •18.3.4 Acute Ischemic Stroke (AIS)
- •18.3.4.1 Cerebral Blood Flow
- •18.3.4.2 Electrophysiology
- •18.3.5.1 Cerebral Blood Flow
- •18.4 Conclusion
- •References
- •19.1 Introduction
- •19.2 Cerebral Blood Haemodynamic Measurements
- •19.3 Cerebral Blood Flow (CBF): Physiology Principles
- •19.4 Vasoreactivity Determining: Methods
- •19.6 Technical Tips
- •19.7 Vasoreactivity: Clinical Importance
- •19.8 Conclusion
- •References
- •20.1 Introduction
- •20.5.4.1 Experimental Endotoxemia
- •20.6 Conclusion
- •Appendix
- •Methods
- •Group 1: Graphic Methods
- •“Beat-by-Beat Method”
- •Method Described by Aaslid
- •Group 2: Multiparameter or Impedance Methods [14]
- •References
- •21.1 Introduction
- •21.2.1 Brain Compliance
- •21.2.2 TCD/TCCS: Cerebral Hemodynamics
- •21.4 Pulsatility Index (PI): Intracranial Pressure (ICP)
- •21.5.1 Cardiovascular Factors
- •21.5.2 Cerebrovascular Factors
- •21.5.3 Cardiopulmonary Factors
- •21.5.4 Metabolism Factors
- •21.5.5 Vascular Factors
- •21.5.6 Other Factors
- •21.6 Conclusion
- •Algorithm
- •References
- •22.1 Introduction
- •22.2 Aneurysmal Subarachnoid Hemorrhage (aSAH)
- •22.3 Cerebral Vasospasm After aSAH
- •22.5.1 TCD/TCCS: Examination Protocol
- •22.5.1.1 Transtemporal Window
- •22.5.1.2 Orbital Window
- •22.5.1.3 Suboccipital/Transforaminal Window
- •22.5.1.4 Submandibular Window
- •22.7 Conclusion
- •Algorithm
- •References
- •23.1 Introduction
- •23.3.1 Premise
- •23.3.3 Limitations
- •23.4.1 Technical Requirements
- •23.4.3 Limitations
- •23.6 Future Directions
- •23.7 Conclusion
- •Algorithm
- •References
- •24.1 Introduction
- •24.2.1 Vasospasm
- •24.2.2 Vasospasm Diagnostic Criteria
- •24.3 TCD/TCCS: Cerebral Vasoreactivity
- •24.4 TCD/TCCS: Intraoperative Monitoring
- •24.7 Conclusion
- •References
- •25.1 Introduction
- •25.4 CAD: Diagnosis
- •25.6 Pupil: Ultrasound Examination
- •25.11 Conclusion
- •Algorithm
- •References
- •26.1 Introduction
- •26.2 Optimal Settings
- •26.2.1 Probe Types
- •26.2.2 Frequencies
- •26.2.3 Focus
- •26.2.4 Depth
- •26.2.5 Pulse Repetition Frequency (PRF)
- •26.2.6 Frame Rate
- •26.2.8 Freeze
- •26.2.9 Cine Loop
- •26.2.10 Smoothing (Interpolation), Interlacing, Correlation
- •26.2.11 Postprocessing
- •26.2.12 Resolution
- •26.2.13 Doppler-Technique
- •26.2.14 PW-Doppler (Pulsed-Wave Doppler)
- •26.2.15 Color Duplex
- •26.3 Indications
- •26.4.1.2 Morphological Differences
- •26.4.1.3 Flow Differences
- •26.4.1.4 Compression
- •26.5 B-Mode Examination
- •26.5.1 Dilation
- •26.5.2 Intima-Media Thickness (IMT)
- •26.5.3 Plaque Analysis
- •26.5.3.1 Location
- •26.5.3.3 Maximal Thickness
- •26.5.3.4 Surface
- •26.5.3.5 Echogenicity
- •26.5.4 B-Flow Imaging
- •26.6.1 Color Doppler Imaging (CDI)
- •26.6.2 Power Doppler Imaging (PDI)
- •26.7.1 Stenosis Measurement
- •26.7.1.1 Diameter Stenosis
- •26.7.1.2 Area Stenosis
- •26.7.1.3 Residual Luminal Diameter
- •26.7.2 Occlusion
- •26.7.3 Subtotal Stenosis: (>95% Stenosis)
- •26.7.4 Long Segment Stenosis
- •26.8 Doppler Spectrum
- •26.10 Contrast Enhanced Ultrasound (CEU)
- •26.11.1 Common Carotid Artery
- •26.11.2 Internal Carotid Artery
- •26.11.2.1 Stenosis
- •26.11.2.2 Dissection
- •26.11.2.3 Occlusion
- •26.11.2.4 Subtotal Occlusion: (95–99% Stenosis)
- •26.11.2.5 Multiple (Tandem) Stenosis
- •26.11.2.6 Long Segment Stenosis
- •26.11.3 External Carotid Artery (ECA)
- •26.11.3.1 Occlusion
- •26.13 Negative Report
- •26.14 Conclusion
- •Algorithm
- •References
- •27.1 Introduction
- •27.2 Anatomy: Vertebrobasilar System
- •27.3 Vertebrobasilar Circulation: Ultrasound Examination
- •27.4 TCD: Aneurysmal Subarachnoid Hemorrhage
- •27.4.1 Delayed Cerebral Ischemia
- •27.4.2 Vasospasm
- •27.5 TCD: Vertebrobasilar Dissection
- •27.6 TCD: Intracranial Stenosis
- •27.7 TCD: Microembolus Detection
- •27.9 Subclavian Steal Syndrome
- •27.10 TCD: Multimodal Monitoring
- •27.11 TCD: Traumatic Brain Injury
- •27.12 TCD: Brain Death Determination
- •27.13 Conclusion
- •References
- •28.1 Introduction
- •28.2 Cerebral Venous System: Anatomy
- •28.3 vTCCS: Ultrasound Investigation Technique
- •28.4 CVST: Venous Ultrasound Findings

