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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

244
bc
A. Y. Denault et al.
a
d e
Fig. 13.8 A 54-year-old woman with a (a) grade IV subarachnoid hemorrhage and left craniectomy shown on computed tomography. Corresponding diencephalic view obtained using twodimensional echocardiography. With rotation (b), the diencephalic view allows close monitoring
of ventricular dimensions which were more signicant on the left side. Note on both images the tip
of the ventricular drainage system. (c, d) Color Doppler allows visual screening of ow velocities
of arteries of the circle of Willis. Direct examination using pulsed-wave Doppler of the left middle
cerebral artery (LMCA) allows more precise quantication. (e) Direct examination using pulsedwave Doppler of the left middle cerebral artery (LMCA) allows more precise quantication.
(Abbreviations: EDV end-diastolic velocity, ICP intracranial pressure, PSV peak systolic velocity,
RI resistant index, RMCA right middle cerebral artery). (Reproduced and adapted by permission
of Taylor and Francis Group, LLC, a division of Informa plc. from Denault etal. [21])
13.5 Pitfalls inCranial 2D Ultrasound andTCD Monitoring
The use of cranial 2D US, ONSD, and TCD/TCCS must be carefully interpreted in
conjunction with extracranial conditions that can be associated with neurological
abnormalities. For instance, intravenous milrinone can induce left ventricular outow tract obstruction in patients with subarachnoid hemorrhage treated for vasospasm (Fig.13.9). This condition can be associated with signicant high- velocity
signals in the cerebral arteries which are unrelated to the degree of vasospasm. We
have observed elevated PI and increased ONSD in various conditions such as left
heart failure, associated with Cheyne–Stokes respiration and possibly intermittent
hypercapnia, right heart failure (Fig.13.10), congenital heart disease with pulmonary hypertension, pneumonia complicating chronic pulmonary hypertension

ab
cd
ef
13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
245
Fig. 13.9 Transcranial Doppler (TCD) and left ventricular outow tract (LVOT) obstruction. A
31-year-old man with subarachnoid hemorrhage receiving intravenous milrinone develops LVOT
obstruction. (a, b) Apical four-chamber view showing a hyperdynamic heart and ow acceleration
in the LVOT using color Doppler. (c) Note the signicant pressure gradient (PG) of 253mmHg and
LVOT velocities of 7.95m/s using the apical ve-chamber view. (d) The associated TCD velocity
of the left middle cerebral artery (MCA) was 2.57 m/s (normal peak velocity 0.9–1.1 m/s).
Following a bolus of 500ml of crystalloid, (e) the LVOT PG drops to 72mmHg and (f) the left
MCA velocity decreases to 1.72 m/s. Examples like this one demonstrates that extra-cranial
pathology can have a profound impact on the left MCA pulsatility index measured by
TCD. (Abbreviations: PSV peak systolic velocity). (Reproduced and adapted by permission of
Taylor and Francis Group, LLC, a division of Informa plc. from Denault etal. [21])

246
ab
cd
A. Y. Denault et al.
Fig. 13.10 A 71-year-old comatose woman with severe right ventricular failure associated with
(a) increased resistance index (RI=0.77) on transcranial Doppler (TCD) of the middle cerebral
artery (MCA), (b) pulsatile TCD cerebral venous ow (CVF) of the petrosal sinus (arrow), (c)
pulsatile portal venous ow (PoVF) (arrow) and (d) elevated pulmonary artery pressure (Ppa)
associated with abnormal right ventricular pressure (Prv) and right atrial pressure (Pra) waveform
suggesting right ventricular dysfunction with signicant tricuspid regurgitation resulting in cerebral and portal venous congestion. The patient died post-operatively of multisystem organ failure.
(Abbreviations: EDV end-diastolic velocity, ETCO
femoral artery pressure, PSV peak systolic velocity). (Reproduced and adapted by permission of
Taylor and Francis Group, LLC, a division of Informa plc. from Denault etal. [21])
end-tidal carbon dioxide, HR heart rate, Pfa
2
(Fig.13.11), and severe aortic regurgitation. All these examples indicate that PI can
signicantly be affected by cardiac conditions and possibly also vascular conditions
such as arterial stiffness [17, 18].
TCD/TCCS can be used in the ICU for continuous monitoring of high-intensity
transient signals (HITS), which represent microemboli (gaseous or solid). HITS can
also be present in hypoxemic patients with a patent foramen ovale. This condition

