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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

6 Transcranial Doppler Ultrasound: Physical Principles
the display device, but where a Doppler shift is detected, it is colour coded to show
the measured relative velocity between the transducer and the detected target.
Usually ow towards the transducer will be coded in one colour (often red), and
ow away from the transducer in another (often blue).
CFI is an extremely good technique for imaging anatomy and related blood ow,
but it has a number of limitations that the operator must bear in mind. First and
foremost, it must be remembered that the Doppler angle, θ, will affect the measured
Doppler shift, and therefore, ow with the same speed in different parts of the image
may be represented by different shades of colour, or even completely different
colours, depending on the component of their velocity relative to the transducer.
Also CFI, just as ordinary PW Doppler, is susceptible to aliasing, and it is important
to differentiate between regions of reverse ow in a vessel and regions of aliasing,
both of which lead to a change in the displayed ow direction. Frame rates in CFI
are signicantly lower than in standard B-mode imaging because in order to detect
and quantify a Doppler shift, it is necessary to interrogate a sample volume several
times (typically between 8 and 16), and this is the reason why the so-called ‘colour
box’ where colour ow information is displayed is often signicantly smaller than
the total area of the scan. Finally, colour ow estimates of velocity are based on a
relatively small number of samples when compared with PW Doppler, and so their
velocity resolution is much lower. Colour ow imaging is an excellent way to gain
an impression of the overall haemodynamics in a region of the body, but if quantitative measurements are to be made, CFI should be used to identify a region of interest and PW Doppler used to make the measurements.
111
6.6.4 Power Doppler Imaging (PDI)
An alternative to coding and displaying the Doppler shift frequency measured from
each sample volume is to measure and display the total Doppler power, which is
determined mainly by the volume of moving blood rather than its velocity. Thus,
changes in angle, and even aliasing, do not alter the colour coding– indeed because
of a mechanism known as intrinsic spectral broadening, it is even possible to image
ow perpendicular to the transducer face, which is not possible with ordinary
CFI.The result of this is that images of tortuous vessel can often be more complete
and easier to understand. Power Doppler is more sensitive than colour Doppler for
imaging of ow but provides no information about the direction of ow.
6.7 Transcranial Doppler Ultrasound (TCD)
Transcranial Doppler ultrasound is the application of Doppler ultrasound techniques
through the intact skull. Where imaging techniques are involved, such techniques
are usually called transcranial coded sonography (TCCS). In general, the skull bone

112
is too thick to penetrate adequately with ultrasound, but there are a number of
‘acoustic windows’ where there is a natural foramina, or the bone is sufciently thin
for a signicant percentage of ultrasound energy to penetrate. The most commonly
used window is the temporal bone window, which allows insonation of the middle,
anterior and posterior cerebral arteries. The foramen magnum window (or suboccipital approach) allows insonation of the basilar and vertebral arteries, and the
orbital approach allows insonation of the ophthalmic arteries and the internal carotid
siphon. TCD techniques have many similarities to ordinary pulsed Doppler techniques but also differ in a number of ways. In order to penetrate the skull, it is necessary to use very low transmitted frequencies (recall that attenuation increases with
frequency), and most simple TCD examinations are performed with 2MHz ultrasound or thereabouts. Low frequencies generate much lower levels of scattering
from blood, (an advantage when monitoring for emboli since small signals from
small emboli are less likely to be masked by the blood ow signal, but a disadvantage if it is the blood ow itself that is to be studied). Low frequencies also give poor
spatial resolution, but the major contribution to poor spatial resolution in transcranial studies is the distortion of the ultrasound beam by the skull.
D. H. Evans
6.7.1 Velocity Measurement
The method used to estimate blood ow velocity in TCD applications is different
from that used elsewhere in the body. The standard method is to average the instantaneous intensity weighted mean velocity over the cardiac cycle, but in TCD it is the
instantaneous maximum velocity that is usually averaged. The reason for this is that
it is easier to extract a good maximum frequency envelope than a good mean envelope when the signal-to-noise ratio is poor. Fortunately, because of the type of ow
found in cerebral vessels, the mean of the maximum over the cardiac cycle is more
or less proportional to the true mean, and the constant of proportionality is approximately 2 [3]. In other words, the true mean velocity is half the gure usually quoted
as ‘mean velocity’. It is vital when reporting TCD velocity measurements that
investigators explain exactly which velocity they have calculated. Another particular issue with TCD velocity measurements is that they are usually made blind, and
the Doppler angle, θ, assumed. Although this may be valid for some patients, in
others it can introduce signicant errors which must be recognised if absolute velocity values are of interest.
6.7.2 Flow Changes
In most arteries in the body, it is reasonable to assume that, in the short term at least,
changes in blood ow velocity are proportional to changes in ow. This is not necessarily a valid assumption in TCD as there is evidence that even the major arteries