438
G. Pánczél et al.
26.1 Introduction
Stroke is an important cause of disability and mortality and has an estimated incidence of 795,000/year [1]. The stenotic diseases of carotids represent 15–20% of
ischemic stroke. Successful medical or surgical therapy prevents the development
of cerebrovascular symptoms due to carotid stenosis. Although screening is not recommended for unselected population, some surveys found high percent of individuals with asymptomatic carotid stenosis without statins and/or antiplatelet therapy.
On the other hand, almost all guidelines recommend carotid screening for people
with numerous vascular risk factors.
Carotid stenosis occurs most commonly at the carotid bifurcation. Carotid ultrasound (CUS) is a noninvasive, cost-effective, bedside, cheap imaging modality for
detecting, grading and monitoring ICA stenosis due to its high sensitivity and specicity, relatively low cost, lack of radiation hazard. Three modalities should be carried out: (a) B-mode (intima-media thickness and plaque morphology) [2], (b) color
Doppler (visualization of ow abnormalities) [3], and (c) velocity measurements
(one of the most important parameter used for grading the severity of carotid stenosis); therefore, the correct positioning, sampling and insonation are important for
accurate assessment [4–6].
26.2 Optimal Settings
The duplex scan makes blood ow audible with the help of the Doppler effect (spectral and color Doppler), and on the other hand, it visualizes the vessels and the surrounding tissues in real time (B-mode). 5–10MHz range is usually used during the
duplex scan of the large vessels of the neck [4, 7].
26.2.1 Probe Types
• Linear array: The piezoelectric crystals are located next to each other, forming
one line.
• Sector probes: (“phased array,” mechanically rotating and mechanically oscillat-
ing US-probes)

26 Carotid Disease: Usefulness oftheUltrasound
439
26.2.2 Frequencies
Higher frequencies (e.g., 7.5MHz) are used for the examination of more supercial
structures (e.g., carotid arteries), while deeper vessels (e.g., vertebral arteries) and
calcied plaques are examined using 5–5.5MHz. Higher frequency US has less
energy but better axial image resolution than lower frequency US beams. The frequency setting of Doppler mode is usually 4–5MHz during duplex scans and these
frequencies should be used for color coding as well.
26.2.3 Focus
The depth where the image resolution is the highest. Linear probes can produce better lateral resolution than sector types.
26.2.4 Depth
It should be set so that the examined structures are located in the optimal focus
distance of the ultrasonic probe. A maximum depth of 4–5cm should be used in
patients with an “average” neck.
26.2.5 Pulse Repetition Frequency (PRF)
It provides information about how often the device sends each “US-pulse.” It should
be set for B-mode image, Doppler-examination and color-coding. It affects the
maximum depth that can be examined and the maximum ow velocity that can be
measured.
26.2.6 Frame Rate
Image refresh rate (in B-mode and color-mode). Typically its value is between 4
and 30Hz.