ab
cd
13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
Fig. 13.11 A 75-year-old man admitted to the intensive care unit for pneumonia and hypercapnic
encephalopathy with right ventricular dysfunction from pulmonary hypertension. (a) Transcranial
Doppler (TCD) of the right middle cerebral artery (MCA) showed a (b) resistance index (RI) of
0.68. (c) The optic nerve sheath diameter was 6.2mm and (d) using a left subcostal view, a pleural
effusion was diagnosed. (Abbreviations: EDV end-diastolic velocity, PSV peak systolic velocity,
RI resistance index). (Reproduced and adapted by permission of Taylor and Francis Group, LLC,
a division of Informa plc. from Denault etal. [21])
247
can be present in up to 20% of the normal population [19, 20]. Intraoperatively,
HITS can be associated with right ventricular dysfunction as microemboli can also
migrate in the right coronary artery. In this situation, reduction in electroencephalographic activity and near-infrared spectroscopy signals can be observed.
13.6 Conclusion
In conclusion, TCD analysis and interpretation should always be performed with
2D ultrasound of the brain, optic nerve, and also careful examination of the extracranial organs that could be altered from cardiac dysfunction.

248
Algorithm
A. Y. Denault et al.
INTENSIVE CARE UNIT (ICU)
EMERGENCY DEPARTMENT (ED)
Clinical Status of the Patient
ABCD
Level of Consciousness (GCS)
Bilateral Pupillary Reactivity?
Hemodynamic Stability?
Oxygenation?
DIAGNOSIS
ACUTE NEUROLOGICAL INJURY
Multimodal Monitoring (MMM)
2D-ULTRASOUND (2D-US)
Low Frequency Probe (1-2 MHz)
Intracranial Approach Extracranial Approach
(A) Transtemporal Acoustic Bone Window Neck Insonation
[ Depth 14-16cm ⇒ See the opposite skull border]
(B) Transtemporal Acoustic Bone Window
[ Mesencephalic Plane / Dincephalic Plane / Ventricular Plane]
(C) Transtemporal Acoustic Bone Window
• Right / Left Middle Cerebral Artery (MCA)
2D-US Imaging
IDENTIFY (Bones)
• Contralateral Skull
• Foramen Lacerum
• Petrous Ridge
• Sphenoidal bone
2D-US Imaging
IDENTIFY (Brain Parenchyma) Normal Abnormal
• Mesencephalon
• Midline
• 3th Ventricle
• Lateral Ventricles
Color Doppler Imaging (blood flow)
[ Mesencephalic Plane ⇒ MCA]
IDENTIFY (Circle of Willis)
Increase MCA Pulsatility Index (> 1.2)
Position the TCD probe in the same 2D-US probe position
Transcranial Doppler (TCD)
Normal Distended
Normal
S > D
AR < 50% of S
Normal
Monomorphic
Consider
Intracranial
Hypertension
2D-US Imaging
IDENTIFY (Vascular structure)
• Internal Jugular Vein
Cardiac Function
2D-US Imaging
[ FOCUS Approach]
Hepatic Venous Flow
2D-US / Doppler Imaging
Portal Venous Flow
Doppler Imaging
Cardiogenic ≠ PI
of Venous Congestion
Abnormal
S < D
AR > 50% of S
Abnormal
Pulsatile > 50%
Consider
Our approach to using TCD in the presence of elevated PI is summarized in the algorithm.
Neglecting the extracranial information in interpreting TCD may lead to inappropriate interventions that would reduce the benet of this type of monitoring.
PI Pulsatility Index, AR atrial reversal hepatic venous ow velocity, D diastolic hepatic venous
ow velocity, S systolic hepatic venous ow velocity, ↑ Increase, MCA middle cerebral artery

13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
249
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A. Y. Denault et al.

Chapter 14
Neurosonology inICU: Transcranial
Color-Coded Duplex Sonography (TCCS)
Protocol
CamiloN.Rodríguez andDeborahPugin
Key Points
1. The transcranial color-coded duplex sonography (TCCS) is a technique that
enables a direct visualization of the basal cerebral arteries. The visualization is
possible through Doppler sonography and the blood ow velocities of the arteries which are color-coded. On the opposite, TCD allows only to record the arterial blood ow velocities without direct visualization. The identication of the
arteries is based on the depth of recording and ow direction.
2. A good knowledge of the anatomy of the intracranial and extracranial arteries is
requested to evaluate them in an efcient way with TCCS.
3. The Circle of Willis is incomplete in 40–65% of the cases.
4. In total, 10–20% of patients do not have an accessible transtemporal acoustic
window to insonate.
5. The insonation angle during the transcranial color-coded duplex sonography
(TCCS) study is very important. It is mandatory to keep it as low as possible
(<60°), for an optimal interpretation of the ow velocity in the cerebral arteries.
6. Transcranial color-coded duplex sonography (TCCS) is very useful to approach the
brain perfusion, but many elements should be taken into consideration to analyze
the results (anemia, fever, systemic blood pressure, angle of insonation, etc.) of
cerebral hemodynamics in many clinical contexts of critical patients. But remember
that we must contemplate that there are certain general limitations at the time of the
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
D. Pugin
Intensive Care Medicine and Neurology, FMH Chez Centre Qorpus. Clinique des Grangettes,
Geneva, Switzerland
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_14
251© Springer Nature Switzerland AG 2022

