Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
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

11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
65. Kumar G, Shahripour RB, Harrigan MR.Vasospasm on transcranial Doppler is predictive of
delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: a systematic review and
meta-analysis. J Neurosurg. 2015:1–8.
66. Vora Y, Suarez-Almazor M, Steinke D, Martin M, Findlay J. Role of transcranial Doppler
monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage.
Neurosurgery. 1999;44(6):1237-47-8.
67. Lindegaard KF, Nornes H, Bakke SJ, Sorteberg W, Nakstad P. Cerebral vasospasm after
subarachnoid haemorrhage investigated by means of transcranial Doppler ultrasound. Acta
Neurochir Suppl (Wien). 1988;42:81–4.
68. Budohoski KP, Czosnyka M, Kirkpatrick PJ, Smielewski P, Steiner LA, Pickard JD.Clinical
relevance of cerebral autoregulation following subarachnoid haemorrhage. Nat Rev Neurol
Nature Publishing Group. 2013;9(3):152–63.
69. Budohoski KP, Czosnyka M, Smielewski P, Kasprowicz M, Helmy A, Bulters D, et al.
Impairment of cerebral autoregulation predicts delayed cerebral ischemia after subarachnoid
hemorrhage: a prospective observational study. Stroke. 2012;43(12):3230–7.
70. Budohoski KP, Czosnyka M, Kirkpatrick PJ, Reinhard M, Varsos GV, Kasprowicz M, etal.
Bilateral failure of cerebral autoregulation is related to unfavorable outcome after subarachnoid hemorrhage. Neurocrit Care. 2014;22(1):65–73.
71. Reinhard M, Roth M, Müller T, Czosnyka M, Timmer J, Hetzel A.Cerebral autoregulation in
carotid artery occlusive disease assessed from spontaneous blood pressure uctuations by the
correlation coefcient index. Stroke. 2003;34(9):2138–44.
72. Demchuk a M, Christou I, Wein TH, Felberg R a, Malkoff M, Grotta JC, et al. Accuracy
and criteria for localizing arterial occlusion with transcranial Doppler. J Neuroimaging.
2000;10(1):1–12.
73. Alexandrov AV, Burgin WS, Demchuk AM, El-Mitwalli A, Grotta JC.Speed of intracranial
clot lysis with intravenous tissue plasminogen activator therapy: sonographic classication and
short-term improvement. Circulation. 2001;103(24):2897–902.
74. Moppett IK, Mahajan RP.Transcranial Doppler ultrasonography in anaesthesia and intensive
care. Br J Anaesth Br J Anaesth. 2004;93(93):710–24.
75. Ducrocq X, Braun M, Debouverie M, Junges C, Hummer M, Vespignani H. Brain death
and transcranial Doppler: experience in 130 cases of brain dead patients. J Neurol Sci.
1998;160(1):41–6.
76. Adams RJ. TCD in sickle cell disease: an important and useful test. Pediatr Radiol.
2005;35:229–34.
77. Cabanes L, Mas JL, Cohen A, Amarenco P, Cabanes PA, Oubary P, etal. Atrial septal aneu-
rysm and patent foramen ovale as risk factors for cryptogenic stroke in patients less than 55
years of age: a study using transesophageal echocardiography. Stroke. 1993;24(12):1865–73.
78. Robba C, Bragazzi NL, Bertuccio A, Cardim D, Donnelly J, Sekhon M, etal. Effects of prone
position and positive end-expiratory pressure on noninvasive estimators of ICP: a pilot study.
J Neurosurg Anesthesiol [Internet]. 2016 Mar 18 [cited 2016 May 19].
79. Robba C, Cardim D, Donnelly J, Bertuccio A, Bacigaluppi S, Bragazzi N, etal. Effects of
pneumoperitoneum and Trendelenburg position on intracranial pressure assessed using different non-invasive methods. Br J Anaesth [Internet]. 2016;117(6):783–91. Available from: http://
bja.oxfordjournals.org/lookup/doi/10.1093/bja/aew356.
80. Joshi B, Ono M, Brown C, Brady K, Easley RB, Yenokyan G, etal. Predicting the limits of
cerebral autoregulation during cardiopulmonary bypass. Anesth Analg. 2012;114(3):503–10.
81. Aggarwal S, Brooks DM, Kang Y, Linden PK, Patzer JF.Noninvasive monitoring of cerebral
perfusion pressure in patients with acute liver failure using transcranial doppler ultrasonography. Liver Transpl. 2008;14:1048–57.
82. Williams K, Galerneau F. Maternal transcranial Doppler in pre-eclampsia and eclampsia.
Ultrasound Obstet Gynecol. 2003;21:507–13.
83. Pierrakos C, Antoine A, Velissaris D, Michaux I, Bulpa P, Evrard P, etal. Transcranial doppler
assessment of cerebral perfusion in critically ill septic patients: a pilot study. Ann Intensive
Care. 2013;3:28.
213