440
G. Pánczél et al.
26.2.7 Preprocessing (Parameters that Should BeSet Before
theExamination)
• Dynamic range:
– 30dB: hard image; 60dB: soft image.
• Edge enhancement:
– Level 1–4, it inuences contours.
• Scan correlation (SCC):
– Level 1–4, it reduces noise by (temporal) averaging image points.
• Fast/detailed (line density):
– Greater line density– better, but slower image.
• Time gain compensation (TGC):
– The waves that are reected from deeper structures are weaker (more are
absorbed); therefore, these require more gain. TGC is suitable for this gain
(that depends on the time of reection).
• Zoom:
– It is used for vessel segments that are difcult to visualize and to examine
plaques and IMT measurements.
26.2.8 Freeze
“Freezing” the image on the display for measurements or documentation. If the US
probe is not in use, the image should always be freezed to prevent unnecessary
warming and untimely deterioration of the probe.
26.2.9 Cine Loop
It stores the most recent sequence preceding the freeze in the system’s memory,
allowing the replay of the last few seconds.
26.2.10 Smoothing (Interpolation), Interlacing, Correlation
Procedures to make the image smoother.

26 Carotid Disease: Usefulness oftheUltrasound
441
26.2.11 Postprocessing
Technical procedures for the optimal display of the screen and the documentation.
These lter out the unnecessary parts of the available grayscale and display the
necessary ones.
26.2.12 Resolution
• Axial resolution: The minimum distance that can be differentiated between two
points that are parallel to the ultrasound beam (frequency-dependent).
• Lateral resolution: The minimum distance that can be differentiated between two
points that are perpendicular to the ultrasound beam (frequency-dependent).
26.2.13 Doppler-Technique
• Doppler shift:
– The frequency of the emitted US changes (shifts) if it is reected from a mov-
ing surface (a reector moving towards the source will increase the registered
frequency and a reector moving away from the source will decrease it).
Since the Doppler shift that is caused by the blood ow is within the hearing
range, therefore the sounds that are produced by the ow are audible.
26.2.14 PW-Doppler (Pulsed-Wave Doppler)
The Doppler probe emits US pulses and the same piezoelectric crystal receives the
reected US.This way, knowing the velocity of the US within the tissue, the depth
of interest and the sample volume can be determined. The number of emitted pulses
in a specic time is characterized by the so-called PRF (pulse repetition frequency).
• Aliasing/Nyquist limit:
– The frequency of a wave can be measured if at least two samplings are per-
formed in each period (Nyquist-limit). In case of high velocities (e.g., highdegree stenosis), the sampling cannot be performed fast enough (PRF can
only be increased until a certain limit and the deeper the examined vessel is
located, the lower this limit is); therefore, the velocity range above the limit
(the top of the spectrum) shifts below the zero line (into the negative range)
and also, color aliasing occurs.

442
• Spectrum:
– The time function of frequency shift (velocity shift in case of angle correc-
tion); it illustrates the change of Doppler shift in time. Since blood ow consists of reectors with different velocities (RBCs), a spectrum is received
instead of a linear curve.
• Angle correction/steering:
– A velocity value is only received from the frequency of the Doppler shift, if
the angle between the US beam and the direction of the blood (reector) is
considered (cos).
• Doppler-gain:
– Its setting is considered optimal if there are no mirror artifacts, the whole
spectrum is visible, and it can be easily differentiated from the background.
G. Pánczél et al.
26.2.15 Color Duplex
• Steering/angle correction:
– As color mode is based on the Doppler effect, angle correction is very impor-
tant in this case as well.
• PRF:
– It should be set at the beginning of the examination according to the expected
velocity and then it can be gradually changed depending on whether we wish
to visualize the vessel or the ow (see there).
• Window size:
– The size of the color window should be adjusted so that it contains the vessel
segment of interest. A smaller window allows faster and more precise
visualization.
• Color gain:
– If the gain is not enough, no color signal is seen in spite of existing ow and
if the gain is too strong, confusing artifacts occur in the color window.
26.3 Indications
• Screening of patients with vascular risk factors (primary prevention)
• Established peripheral artery and coronary disease
• TIA, hemi-or brainstem symptoms suggesting stroke