252
examination (acoustic windows, clinical interpretation of pulsatility index (PI), etc.)
and certain specic aspects that we should consider when we approach the patient
in a critical pathology determined with or without acute neurological injury.
C. N. Rodríguez and D. Pugin
14.1 Introduction
The insonation of intracranial blood vessels through the skull was rst reported by
Aaslid and colleagues in 1982 with transcranial Doppler (TCD). Transcranial
Doppler (TCD) is based on the use of low-frequency ultrasound probe through various anatomical windows (area of thin skull), allowing an exploration of the Doppler
signal of the basal cerebral arteries [1].
The TCD records the blood ow velocities of these arteries, and they are identied by the position of the probe, the depth of recording, and the ow direction.
Sometimes, the exact identication of the arteries may be challenging, especially in
anatomical variations.
The major limitations of the TCD are the lack of
1. Visualization of the insonated arteries.
2. Evaluation of the angle between the beam of insonation and the vessel, and the
potential misidentication of the artery.
Unlike the Transcranial Doppler (TCD), TCCS allows a direct visualization of
the basal cerebral arteries through the temporal window of the skull, a thorough
identication, and a potential correction of the angle is therefore possible.
TCCS is a non-invasive ultrasound that combines images of parenchymal structures (B-Mode) allowing the visualization of different brain structures through the
temporal window and the Doppler evaluation of basal cerebral arteries. The main
cerebral arteries of the Circle of Willis may be insonated. The blood ow velocities
may be recorded and are color-coded according to the direction of the ow (Doppler).
This helps to better identify the different basal cerebral arteries, and the direct visualization of the arteries may show arterial stenosis or kinking.
The scope of TCCS allows an evaluation of the parenchyma, midline shift, visualization of intra- or extracranial hematoma, monitoring of vasospasm, monitoring
of indirect signs of increased intracranial pressure, and diagnosis of cerebral circulatory arrest.
To analyze correctly the ow velocities and B-Mode (2D) images, special attention should be paid to possible anatomical variations [2–5].
14.2 TCCS: Anatomical Aspects
The objective of the study by transcranial Doppler (TCD) is the evaluation of blood
ow velocities in basal cerebral arteries, and transcranial color-coded duplex sonography (TCCS) includes also the evaluation of cerebral blood ow velocities in the

ACA(A2)
ACA(A2)
G.N. Rodriguez, 2019
14 Neurosonology in ICU: Transcranial Color-Coded Duplex Sonography (TCCS…
253
cerebral intracranial and extracranial arteries and the evaluation of extravascular
structures.
A basic knowledge of anatomy is mandatory to realize an effective study of these
parameters.
The intracranial and extracranial vascular and the parenchymal structures can be
accessed through the transcranial color-coded duplex sonography (TCCS).
Remember, 10–20% of patients do not have an accessible transtemporal acoustic
window to insonate.
14.3 Basal Cerebral Arteries: Circle ofWillis
The Circle of Willis is a vascular structure located in the brain base connecting two
arterial systems: the anterior system constituted by both Internal Carotid Arteries
and the posterior system, originating from the vertebro-basilar circulation [6]. From
the Circle of Willis, intracranial arteries can be individualized: Middle Cerebral
Artery (MCA), Anterior Cerebral Artery (ACA), Posterior communicating Artery
(PcomA), and Posterior Cerebral Artery (PCA) (Figs.14.1 and 14.2).
MCA(M1)
ACA(A1)
ICA
ICA
ACA(A1)
Fig. 14.1 Scheme: Circle of Willis and most common blood ow direction; ACA anterior cerebral
artery, MCA middle cerebral artery, PCA posterior cerebral artery, ICA internal carotid artery,
AComA anterior communicating Artery, PComA posterior communicating artery, M mesencephalon, (Arrows): points out the most common direction of ow
PComA
BAAComA
PComA
MCA(M1)
PCA(P1)
PCA(P1)
PCA(P2)
M
PCA(P2)
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