Chapter 12
Neurosonology intheICU: Transcranial
Doppler (TCD) Protocol
CorinaPuppo
Key Points
1. TCD is a non-invasive ultrasound technique at the patient’s bedside, measuring
cerebral blood ow velocities (CBFV) of basal cerebral arteries.
2. It measures ow velocities and estimates changes in cerebral blood ow but does
not measure cerebral blood ow in absolute values.
3. It uses areas or natural orices of the skull as acoustic windows to insonate intra-
cerebral hemodynamic changes.
4. The most used acoustic window to evaluate global cerebral hemodynamics is the
transtemporal window through the middle cerebral artery (MCA) insonation.
5. TCD, through an envelope wave, determines the three ow velocities and the
derived hemodynamic indexes: PSV, EDV, MFV, PI, RI, and LR.
6. In normal conditions, the intracranial blood ow circulates only in one direction,
accelerating during systole and decelerating during diastole, without ever stopping or reversing its direction.
7. The cerebral arteries’ blood ow is less pulsatile than in the rest of the arteries of
the body, given the important collateral circulation of the system (circle of
Willis) that maintains a low resistance pattern.
8. It is essential to repeat the TCD examinations in order to measure the hemody-
namic changes in real time and to assess the trends of the parameters evaluated
and/or the response to an established therapeutic trial.
C. Puppo (*)
Intensive Care Unit, Clinics Hospital, Universidad de la Republica School of Medicine,
Montevideo, Uruguay
e-mail: coripuppo@gmail.com
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_12
215© Springer Nature Switzerland AG 2022

216
C. Puppo
12.1 Introduction
Transcranial Doppler (TCD) is a non-invasive ultrasound method that measures
cerebral blood ow velocities (CBFVs) in the basal cerebral arteries (circle of
Willis), without transferring the patient out of the ICU.
It measures the circulatory velocity of the blood. It does not measure cerebral
blood ow (C BF). However, under certain conditions, changes in CBFV are
proportional to changes in CBF.
In intensive care unit (ICU), it can be used (a) uniquely, (b) repeatedly, observing
the trend of changes in CBFVs and pulsatility, (c) continuously alone, or (d) combined with other variables, for example, arterial blood pressure and intracranial
pressure (ICP), constituting multimodal neuromonitoring.
12.2 TCD: Spectral Wave
The screen of the TCD equipment shows the circulation velocity in time. The circulatory velocity of a complete arterial pulse cycle is called sonogram.
At each instant the blood particle velocities can be seen. Since the ultrasound is
reected by multiple moving blood particles in a certain segment of the artery (the
depth and size of this segment are chosen by the operator), a “spectrum” of velocities is generated [1]. This spectrum is different if the ow is laminar or turbulent
(Fig.12.1). In arterial segments without stenosis or bifurcations, the ow is laminar.
By taking only the maximum velocities at each point in this spectrum, the TCD
equipment outlines an “envelope” wave. The envelope wave, therefore, shows the
values of the particles moving at the highest velocity within the arterial vessel. The
values of the envelope wave thus generated are those analyzed and displayed by the
ultrasound equipment. In the graph of the envelope wave of each arterial pulse, three
variables are dened: peak systolic velocity (PSV), mean ow velocity (MFV), and
end-diastolic velocity (EDV) (Fig.12.2).
Spectrum and envelope wave characteristics: Under normal conditions, cerebral
blood ow moves in a single direction within the vessel, slows down in the diastole,
and accelerates when a new blood pulse arrives. It does not stop or reverse its direction. The nal diastolic rate is the lowest of each pulse, greater than zero.
By convention, the ow toward the transducer is given a positive value and the
ow away from it is given a negative value. In the arterial bifurcations, a bidirectional ow is seen.
A relatively constant diameter of the studied vessel is assumed, and thus the
changes of CBFV are directly proportional to the changes of CBF. For this, the
transducer must remain xed without changes in its angulation.
TCD measures CBFV and estimates changes in CBF but does not measure CBF
in absolute values.

