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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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

234
A. Y. Denault et al.
2. Two-dimensional (2D) ultrasound and TCCS can facilitate placement of a con-
tinuous TCD monitoring system.
3. 2D ultrasound and Doppler (TCCS) can also be used in order to optimize TCD
acquisition and improve its interpretation by differentiating between an intracranial and an extracranial source of an abnormal TCD signal.
4. 2D ultrasound and Doppler (TCCS) can be used to image intra- and extracranial
structures which can be the source of neurological disorders.
13.1 Introduction
Transcranial Doppler (TCD) ultrasound (US) is a simple, non-invasive, relatively
inexpensive bedside tool that can provide real-time dynamic information regarding cerebral blood ow velocity (CBFV) in the proximal cerebral blood vessels.
Since its rst clinical application in 1982 [1], the use of TCD has expanded rapidly over the past two decades. The portability and non-invasive nature of TCD
allow both assessments during emergencies and continuous or serial monitoring
in the intensive care unit (ICU). The clinical applications of TCD in the ICU are
summarized in Table13.1. TCD is commonly used in neuro-critical care units,
Table 13.1 Applications of transcranial Doppler (TCD/TCCS) in the operating room and the
intensive care unit
1. Neuro-critical care
(a) Cerebral vasospasm screening and monitoring to assess progression and treatment effect
(angioplasty or medical treatment) after aneurysmal subarachnoid hemorrhage
(b) Non-invasive intracranial pressure (ICP) screening and monitoring, combined with optic
nerve sheath diameter, in the absence of invasive ICP monitoring (fulminant hepatic
failure, etc.)
(c) Assessment of the degree of hyperemia after arteriovenous malformation resection,
carotid endarterectomy, carotid surgical or endovascular angioplasty and in patients with
malignant hypertension
(d) Assessment of cerebral circulatory arrest in suspected brain death
2. Stroke Unit
(a) Diagnosis of proximal arterial occlusion in acute ischemic stroke
(b) Assessment of arterial patency after thrombolytic treatment
(c) Diagnosis of hyperemia after conversion of acute ischemic to hemorrhagic stroke
3. Various
(a) Assessment of cerebral autoregulation and cerebrovascular carbon dioxide reactivity
(b) Diagnosis of intracranial artery stenosis
(c) Guiding chronic red cell transfusion therapy in patients with sickle cell disease who are at
risk of developing stroke
(d) Intraoperative monitoring during carotid endarterectomy and procedures at risk of
causing systemic emboli and hypoperfusion
(e) Detection of cardiac or pulmonary right to left shunt (e.g. patent foramen ovale)
Adapted with permission of Taylor and Francis Group, LLC, a division of Informa plc. from
Denault etal. [21]
Abbreviations: TCD transcranial Doppler

13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
acute stroke units, operating rooms, ICUs, and emergency departments. It can
even be useful in an outpatient setting to assess the hemodynamic changes associated with stenosis of major cerebral arteries or to determine the risk of stroke in
patients with sickle cell disease. For the experienced vascular neurologist, neurointensivist, and neuro- anesthesiologist, the small portable TCD device serves as a
“stethoscope for the brain” [2]. The addition of two-dimensional (2D) US to a
standardized TCD assessment allows optimization of TCD acquisition and
improves its interpretation by differentiating an intracranial from an extracranial
source of an abnormal TCD signal. Finally, 2D US and Doppler can be used to
image intracranial as well as extracranial structures, which can be the source of
neurological disorders.
235
13.2 Acoustic Windows
In order to interrogate the brain, it is essential to obtain an acoustic window through
the skull. Normally, US waves undergo gradual loss of intensity as they move
through different body structures. The degree of attenuation is directly proportional
to the attenuation coefcient of the medium and to the emitted US frequency. Since
bone has a relatively high attenuation coefcient, it is difcult to measure CBFV
using a conventional 5–10 MHz Doppler probe. The use of a lower frequency
(1–2MHz) probe is required. TCD examinations are commonly performed through
four acoustic windows where the bone is relatively thin or absent. However, in the
ICU, for monitoring purposes, we typically concentrate on the temporal window.
The middle cerebral artery, anterior cerebral artery, posterior cerebral artery, and
terminal internal carotid artery can be examined (Fig. 13.1) through the transtemporal window.
13.3 2D-Guided TCD Monitoring
In order to examine the brain through the temporal window, the depth has to be
adjusted to at least twice the distance from the midline cerebral falx which is typically at 8cm. The skull is formed by two layers of compact bone separated by a
porous layer called diploë that allows US wave propagation by creating an acoustic
interface [3]. However, in up to 38% of patients, Doppler signals cannot be acquired
because of an inadequate or narrow temporal acoustic window [4]. Blind placement
of a TCD probe in these patients can be time-consuming and may ultimately result
in an inadequate signal. The use of 2D cranial ultrasonography can potentially facilitate localization of the temporal acoustic window prior to TCD probe placement.
The most commonly used planes are the mesencephalic plane, the diencephalic
plane, and the diencephalic-ventricular plane which includes the lateral ventricles

