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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

7 Transcranial Doppler (TCD) and Trancranial Color-Coded Duplex Sonography…
141
7.6.1.2 Basal Vein (of Rosenthal)
Identication: The basal vein is very close (slightly cranial) to the P2A segment of
the posterior cerebral artery.
TCCS
Acoustic bone window: Transtemporal.
Insonation plane: It starts in the mesencephalic plane and then the probe is positioned with a slight angulation to the diencephalic plane (thalamic), following the
direction of the posterior cerebral artery.
Duplex: Flow away from the probe to venous sinus of dura mater (blue color).
Note: Decrease the depth [11, 33].
TCD
Acoustic bone window: Transtemporal.
Flow: Increase in the ow velocity (thrombosis?) [35, 37].
7.6.1.3 Great Cerebral Vein (of Galen)
Identication: It is immediately behind the pineal gland (hyperechoic structure)
behind the two lines (hyperechoic) corresponding to the third ventricle (diencephalic plane).
TCCS
Acoustic bone window: Transtemporal.
Insonation plane: Diencephalic (thalamic).
Duplex: Flow away from transducer to venous sinus of dura mater drainage
(blue color).
Note: Decrease the depth [11, 33, 37].
7.6.2 Dural Venous Sinuses (Fig.7.17)
7.6.2.1 Sphenoparietal Sinus
Identication: Identify the edges of the lower wing of the sphenoid and the pyramid
that makes up the sphenoid bone. The sphenoparietal sinus is located at the hyperechoic edge of the sphenoid wing.
TCCS
Acoustic Bone window: Transtemporal.
Insonation plane: Superior pons plane and inferior pontine plane.
Duplex: Blue color (ow away from transducer).

142
ab
Fig. 7.17 (a) Scheme: sinuses detectable by TCCS (oor of the cranial cavity); (1) foramen magnum, (2) cerebellar tentorium, (3) transverse sinus, (4) straight sinus, (5) superior petrosal sinus,
(6) inferior petrosal sinus, (7) optic nerve, (8) internal carotid artery. (b) Scheme: sinuses detectable by TCCS (oor of the cranial cavity, left cerebellar tentorium removed); (1) foramen magnum, (2) cerebellar tentorium, (3) transverse sinus, (4) straight sinus, (5) superior petrosal sinus,
(6) inferior petrosal sinus, (7) optic nerve, (8) internal carotid artery, (9) sphenoparietal sinus, (10)
sigmoid sinus, and (11) cavernous sinus. (Author: Camilo N.Rodríguez)
C. N. Rodríguez and R. Splittgerber
7.6.2.2 Superior Petrosal Sinus
Identication: Identify the edges of the lower wing of the sphenoid and the pyramid
that makes up the sphenoid bone. The sphenoparietal sinus is located at the hyperechoic edge of the sphenoid wing.
TCCS
Acoustic window: Transtemporal.
Insonation plane: Superior pons plane and inferior pontine plane.
Duplex: Blue color (ow away from transducer).
7.6.2.3 Inferior Petrosal Sinus
Identication: It runs close to the basilar artery. Close to this artery, the vertebral
venous plexus and the inferior petrosal sinus can be identied.
TCCS
Acoustic Window: Transforaminal.
Duplex: Red color (ow forward to the transducer close to the Basilar artery).
7.6.2.4 Cavernous Sinus
Identication: Difcult insonation.

7 Transcranial Doppler (TCD) and Trancranial Color-Coded Duplex Sonography…
143
TCCS
Acoustic bone window: Transtemporal.
7.6.2.5 Transverse Sinus
Identication: From the plane of insonation of the straight sinus, it is necessary to
perform a downward (and posterior) probe rotation for the location of the contralateral transverse sinus.
TCCS
Acoustic bone window: Transtemporal.
Duplex: Blue color (contralateral transverse sinus)/red color (ipsilateral transverse sinus). Both transverse sinuses drain to sigmoid sinuses [11, 32, 37].
7.6.2.6 Straight Sinus
Identication: From the diencephalic plane, it is necessary to rotate the transducer
upwards to align the plane of insonation with the beginning of the tentorium of the
cerebellum (hyperechoic). The straight sinus is directed, on this anatomical structure, until its drainage in the conuent sinus.
TCCS
Acoustic Bone window: Transtemporal.
Duplex: Blue color (ow away from the transducer to conuent sinus) [32].
TCD
Acoustic Bone window: Transforaminal.
Flow: Increase in the ow velocity (thrombosis) [34, 37].
Operator training requires more time and patience. The insonation and identication of the intracerebral venous system is more difcult, given the low ow of the
system under normal conditions.
There is evidence of an alternative frontal acoustic window (paramedian projection and lateral projection) at the access of the deep venous system and/or anterior
cerebral artery (A2 segment). It presents a lower efciency than the transtemporal
window, a difculty that can be resolved with the administration of contrast [38].
7.7 Conclusion
To introduce transcranial Doppler (TCD) or transcranial color-coded duplex
Sonography (TCCS) into critical care practice, the operator should be fully trained
into acquiring the following:
• Adequate knowledge of cerebrovascular and brain parenchyma anatomy.