6 Transcranial Doppler Ultrasound: Physical Principles
exhibit considerable vasoactivity. Certainly arterial spasm leads to dramatic
increases in blood ow velocity that are not representative of changes in ow, and
other stimuli are thought to affect cerebral arterial diameter. It is vital that this fact
is borne in mind when interpreting velocity changes in TCD.Unfortunately, cerebral vessels are too small to have their diameters accurately measured by ultrasound, but attempts have been made to monitor changes in diameter by measuring
changes in the total amount of power backscattered by the moving blood within the
sample volume. This technique can only be partially successful because it relies on
uniform insonation of the blood vessel, which cannot be achieved due to the distortion of the ultrasound beam by the skull bone.
113
6.7.3 Cerebrovascular Resistance
Cerebrovascular resistance (CVR) can be calculated by dividing mean blood pressure by mean blood ow. TCD, however, measures velocity (i.e. ow divided by
vessel cross section). Therefore, dividing mean blood pressure by mean blood ow
velocity leads to a value of CVR multiplied by vessel cross section (at the point of
ultrasound insonation). This quantity has been called ‘resistance-area product’ or
RAP [4], both to distinguish it from true CVR, and to emphasise that it is also
dependent on any changes in the cross section of the vessel where the measurement
is being made.
6.7.4 TCD– Embolus Detection
Embolus detection has become a major application of TCD.The basis of embolus
detection is very simple. As an embolus passes through the Doppler sample volume, if its scattering cross section is sufciently large, it will give rise to an additional Doppler component that can be heard or seen on the Doppler display.
Whether or not an embolus can be detected depends on its size and composition,
the ultrasound frequency, the size of the sample volume, the embolus trajectory and
its interaction with the ultrasound beam. In general, even relatively small gas bubbles will be detected, but some larger solid emboli may not. Several techniques
have been proposed for distinguishing between different types of emboli, and while
some progress has been made towards this goal, there are still signicant challenges. Microembolic signals are discussed in a later chapter in this book, and for
an in- depth discussion of the physics of embolus detection, the reader is
referred to [5].

114
D. H. Evans
6.8 Transcranial Colour-Coded Duplex Sonography (TCCS)
Transcranial colour-coded sonography is simply CFI or PDI performed through the
cranial bones. As for simple TCD, it can only be done through the ‘bone windows’,
must be done at relatively low frequencies to achieve adequate penetration and is
subject to the effects of beam distortion (and, therefore, image distortion) by
the skull.
Transcranial color-coded duplex ultrasonography (TCCS) provides the imaging
of large intracranial arteries through the intact skull by colour coding of blood ow
velocity. The circle of Willis can be identied by their anatomic location with
respect to the brain stem structures and by the ow direction. TCCS is an important
imaging method due to its excellent time resolution. This technique is useful for
detecting vasospasm. Application of echo-contrast agent can increase the accuracy
of investigation [6].
6.9 Ultrasound Safety
No chapter on the physical and technical principles of neurovascular ultrasound
would be complete without the mention of ultrasound safety. Diagnostic ultrasound
is generally assumed to be perfectly safe, and even if there are potential hazards,
these are greatly outweighed by the benets to the patient. It is, however, important
to remember that this may not always necessarily be the case. There are two broad
classes of mechanism by which ultrasound is capable of damaging tissue, the ‘thermal effects’ and the ‘non-thermal effects’, which may be further broken down into
cavitation, streaming and other direct effects.
Thermal effects, that is, heating of the tissue, are related to the conversion of
ultrasound energy into heat energy, and hence to the temporal average intensity of
the ultrasound beam and the rate at which it is absorbed by the tissue. Non-thermal
effects are related to the peak negative pressure of the ultrasound wave as it propagates through the tissue. It should be noted that these two mechanisms are virtually
independent of each other, as the relationship between average intensity and peak
negative pressure depends on the pulsing regime selected. One potential area for
caution in neurovascular ultrasound is TCD.There are three reasons for this. Firstly,
in order to overcome the rapid attenuation of ultrasound by the skull, it is necessary
to use relatively high ultrasound intensities; secondly, bone is a rapid absorber of
ultrasound and thirdly, TCD monitoring may last for considerable periods of time
where the same region of tissue is being insonated continuously. All these effects
can lead to signicant heating of the skull bone, and potentially to secondary heating of brain tissue by conduction from the bone.
There are two indices that are of value in evaluating the potential hazard of ultrasonic examinations, the thermal index (TI) and the mechanical index (MI). The TI