236
MCA
ag
b
c
d
e
f
A. Y. Denault et al.
gate depth 4.5 - 5.5 cm
ACA A2
MCA/ACA befurcation
gate depth 5.5 - 6.5 cm
ACA
gate depth 6.0 - 8.0 cm
TICA
gate depth 6.0 - 7.0 cm
PCA (pre communicating)
gate depth > 5.5 cm
PCA (post communicating)
gate depth > 6.5 cm
ACA A1
MCA
A
PcomA PcomA
F
PCA2 PCA2
C
D
B
PCA1 PCA1
Fig. 13.1 Transcranial Doppler signals. Probe position in the temporal window and normal transcranial Doppler (TCD) signals are shown for the (a) middle cerebral artery (MCA), (b) bifurcation of the MCA and anterior cerebral artery (ACA), (c) ACA, (d) terminal internal carotid artery
(TICA), (e) pre-communicating posterior cerebral artery (PCA) and (f) post-communicating PCA
(PcomA). (g) Corresponding position in the circle of Willis. (Abbreviations: AcomA anterior communicating artery, BA basilar artery). (Reproduced and adapted by permission of Taylor and
Francis Group, LLC, a division of Informa plc. from Denault etal. [21])
AcomA
TICA
MCA/ACA
befurcation
E
BA
ACA A2
C
D
E
ACA A1
B
MCA
A
F
(Fig. 13.2) [5]. The probe is placed over the area just above the zygomatic arch
along the orbitomeatal line which extends from the lateral canthus of the eye to the
midpoint of the external auditory meatus. The acoustic window can be located in the
anterior part of the temporal bone, close to the vertical portion of the zygomatic
bone, or, more frequently, posterior and close to the tragus of the ear.
Any transthoracic or hand-held low-frequency transducer probe (1–2MHz) can
be used. In patients with prior craniectomy (Fig.13.3b), visualization of cerebral
anatomy and TCD signals are easily obtained (Fig.13.3b–d). The gain and depth
(14 to 16cm) are adjusted to localize the bony structures (Fig.13.4). The contralateral cranial bone is rst located in the far eld. In the mid-eld, the petrous ridge
can be identied posteriorly and sphenoid wing anteriorly. The carotid siphon and
foramen lacerum can be localized anteriorly. The cerebral peduncle, third ventricle,
and the cerebral falx can be localized in the middle eld with the mesencephalic

ab
13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
Mesencephalic view
237
c
Fig. 13.2 Axial trans-temporal brain computed tomography (a) and ultrasound at 3 different levels. (b) Upper brainstem or mesencephalic view at the level of the zygomatic arch, (c) diencephalic
view at the level of the third ventricle obtained by tilting the probe 10
ventricular view obtained by tilting the probe another 10
can be seen. (Reproduced and adapted by permission of Taylor and Francis Group, LLC, a division
d
Diencephalic-ventricular viewDiencephalic view
o
o
upward. In this view, the lateral ventricle
upward and (d) diencephalic-
brainstem appearing as a ¨buttery shape¨ surrounded by the echogenic basal cisterns in the axial plane, parallel to the orbitomeatal line [6].
Doppler imaging (scale between 20 and 100cm/s) allows identication of the
major vascular structures. Depth and direction of ow are the main characteristics
of the Doppler signal that help to differentiate the various vessels [7]. Identication
of the vascular structures usually takes less than one minute. TCD monitoring
probes are then positioned, adjusted, and stabilized with the other cerebral monitoring modalities. The above TCD monitoring technique has been used at our institution as part of a multimodal neurologic monitoring strategy since 2015. We recently
reported that 95 patients out of 100 had at least a unilateral adequate temporal
acoustic window available for TCD monitoring during cardiac surgery. An adequate
bilateral window was found in 70 patients. In ve patients, neither right nor left
temporal acoustic window was present and TCD could not be used [8]. The use of