144
INTENSIVE CARE UNIT (ICU)
C. N. Rodríguez and R. Splittgerber
• A correct understanding of the anatomical US landmarks and hemodynamics
measures for an accurate interpretation of the results.
This knowledge will allow the operator to choose the most appropriate acoustic
window in correlation with the current clinical condition of the patient, patient’s
decubitus, insonation technique, and the anatomical objective to be studied.
Algorithm
EMERGENCY DEPARTMENT (ED)
IDENTIFY
Neuro-Critical Care Patient ? ABCD
Position of the Patient ? Level of Consciousness (GCS)
Conservation of Head Anatomy ? Hemodynamic Stability
Structure or Vessel of Interest
Transcranial Color-Coded Sonography
Intra-axial collections Circle of Willis
Extra-axial collections
Volume of the Collections Extracranial Carotid System
3th Ventricle Size
Lateral Ventricle Size
Mesencephalon
Midline Shift (MLS)
CEREBRAL HEMODYNAMICS
Circle of Willis
(ACA / MCA / PCA / VA / BA)
Carotid System
(ICA / ECA)
Spectral Doppler Waveform (Indexes)
(PI / RI / LI)
Cerebral Autoregulation (CA)
Cerebral Venous System
Dural Venous Sinuses
(TCCS)
CEREBRAL PARENCHYMA
(B-Mode)
(Doppler Mode)
DEFINE
Acoustic Window
CEREBRAL HEMODYNAMICS
(Doppler mode and M-Mode)
(MCA / ACA / PCA / VA / BA)
(ICA / ECA)
T (Time): Dedication 45 Minutes
C (Color –Grayscale): B-Mode (Brain Parenchyma)
C (Color –Coded): Doppler Mode
(Blodd Flow Direction and Insonation angle)
S (Side): Bilateral Ultrasound (Always)
T (Time): Dedication 45 Minutes
C (Color): Doppler Mode and M-Mode
D (Double): Bilateral Ultrasound (Always)
Clinical Status of the Patient
Oxygenation? (MV?)
TranscranIal Doppler
(TCD -¨Blindapproach¨)
ATTENTION
ATTENTION
ABCD airway-breathing-circulation-disability, MV mechanical ventilation, ACA anterior cerebral
artery, MCA middle cerebral artery, PCA posterior cerebral artery, VA vertebral artery, BA Basilar
artery, PI Pulsatility index, RI resistance index, LI Lindegaard index, ICA internal carotid artery,
ECA external carotid artery

7 Transcranial Doppler (TCD) and Trancranial Color-Coded Duplex Sonography…
145
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C. N. Rodríguez and R. Splittgerber

Chapter 8
Transcranial Doppler (TCD/TCCS)
andCerebral Blood Flow: Applications
intheNeurological Intensive Care Unit
EdwardM.Manno andFarzenehSorond
Key Points
1. Cerebral blood ow originally directly measured more recently is measured
through external detection systems. Transcranial Doppler ultrasound can serve
as a surrogate for measurements under select circumstances.
2. Cerebral autoregulation is a pressure phenomenon that maintains relatively con-
stant cerebral blood ow over a wide range of cerebral perfusion pressures. CO
vasoreactivity measures the response of cerebral blood ow to alterations
in PCO2.
3. Transcranial Doppler ultrasound represents a noninvasive method to measure
direction of ow and velocities of the basal cerebral arteries. Cerebral autoregulation can be tested under static and dynamic conditions.
4. Transcranial Doppler ultrasound is used in a variety of pathologies in the neuro-
logical intensive care unit. Its main use is for the detection of cerebral vasospasm
after subarachnoid hemorrhage.
5. Transcranial Doppler ultrasound has attained greater acceptance as a conrma-
tory test in the diagnosis of brain death.
2
8.1 Introduction
In 1982, Rune Aaslid reported the capability of insonating through the skull using a
low-frequency pulsed Doppler ultrasound wave [1]. Thus, with the development of
transcranial Doppler ultrasound (TCD), the cerebrovascular tree could be mapped.
E. M. Manno (*) · F. Sorond
Department of Neurology, Northwestern University Feinberg School of Medicine,
Chicago, IL, USA
e-mail: edward.manno@nm.org; Farzaneh.Sorond@nm.org
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_8
147© Springer Nature Switzerland AG 2022