12 Neurosonology intheICU: Transcranial Doppler (TCD) Protocol
217
Fig. 12.1 Difference between laminar ow spectrum (upper) and turbulent ow spectrum (lower).
In the rst one most of the circulating particles are of high velocity and therefore form a thick line
near the maximum velocity in each instant; the different colors translate more or less particles
concentration. A lower triangle remains where there is a spectral window, indicated by a red circle.
In turbulent ow, which can be seen in bifurcations, or in severe stenoses, the angles of intonation
are formed between the direction of the particles rotating in turbulent form and the direction of the
ultrasound emitted by the transducer are large, so they look as low velocities. The vascular murmur
is marked with a circle, evidencing the turbulence, which has a special sound, like that of a
¨seagull's song¨, superimposed on the normal sound
12.3 TCD: Identication ofVessels
Transcranial Doppler identies the different arteries according to
1. Characteristics of the Doppler signal.
2. Topography of the Doppler signal (acoustic window, direction of the ultrasound
beam, and depth).
3. Hemodynamic response to maneuvers.
1. Characteristics of the Doppler Signal:

218
Fig. 12.2 On the left you can see a Doppler spectrum velocities (sonogram) in the rst four cycles.
In the following cycles the spectrum has been erased and only the envelope wave is seen. The
arrows show the point where the PSV, the EDV and the MFV.You can also see the graphical calculation of the average velocity which in this case coincides with the value calculated by the equipment since the envelope wave correctly follows the maximum values of the Doppler spectrum. The
average velocity calculated graphically is the one that marks a horizontal line that divides the
envelope wave in two parts of similar area as seen in the gure
C. Puppo
By convention, if the ow is directed toward the transducer, it is shown as
positive spectrum wave; if it is directed in the opposite direction, it is shown as
negative spectrum wave. If a bifurcation is insonated, it is displayed as a bidirectional spectrum wave.
2. Topography:
Different acoustic windows allow to insonate different arteries of the circle of
Willis. From each acoustic window, the direction of the ultrasound beam from
transducer allows the identication of the different basal cerebral arteries, as
well as the depth at which each of them is located.
3. M-Mode: Power Motion Mode Doppler
Transcranial Doppler emits pulsed ultrasound. This means that it obtains
information only from a small volume of the intracranial space whose depth is
permanently dened throughout the examination. This small volume is called
the “sample volume.” The operator must, therefore, know which vessel he is
going to look for, through which window, and at what depth he is going to
look for it.
The operator must also know the insonation angle that he must give to the
transducer. This generated the concept that the technique is operator dependent.
The introduction of the M-mode (PMD) facilitates the examination, even for
inexperienced operators, since it makes it possible to simultaneously see the