238
ab
c d
A. Y. Denault et al.
Fig. 13.3 (a) Normal position of hand-held ultrasound on the temporal region. (b) Patient after
right-sided craniectomy for cerebral edema is shown. (c) 2D cerebral ultrasound image with color
Doppler (Nyquist 13cm/s) that shows part of the circle of Willis. Note the buttery aspect of the
midbrain. (d) Transcranial Doppler investigation of the right middle cerebral artery (RMCA)
velocity. (Reproduced by permission of Taylor and Francis Group, LLC, a division of Informa plc.
from Denault etal. [21])
2D cranial US can rapidly facilitate TCD monitoring in most patients despite the
high reported failure rates in TCD monitoring [4]. Table 13.2 summarizes the
approach used for obtaining continuous TCD monitoring from the temporal acoustic window. Transcranial Color-Coded Duplex Sonography (TCCS) can also help
identify the cerebral vascular anatomy and allow proper angle correction when
assessing ow velocities [9].
13.4 Applications ofTCD Monitoring intheICU
We use TCD monitoring as part of multimodal monitoring mostly in the cardiac
operating room but also in the cardiothoracic, general, and neuro ICU.The following signals will be displayed:

13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
239
a
b
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Fig. 13.4 Temporal windows. (a, b) Using 2D imaging, anatomic reference points shown with
these cut portions of the skull are the petrous bone, foramen lacerum, sphenoid wing and the opposite cranial wall (arrows). (c) Color Doppler (Nyquist 27cm/s) showing blood ow in the petrous
bone (arrows). The sphenoid wing is shown (triangles). (d) The display depth is initially adjusted
in order to see the contralateral skull at the mesencephalic level. (Abbreviations: ACA anterior
cerebral artery, MCA middle cerebral artery, PCA posterior cerebral artery). (Reproduced by permission of Taylor and Francis Group, LLC, a division of Informa plc. from Denault etal. [21])
1. The peak systolic ow velocity (PSV)
2. The end-diastolic ow velocity (EDV)
3. The mean ow velocity (MFV)
4. The pulsatility index (PI)
5. The resistance index (RI)
US machines with automatic or manual spectral waveform tracing calculate
MFV as the area under the traced curve.
• Mean ow velocity (MFV)=(PSV+(2xEDV))/3 or (PSV–EDV)/3+EDV
• Pulsatility Index (PI)=(PSV–EDV)/MFV (normal 0.8–1.2)
• Resistance Index (RI)=(PSV–EDV)/PSV (normal 0.6±0.1)
Velocity signals will be signicantly altered in the presence of increased intracranial pressure (ICP). However, there are several other roles of cranial and