148
Subsequent techniques were developed that allowed for the identication of vessel
narrowing or occlusion, the assessment of cerebral blood ow and autoregulation,
and the discovery of high-intensity transient signals (HITS). TCD became increasingly important in its use for discovering patients at risk for cerebral infarction from
a variety of neurological conditions. The technology became increasingly widespread due to its portability, low cost, and ease of use. Due to the overall utility of
the technology, TCD became a critical diagnostic tool in the neurological intensive
care unit. This chapter will review basic cerebrovascular physiology and describe
TCD technology and its application in the neurological intensive care unit for a
variety of pathological conditions.
E. M. Manno and F. Sorond
8.2 Cerebral Blood Flow Measures
In the 1940s, Kety and Schmidt using the Fick principle described a direct method
of quantifying cerebral blood ow (CBF) [2]. Using nitrous oxide, an inert, diffusible, non-metabolizable tracer, they were able to calculate CBF based on a differential equation incorporating arterial and venous concentrations of nitrous, the time to
reach equilibrium, and the partition coefcient of the brain [3]. All methods of CBF
are subsequently compared to the Kety–Schmidt measures which are considered the
gold standard.
The development of external detection systems permitted the use of radioactive
tracers to measure global and regional areas of CBF.Perfusion and the time to washout of radioactivity are used to determine regional ow. A variety of substances have
been used with increasingly sophisticated methods to detect regional ow. Some
commonly employed methods now include single-photon emission computed
tomography SPECT and positron emission tomography [4].
Both computed tomography (CT) and magnetic resonance imaging (MRI) have
developed the bolus-tracking methods to determine and quantify regional blood
ow. MRI uses gadolinium to detect a decrease in the T2 signal caused by the magnetic susceptibility of this agent [5]. CT is able to similarly detect the rate of appearance and disappearance of a contrast bolus to detect regional ow. CT and MRI
perfusion is now commonly used in emergency departments to detect acute large
vessel occlusions and to determine if additional brain tissue is at risk for infarction.
All of the above-listed methods, however, are relatively invasive and require
transport of the patient to radiology.
8.3 Transcranial Doppler (TCD/TCCS)
TCD/TCCS represents a noninvasive method to evaluate ow velocities through the
basal cerebral arteries. By evaluating the ow velocity spectrum of the cerebral
arteries, TCD/TCCS can provide information on the direction of ow, patency of

Transorbital
8 Transcranial Doppler (TCD/TCCS) and Cerebral Blood Flow: Applications…
Fig. 8.1 Multiple
approaches to obtain ow
velocities of the basal
cerebral arteries.
Approaches listed include
transtemporal,
transforaminal,
transorbital, and
submandibular. These
“windows allow for
insonation of these vessels.
(Aaslid [5])
Transforaminal
Submandibular
Transtemporal
149
vessels, focal stenosis, and cerebrovascular reactivity [5]. TCD/TCCS utilizes a
2MHz ultrasound probe to emit a pulsed Doppler wave which is both range gated
and directionally sensitive. Range gating allows for the depth to be adjusted by
altering the time the pulsed wave is received. The Doppler principle allows the
determination of direction of ow. The ultrasonic beam encompasses the insonated
artery, thus reecting a wave of erythrocyte velocities that have the highest velocities detected at the center of the artery [6]. Systolic peak velocities can be measured,
and mean ow velocities calculated form the waveform. The shape of the waveform
will determine a pulsatility index (PI) with a low PI representing a dampened waveform. High PIs are generally believed to be a marker for increased downstream
resistance [7].
Using a low-frequency transmitted wave, TCD can insonate through the temporal bone. Examination is performed through the use of transtemporal, ophthalmic,
and posterior approaches or “windows” (Fig.8.1). Through these approaches, a map
of the cerebrovascular tree can be generated (Fig.8.2). Normal ranges for TCD ow
velocities of the cerebral arteries are well documented [6].
8.4 TCD/TCCS: Assessment ofCerebral Blood Flow
TCD has been used to assess both volume ow and relative changes in CBF after
dynamic changes in blood pressure. Absolute blood ow can be estimated for TCD
ow velocities only when the diameter of the vessel lumen is known [8]. Calculations
of CBF using TCD ow velocities under “static” or non-changing conditions have
determined values similar to expected values of CBF but direct comparisons with
other measures of CBF are lacking [9]. Similarly, due to the nature of the disease
processes in the intensive care unit, the two variables of lumen diameter and arterial

150
E. M. Manno and F. Sorond
Fig. 8.2 Transcranial waveforms and directions of the basal cerebral arteries obtained through the
multiple approaches. (LACA=left anterior cerebral artery; LMCA=left middle cerebral artery;
LPCA=left posterior cerebral artery; LVA=left vertebral artery; BA=basilar artery; RACA=right
anterior cerebral artery; RMCA= right middle cerebral artery; RPCA=right posterior cerebral
artery; RVA=right vertebral artery.) (Saver and Feldmann [6])
perfusion territories are rarely constant. Thus, calculation of absolute CBF in the
neurological intensive care unit is fraught with difculties. Transcranial color-coded
duplex sonography can provide a better estimate of luminal diameter but is rarely
used under dynamic testing [10].
A more practical use of TCD/TCCS in the neurological intensive care unit is
measuring relative changes in ow velocities [11–16]. Several studies have investigated the relationship between changes in TCD ow velocities and CBF.A linear
relationship has been reported between ow velocities and the mean transit time of
technetium [14], and percentage changes in ow velocities and percentage changes
in CBF [15]. Flow velocity and CBF changes to hyperventilation in normal volunteers revealed changes that reected a slope 0.8 with a y-intercept close to zero,
again suggesting that relative changes in ow velocities approximated changes in
CBF [16].
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