12 Neurosonology intheICU: Transcranial Doppler (TCD) Protocol
219
intensity and direction of the ow along 6cm or more of the intracranial space
that the ultrasound beams cross.
When using the PMD, the screen of TCD machine is divided into two sectors:
1. In the main sector (generally upper), you can see the sonogram of the vessel
under examination (at a predetermined depth), that is, the full characteristics
(spectrum, envelope wave, PSV, EDV, MFV, PI) of the ow velocity at the chosen point of the artery under study.
2. In the M-mode sector screen (generally lower), the different ows that appear
along the path (3–6cm or more, congurable by the examiner) of the ultrasound
beam in that direction are shown simultaneously (Fig.12.3). This sector graphs
the ows along the beam path, showing in the different depths, if there is any
ow or not, and in case there is, in red or blue color if it is directed toward or
moves away from the transducer, respectively.
Over time these segments are seen as red or blue horizontal bands crossing
the screen. The display allows to choose any point of interest in this sector, so
that the main screen shows the sonogram of the ow at the chosen point and the
characteristics of both the spectrum and its envelope waves (PSV, EDV, MFV,
PI, etc.).
Normal values of CBFVs vary according to (a) insonated vessel and (b) physiological variables. CBFV in the cerebral arteries varies with age, where they are
greatest in childhood and decrease with age. Normal values of CBFV in healthy
adults for three age groups are shown in Table12.1.
To have a global idea of the values in mind, the following scheme is useful: average velocity in cm/s (±10): ACM 60, ACA 50, ACP 40, and posterior circulation
sector 35.
Other important physiological variables that inuence the CBFV in the cerebral
arteries are blood viscosity (one of whose main determinants is hematocrit), temperature, PaCO2, and heart rate.
The trends of values are more important than a single CBFV value.
12.4 TCD: Clinical Utility
TCD is known as the “Stethoscope of the brain.” The use of the TCD is directed to the
detection and follow-up of cerebral hemodynamics alterations in the patients with neurological injury: acute ischemic stroke (AIS), subarachnoid hemorrhages (SAH), intracerebral hematoma, traumatic brain injury (TBI), and other pathologies such as central
nervous system (CNS) infections, cerebral vasculitis, etc. It is especially useful in neurocritically ill patients whose state of consciousness is altered (secondary to different
injuries and/or sedation/analgesia/neuromuscular block requirements), and complete
neurological examination is not possible. Unlike the TCCS, it does not show anatomical images (B-mode) but only the blood ow velocities in the basal cerebral arteries.

220
C. Puppo
Fig. 12.3 The M mode or "Power Mode". The two panels that appear on the computer screen
when using this mode are shown. The insonation is through transtemporal acoustic window. In the
upper panel you can see the Doppler spectrum, where equipment has delineated the spectral
Doppler envelope. In this case it is a laminar blood ow. The lower panel shows the M-mode,
which displays all the ows in the path of the ultrasonic beam, their depths in relation to the surface
of the transducer and their directions (towards the transducer in red and away from it in blue). The
scale on the left shows at what depth, in mm, these ows are seen. Between 40 and 60mm there is
a ow that approaches the transducer, which corresponds to the middle cerebral artery (MCA). In
this red band there is a dotted line, which shows the depth at which the artery is being observed, in
this case about 48 mm; at this depth corresponds the spectrum seen in the upper panel. Any point
can be chosen, so that the volume of the sample will inspect and show on the upper display the
spectrum and the corresponding envelope with its PSV, MFV, EDV and PI.Between 70 and 75mm
a ow is seen that moves away, corresponding to the anterior cerebral artery (ACA). The carotid
bifurcation is not clearly seen in this image, but at about 62mm a blue band can be seen at times,
so it can be thought that this is the bifurcation and that by slightly angulating the transducer it could
be clearly found
The alterations of cerebral hemodynamics, monitored by TCD, are generally
secondary to
1. Increase of ICP.
2. Vasospasm.
3. Hyperemia.

12 Neurosonology intheICU: Transcranial Doppler (TCD) Protocol
Table 12.1 Normal values of CBFVs in adults [32]
Artery
(Depth / mm)
MCA
(50 mm)
ACA
(70 mm)
PCA
(60 mm)
VA / BA
(75 mm)
MCA Middle cerebral artery, ACA Anterior cerebral artery, PCA Posterior cerebral artery, VA
Vertebral artery, BA Basilar artery
PSV
(cm/s)
95±14 46±7 58±8 <40
91±17 44±10 58±12 40–60
78± 15 32±9 45±11 >60
76±17 36±9 47±14 <40
86± 20 41±7 53±11 40–60
73± 20 34±9 45±14 >60
53±11 26±7 34±8 <40
60±21 29±8 37±10 40–60
51±12 22±7 30±9 >60
56±8 27±5 35±8 <40
60±17 29±8 36±12 40–60
51±19 21±9 31±12 >60
EDV
(cm/s)
MFV
(cm/s)
Age
(yr.)
221
4. Alterations in cerebrovascular reactivity.
5. Coexistence of two or more of the previously mentioned points.
When the interest is to assess whether there are global alterations of the cerebral
hemodynamics, we must insonate the anterior circulation; middle cerebral artery
(MCA), anterior cerebral artery (ACA), and the posterior circulation; and basilar
artery (BA) and vertebral arteries (VA). When the interest of the study is to detect a
segmental alteration (vasospasm), the assessment must be global initially and then
detailed, along each vessel.
12.5 TCD: Frequent Uses inIntensive Care Unit
1. Detect and estimate changes of intracranial pressure (ICP) [2–11].
2. Diagnose cerebral circulatory arrest [12–18], collaborating in the diagnosis of
brain death.
3. Diagnosis and monitoring of cerebral artery vasospasm in the clinical evolution
of SAH [19, 20], TBI [21, 22], and CNS infections [23–27].
4. In AIS: Monitor arterial recanalization when thrombolytics are performed [28].
To increase the action of these drugs (sonothrombolysis) [29, 30]. To evaluate
the presence of microembolism signals and the presence of right–left shunt in
cryptogenic AIS.
5. To evaluate the state of cerebral autoregulation (CA) [31], by means of inte-
grated neuromonitoring through mean ow reactive index (Mx).
6. Cerebral vasomotor reactivity to CO
critical closing pressure.
. Time constant of cerebral circulation and
2