26 Carotid Disease: Usefulness oftheUltrasound
• Follow-up of stroke patients (secondary prevention)
• Bruits during auscultation of the supra-aortic vessels
• Unilateral visual disturbance (amaurosis fugax, ischemic ophthalmopathy, visual
eld defect)
• Syncope
• More than 20 mmHg difference between blood pressures measured on the
two arms
• To look for plaques before carotid massage
• Preceding major surgeries (e.g., coronary bypass surgery)
• Regular follow-up after vascular intervention (endarterectomy, stenting)
• Neck tumor
• Sudden neck pain (if dissection suspected)
• Follow-up after transplantation [4].
443
26.4 Carotid Ultrasound: How toStart theInvestigation?
The patient is in the semi-sitting or supine position, and the examiner is next to or
behind the patient. The examination starts with B mode scan of the vessels. First,
the proximal segment of the common carotid artery is visualized: the probe is positioned dorsal to the sternocleidomastoid muscle, above the clavicle. The common
carotid artery is followed until its bifurcation and then the internal carotid artery is
visualized by positioning the probe and continuing cranially. It should be followed
until its most distal segment (it is usually possible until the lower edge of the mandible) and then the external carotid artery should be examined after returning to the
bifurcation [4].
26.4.1 Differentiating theInternal andExternal Carotids
26.4.1.1 Positioning theProbe
The longitudinal section of the common carotid artery is visualized until its bifurcation and then the cranial side of the probe is rotated forward toward the mandibular
angle to visualize the internal carotid. Caution: the initial portions of the external
and internal carotids might be located inversely.
26.4.1.2 Morphological Differences
The bulb of the internal carotid is dilated similar to an onion and has no side branches
in its cervical segment. The external carotid is usually more gracile and branches
(especially the superior thyroid artery) are usually visible.

444
G. Pánczél et al.
26.4.1.3 Flow Differences
The spectrum of the internal carotid is less pulsatile (the end diastolic velocity is
higher than in the external carotid) which is caused by the lower resistance of the
cerebral vessels (Fig.26.1). The spectrum of the external carotid is more pulsatile
and features “spikes” and its end diastolic velocity is lower (the arteries that supply
the muscles and the skin are more resistant), frequently triphasic (Fig.26.2).
26.4.1.4 Compression
Repeated tapping/compression of the supercial temporal artery creates retrograde
pulse waves that appear as oscillations in the spectral analysis of the external carotid
(Fig.26.2).
During the examination of the carotid system, the course, dilation and mural
abnormalities of the vessels are described in the report (see the end of the chapter).
It is followed by the color duplex scan. The vessels are examined using the color
window and their course, caliber and mural abnormalities are reported. The morphological examinations are followed by Doppler spectral analysis to describe
hemodynamic conditions. Pathological abnormalities must be also recorded.
Finally, if needed, contrast-enhanced ultrasound should be performed [8].
Fig. 26.1 The normal internal carotid artery. The spectrum is biphasic (less pulsatile), the peak
systolic velocity 110cm/s

26 Carotid Disease: Usefulness oftheUltrasound
Fig. 26.2 The spectrum of the external carotid is more pulsatile (left picture), the end diastolic
velocity is lower, frequently triphasic. Repeated tapping/compression (arrows) of the supercial
temporal artery creates retrograde pulse waves that appear as oscillations in the spectral analysis of
the external carotid (right picture)
445
26.5 B-Mode Examination
Longitudinal and then cross-sectional scans of the vessels of interest are performed
in caudocranial direction, rst in B-mode and then in color mode. Any occurring
abnormalities are documented:
I. Elongation
II. Kinking (acute angulation of the artery, it might be mild in case of larger angles
or lead to distortion that could result in ow obstruction).
III. Coiling (a complete loop of the artery, it usually does not cause ow
disturbances).
IV. Bifurcation level. In case of a high bifurcation (that is near the lower mandibu-
lar ramus), the internal carotid artery is often difcult to visualize if it can be
visualized at all.
Mean diameters of ICA (4.7+/−0.8mm) and CCA (6.1+/−0.8mm) in women
are signicantly smaller than in men: 5.1+/−0.9mm and 6.5 +/−1.0mm, respectively [4].
26.5.1 Dilation
The caliber of the vessel and any occurring abnormalities are observed.
• Dilated:
– Diffuse dilation: anatomical variation; circumscribed dilation: aneurysm
(fusiform); but the carotid bulb is often dilated, and it is not an aneurysm
in itself.