6 Transcranial Doppler Ultrasound: Physical Principles
115
is an estimate of the rise in tissue temperature in °C under worse case conditions.
The MI is an attempt to indicate the probability of mechanical damage by nonthermal processes. When these indices have a value of 1 or more, the possibility of
hazard should be considered. There are in fact three different thermal indices, the
soft tissue index (TIS) and bone index (TIB), and most relevant to TCD, the cranial
index (TIC), which is the TI that should be used when there is bone at the surface
(this is because, in this situation, the greatest temperature rise occurs in the bone and
adjacent tissue). Operators of TCD instruments should strive to maintain as low a
value of TIC as is compatible with obtaining a good signal, and have clear justication for using unusually high values.
One nal area of caution with TCD is in relation to the use of contrast agents, as
they may potentially lower the threshold for cavitational activity. Clearly, it is
important with respect to any potential for hazard related to the ultrasound that the
operator must do all they can to reduce unnecessary exposure, and to ensure that the
benets to the patient outweigh potential hazards. It is also important that ultrasound practitioners keep up to date with the current literature on safety. The
European Federation of Societies for Ultrasound in Medicine and Biology
(EFSUMB) issue safety statements regularly and can be found on their website at
www.efsumb.org. Much more in-depth discussions of ultrasound safety can be
found in [7, 8].
6.10 Conclusion
Ultrasound is a powerful diagnostic technique. It is important that any user of the
technique is familiar with the physical and technical principles behind the method,
as these provide an insight into its strengths and weaknesses, and sources of possible artefacts.
References
1. Hoskins PR, Martin K, Thrush A, editors. Diagnostic ultrasound: physics and equipment. 3rd
ed. FL, USA: CRC Press; 2019.
2. Evans DH, McDicken WN.Doppler ultrasound: physics, instrumentation and signal process-
ing. 2nd ed. Chichester: Wiley; 2000.
3. Evans DH.On the measurement of the mean velocity of blood ow over the cardiac cycle using
Doppler ultrasound. Ultrasound Med Biol. 1985;11(5):735–41.
4. Evans DH, Levene MI, Shortland DB, Archer LNJ.Resistance index, blood ow velocity, and
resistance-area product in the cerebral arteries of very low birthweight infants during the rst
week of life. Ultrasound Med Biol. 1988;14(2):103–10.
5. Evans DH.Ultrasonic detection of cerebral emboli. In Yuhas DE and Schneider SC, editors.
Proc. 2003 IEEE ultrasonics symposium, IEEE, Piscataway, 2003. p.316–26.

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6. Bartels E.Transcranial color-coded duplex ultrasonography in routine cerebrovascular diag-
nostics. Pers Med. 2012;1(1–12):325–30.
7. Ter Haar G, editor. The safe use of ultrasound in medical diagnosis. 3rd ed. London: British
Institute of Radiology; 2012.
8. Csiba L, Baracchini C, editors. Manual of neurosonology. Cambridge, Uk: Cambridge
University Press; 2016. p.1–322.
D. H. Evans

Chapter 7
Transcranial Doppler (TCD)
andTrancranial Color-Coded Duplex
Sonography (TCCS): Applied
Neuroanatomy
CamiloN.Rodríguez andRyanSplittgerber
Key Points
1. It is important to know the anatomy of the parenchymal brain and cerebral vas-
cular landmarks (circle of Willis) for an adequate US approach and interpretation of the ndings in the critical patient bedside.
2. Within the circle of Willis the most frequent anatomical variation is hypoplasia
or absence of the posterior communicating artery (PComA).
3. It is paramount to choose the most appropriate bone window according to the
clinical condition of the patient, his decubitus, and the specic objective to be
studied.
4. The transtemporal acoustic window is the most used because it allows access to
the most important axial exploration planes: mesencephalic, diencephalic, and
ventricular.
5. The submandibular acoustic window is an alternative and very useful access,
especially in the critically ill patient and his frequent supine decubitus, when
studying the vertebrobasilar system.
6. The anatomical identication of the deep venous cerebral system and the dural
venous sinuses is not easy. It requires training and dedication to the bedside of
the patient.
C. N. Rodríguez (*)
Intensive Care Medicine, Hospital Nacional Prof. Dr. A. Posadas, University of Buenos Aires
(UBA), Neurointensive Care Section - ESICM, Neurointensive Care Section - AMCI,
Neurointensive Care Committee - FEPIMCTI, Member of ESNCH, Buenos Aires, Argentina
e-mail: camilo.rodriguez@nesccco.com
R. Splittgerber
Department of Surgery, Vanderbilt University Medical Center, Ofce of Health Sciences
Education, Vanderbilt University School of Medicine, Nashville, TN, USA
e-mail: ryan.splittgerber@vanderbilt.edu
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_7
117© Springer Nature Switzerland AG 2022