222
C. Puppo
12.6 TCD: Technique
12.6.1 Position ofthePatient andExaminer
Frequently, the neurocritical patient is in dorsal decubitus, with the head elevated
about 30°, aligned with the trunk. It is not necessary to modify the patient’s position. The examiner can be placed at the patient’s bedside, but given the large number
of catheters and devices that are frequently found around critical patients, it is usually placed at the side of the bed.
The different vessels are insonated through the different acoustic windows
(Fig. 12.4). Acoustic windows are areas of the skull that are more permeable to
ultrasound beams, because they are thinner or because they are natural orices. The
transducer should be placed by exerting moderate pressure (except when using
transorbital window), with abundant gel to ensure proper coupling between the
transducer and the skin. It must be known in which direction the ultrasound beam
will be emitted, and at what depth each artery will be searched. In this way, the
depth will be xed in advance.
The exploration will begin more supercially and will be deepened by a few millimeters, optimizing the angle of insonation at each point to nd the spectrum whose
blood ow velocity is maximum, which is the one that will coincide with the minimum angle of insonation (angle between the ultrasonic beam and the direction of
blood ow at the point of insonation).
12.6.2 Transtemporal Acoustic Window
TCD assessment begins through the transtemporal acoustic window to insonate
middle cerebral artery (MCA). The transtemporal acoustic window extends above
the zygomatic arch, in front of the swallow, and behind the lateral corner of the
homolateral eye. It has a projection that can be anterior, medial, and posterior. Each
patient is different, so the best approach should always be sought in each case.
12.6.2.1 Anterior Circulation
Middle Cerebral Artery (MCA)
1. Acoustic Window: Transtemporal
2. Depth: (M1 Segment)
The depth should be between 45 and 60–65 mm and followed along its
entire length.
3. Acoustic Window: Transtemporal
4. Depth: (M2 Segment)

ab
cd
12 Neurosonology intheICU: Transcranial Doppler (TCD) Protocol
223
Fig. 12.4 The circle of Willis and their relationships to the different acoustic windows. In (a) it is
shown the whole circle of Willis, its main branches and the vessels that form it, the transducer in
transtemporal acoustic window and the different intonation angles that must be given to it (in this
plane) to nd the lowest angle of insonation with the MCA and. In (b) the transoccipital acoustic
window and its relationship with the blood ow in the posterior circulation can be observed. In (c)
the anterior sector is seen in a coronal view and, in (d) the transorbital acoustic window and its
relationship with the vessels of the carotid siphon and OA is observed in a sagittal section
In certain cases, it is important to insonate more supercially, from 45mm to
30mm (e.g., distal vasospasm).
In all cases, the transducer will be slightly rotated to apical (about 10°), caudal
(about 10°), occipital, and frontal direction [7], independent of the sector of the
transtemporal window that the operator is located to record Doppler signals.
As the ow of the MCA is toward the transducer, it will be seen as a positive
sonogram.
At 65mm depth of insonation is the carotid bifurcation, where the MCA and the
anterior cerebral artery (ACA) originate. The carotid bifurcation is insonated as a
bidirectional blood ow, with a simultaneous positive and negative sonogram.
Соседние файлы в папке Библиотека им академика М.И. Перельмана