446
G. Pánczél et al.
• Narrowed:
– Diffuse narrowing in the whole vessel: hypoplasia; a decrease in caliber can
often be observed distally from an occlusion due to a fall in transmural pressure; segmental narrowing: bromuscular dysplasia (rare in the cervical area).
26.5.2 Intima-Media Thickness (IMT)
A zoomed, longitudinal scan of the CCA is performed and the measurement is carried out 1–3cm below the bifurcation (if a plaque is located at this level, then right
below the plaque), on the wall that is farer from the probe (dorsomedial wall). A thin
white stripe, the blood-intima interface (A) is located between the arterial lumen (in
black) and the vessel wall. Below the white stripe, a black and then another white
stripe (usually the thickest layer) are seen. The border between the latter two is the
media-adventitia interface (B). IMT equals to the distance between A and B and its
normal value is 0.4–0.8 (Fig.26.3). Aging, hypertension, hyperlipidemia, diabetes,
smoking, and extreme alcohol consumption increase the IMT and numerous observations prove the correlation between the pathological thickness of IMT and risk of
vascular events. Similarly, an IMT decrease after long lasting pharmacotherapy
(e.g., statin) is associated with decreased vascular risk. The standards of IMT measurement were published by the Mannheim Consensus Meeting [9].
26.5.3 Plaque Analysis
During B-mode examination, every circumscribed plaque is detected in the vessel
segments that are in the eld of view. Plaques are characterized based on the following features:
Fig. 26.3 IMT.A thin
white stripe, the bloodintima interface (A) is
located between the arterial
lumen (black) and the
vessel wall. Below the
white stripe, a black and
then another white stripe
(usually the thickest layer)
are seen. The border
between the latter two is
the media-adventitia
interface (B). IMT equals
to the distance between
(A, B)

26 Carotid Disease: Usefulness oftheUltrasound
447
26.5.3.1 Location
Which vessel portion, which wall (according to their relation to the probe, near, far
or lateral walls are distinguished).
26.5.3.2 Shape andConguration
In cross-sectional scans, plaques can appear circumscribed, sickle-like and attached
to the lateral wall, concentric or semicircular (eccentric); connecting plaques can
form plaque systems.
26.5.3.3 Maximal Thickness
The thickness of the plaques that seem the thickest is measured during crosssectional scan of the artery.
26.5.3.4 Surface
Smooth (usually soft plaques), moderately irregular (usually brous or calcied
plaques), severely irregular (usually calcied plaques), ulcerated (focal, sudden
excavation of the surface with a usual depth of >2mm). Its signicance: irregular,
especially ulcerated surfaces signicantly increase the risk of stroke.
26.5.3.5 Echogenicity
It indicates which range of the grayscale the plaque belongs to. Echolucent (soft)
plaque: dark, its density is similar to blood; such are lipid-rich, hemorrhagic plaques
and newly formed thrombi. Isodense (moderately dense): its density is similar to the
sternocleidomastoid muscle (such are brous plaques and chronic thrombi.
Hyperdense, hyperechoic plaque: its density is similar to the cervical vertebra, it is
white (such are collagen-rich, brous and calcied plaques, the latter also produce
an acoustic shadow). Importance: echolucent plaques indicate a signicantly
increased risk of stroke. Measurement: the density of blood is set between 0 and 5,
and the density of the adventitia is set to 230. Echolucent plaques with a density
below 32 indicate increased risk of stroke [10–12].
26.5.3.6 Homogeneity– Heterogeneity
It indicates how similar or different are the parts of a plaque (Figs.26.4, 26.5, 26.6,
and 26.7).
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