118
C. N. Rodríguez and R. Splittgerber
7.1 Introduction
Transcranial Doppler (TCD) and/or transcranial color-coded duplex sonography
(TCCS) are frequently used as noninvasive and rapid access neurological monitoring tools in the intensive care unit [1, 2].
The anatomical correlation of the brain parenchyma and its vascular components
will be better scanned when approaching the patient with the TCCS technique
where the 2D image (parenchyma and brain structures) is combined with the colorcoded Doppler of the patients’ vessels corresponding to the circle of Willis.
7.2 Brain Parenchyma: Anatomy andUltrasound
There are two main techniques for transcranial Doppler: the conventional TCD
(“blind”) and the transcranial color-coded duplex sonography (TCCS). The main
advantage of TCCS versus TCD (¨blind technique¨) is that the intracranial vessels
can be identied in relation to some anatomical landmarks. Within this fact lies the
importance of recognizing the anatomical structures and their access windows [3].
We will approach the intracerebral anatomy from the insonation windows, which
are most commonly used in clinical practice.
7.2.1 Anatomy ofAcoustic Windows
7.2.1.1 Transtemporal Acoustic Window (Fig.7.1)
The transtemporal window is the most frequently used as it allows access to the
most important axial exploration planes: mesencephalic, diencephalic, and ventricular [3, 4].
Mesencephalic Plane
This plane is obtained by projection of the transducer at a 90° angle to the temporal
bone via the transtemporal bone window.
A. Brain parenchyma structures identied by TCCS (Fig.7.2).
• TCCS: B-mode.
• Depth: 14–16cm.
a. Cerebral peduncles [Mesencephalon] (hypoechoic >> “Buttery”) [5, 13]
b. Basal cisterns (space around the mesencephalon).
c. Contralateral skull bone (hyperechoic).

b
a
7 Transcranial Doppler (TCD) and Trancranial Color-Coded Duplex Sonography…
Fig. 7.1 (a) Scheme: anatomy of transtemporal acoustic window and different approaches; (F)
frontal, (A) anterior, (M) medial, and (P) posterior above zygomatic process of temporal bone. (b)
Scheme: anatomy of the oor of the cranial cavity: (1) anterior fossa, (2) sphenoid bone, (3) middle
fossa, (4) posterior fossa, (5) parietal bone, (6) foramen magnum, and (7) sphenoid bone. (blue
arrows): direction of insonation beam from transducer through temporal bone. (Author: Camilo
N.Rodríguez)
119
a
Fig. 7.2 (a) Mesencephalic plane by TCCS: (M) mesencephalon; (arrow) contralateral skull. (b)
Brain anatomy by CT scan: (M): mesencephalon; (1) ambient cistern and (2) quadrigeminal cistern. (Author: Camilo N.Rodríguez)
b

120
C. N. Rodríguez and R. Splittgerber
These are (Fig. 7.2a) the neuroanatomical landmarks used to localize the
circle of Willis with Doppler technique [3, 4, 6].
B. Vascular structures identied by TCCS.
• TCCS: Doppler mode.
1. Circle of Willis [7–9] (Fig.7.3).
1.1 Internal carotid artery (ICA).
1.2 Middle cerebral artery (MCA).
1.3 Anterior cerebral artery (ACA).
1.4 Posterior cerebral artery (PCA).
7.2.1.2 Diencephalic Plane (Thalamic Plane)
This plane is obtained by a slight displacement of the transducer toward the cephalic
10° from the mesencephalic plane through the transtemporal window.
A. Brain parenchyma structures identied by TCCS (Fig.7.4).
• TCCS: B-mode.
• Depth: 14–16cm.
1. Third Ventricle.
[Two hyperechoic horizontal parallel lines]
a
Fig. 7.3 (a) Circle of Willis by TCCS through transtemporal acoustic window: (1) mesencephalon, (M1) ipsilateral M1 segment of middle cerebral artery (red), (M2) M2 segment of middle
cerebral artery, (ACA) anterior cerebral artery, (MCAc) contralateral middle cerebral artery (blue),
(arrow) contralateral skull. (b) Angio-MRI of circle of Willis: MCA (M1): M1 segment of middle
cerebral artery, (M2) M2 segment of MCA, (ICA) internal carotid artery, (PCA) posterior cerebral
artery, (BA) Basilar artery, (ACA) anterior cerebral artery, and (MCAc) contralateral middle cerebral artery. (Author: Camilo N Rodríguez)
b
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