240
Table 13.2 General procedural steps in echo-guided transcranial Doppler monitoring through
temporal window
1. Probe selection: select a low frequency probe (1–2MHz) and the transcranial prole
2. Patient: Supine position
3. Position the ultrasound machine so that the ultrasound images and the chosen site for vascular
investigation will be in the same visual eld
4. Position of the operator: head of the bed while stabilizing the hand using a pillow
5. Preparation: adjust gain, depth (14–16cm for contralateral skull bone and 5–6cm for MCA),
color scale, M-mode and pulsed-wave Doppler. Use a 10–15mm sample volume initially,
then adjust
6. Identify with 2D US the petrous ridge posteriorly, carotid canal (C2-C3 segments), foramen
lacerum, cerebral falx, sphenoid wing anteriorly, cerebral peduncle and the contralateral
cranial bone (Fig.13.1). Use color Doppler (scale 25cm/s) to identify the vessels in the
following order: bidirectional « buttery » TICA signal (C7 segment) in the foramen lacerum,
MCA, ACA, ACoA, then move back to TICA and nd the PCoA then the PCA, proximal (P1
segment) and distal (P2 segment) portion around the cerebral peduncle
7. Position the TCD: Position in the acoustic bone window into the same probe position
8. Report velocities and refer to normal values adjusted by age
Adapted with permission of Taylor and Francis Group, LLC, a division of Informa plc. from
Denault etal. [21]
Abbreviations: 2D two-dimensional, ACA anterior cerebral artery, ACoA anterior communicating
artery, C carotid segments (C2,petrous segment; C3, lacerum segment; C7, communicating or
terminal (t) segment), MCA middle cerebral artery, PCA posterior cerebral artery, PCoA posterior
communicating artery, TICA terminal internal carotid artery, US ultrasound
A. Y. Denault et al.
extracranial 2D US.In the presence of signs of increased ICP, 2D US of the brain
can be used to diagnose dilated ventricles in patients with previous craniotomy
(Fig.13.5), midline shift (Fig.13.6), and regional increase in ICP (Fig.13.7), and
facilitate the monitoring of vasospasm versus hyperemia through direct visualization of the circle of Willis (Fig.13.8). In addition, examination of the optic nerve
sheath diameter (ONSD) is another method of evaluating increased ICP.For adults,
normal values taken at 3mm of the optic disk are 5.4±0.6mm, and abnormal values range between 6 and 7mm [5]. As mentioned by Harrer etal., overlaps between
normal and pathological values are possible given the nature of the dynamic process
[5]. The diagnosis of papilledema can be easily performed; however, the ONSD will
change more rapidly than the appearance or disappearance of papilledema [5]. In
patients with increased ICP, both ONSD and CBF velocities obtained by TCD will
be abnormal. However, ONSD seems to be more sensitive and specic than CBF
velocities obtained by TCD in detecting elevated ICP [10–15].
Furthermore, a recent study by Chelly etal. demonstrated that ONSD on the rst
day after cardiac arrest was signicantly associated with in-hospital mortality (OR
6.3; 95%CI [1.05–40] per 1mm of ONSD above 5.5mm; p=0.03) and correlated
with brain edema measured using computed tomography [16].

ab
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13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
241
Fig. 13.5 (a) Transcranial sonography (TCS) using a hand-held pocket ultrasound device (GE
Vingmed Ultrasound AS, Horten, Norway) on a patient with craniectomy. (b) Prior to external
ventricular drain (EVD) clamping, TCS showed a measurement of the 3rd ventricle at approximately 1.16cm. (c) On the third day, TCS showed a dilated 3rd ventricle measuring 1.37cm. (d)
Computed tomography scan showed a dilated 3rd ventricle measuring 13.1mm. (e) One day after
reopening the EVD, the size of the 3rd ventricle decreased to 0.99cm as measured by TCS. (f) The
following day, it went down to 0.69cm. (Abbreviations: IM mechanical index, IT thermal index).
(With permission of Najjar etal. [22])

242
ef
ab
Fig. 13.5 (continued)
A. Y. Denault et al.
Fig. 13.6 Cerebral hematoma. (a) Transcranial 2D diencephalic-ventricular image of an intraparenchymal hematoma (dotted line) with a (b) persistent left midline shift (arrow). (c) Initial computed tomography upon presentation with midline shift (arrow) and (d) magnetic resonance
imaging following craniectomy taken at different axial planes are presented for comparison.
(Reproduced by permission of Taylor and Francis Group, LLC, a division of Informa plc. from
Denault etal. [21])

cd
ab
cd
13 Transcranial Doppler (TCD/TCCS) Monitoring in the Intensive Care Unit…
Fig. 13.6 (continued)
243
Fig. 13.7 A 47-year-old man with (a) grade V subarachnoid hemorrhage, bilateral intra-cranial
pressure (ICP) monitoring and left-sided craniectomy shown on computed tomography. (b)
Mesencephalic brain ultrasound view with color Doppler showing parts of the circle of Willis.
Note the increased velocity of the left middle cerebral artery (LMCA), greater than the 123cm/s
Nyquist limit (normal peak velocity 90–110cm/s). (c, d) Transcranial Doppler velocities of both
the LMCA and right middle cerebral artery (RMCA). The latter was obtained through a normal
right temporal window. The peak systolic velocity (PSV), end-diastolic velocity (EDV), resistance
index (RI) and ICP were higher in the LMCA compared to the RMCA. (Abbreviations: RPCA
right posterior cerebral artery). (Reproduced and adapted by permission of Taylor and Francis
Group, LLC, a division of Informa plc. from Denault etal. [21])
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