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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5813_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Acknowledgements
- •Contents
- •List of Videos
- •2.1 Introduction
- •2.2 Vascular Anatomy
- •1.1 Introduction
- •1.3 Transcranial Colour-Coded Duplex Ultrasonography
- •1.4 Final Remarks
- •References
- •2.3.1 Anatomic Landmarks
- •2.3.2 Clinical Implications
- •2.3.2.1 Intracranial Hemorrhage
- •2.3.2.2 Epidural/Subdural Hematomas
- •2.3.2.3 Brain Midline Shift
- •2.3.2.4 Hydrocephalus
- •2.3.2.5 Stroke
- •2.4 Conclusion
- •References
- •3.1 Introduction
- •3.2 Anatomy Abnormalities
- •3.4 Setup
- •3.5 The MOTOr Approach
- •3.5.1 Mandibular
- •3.5.2 Occipital
- •3.5.3 Transtemporal
- •3.5.4 Orbital
- •3.5.4.1 Optic Nerve Sheath
- •3.6 Troubleshooting
- •3.7 Summary
- •References
- •4: Optic Nerve Sheath Diameter
- •4.1 Introduction
- •4.2 Anatomical Background
- •4.3.1 Technology
- •4.3.2 Methods
- •4.3.3 Normal Views
- •4.4.1 Limits
- •4.4.2 Safety
- •4.6 Conclusion
- •References
- •5.1 Introduction
- •5.2 Technical Considerations
- •5.2.3 Ultrasound-Related Artifacts
- •5.3 Anatomical Considerations
- •5.4 Clinical Considerations
- •5.4.4 Cerebral Circulatory Arrest
- •5.5 Summary
- •References
- •6.1 Introduction
- •6.3 Training Strategies
- •6.6 Competence
- •References
- •7.1 Introduction
- •7.2 Flow Velocity
- •7.3 Pulsatility Index
- •7.4 Critical Closing Pressure
- •7.5 Autoregulation
- •7.5.1 Static Autoregulation
- •7.5.2 Dynamic Autoregulation
- •References
- •8.1 Introduction
- •8.4.3.2 Data Mining
- •8.7 Final Remarks
- •References
- •9.1 Introduction
- •9.2 TCD: Velocity or Flow?
- •9.3.2 Cerebral Vasospasm
- •9.3.3 Hyperperfusion
- •9.3.4 Hypoperfusion
- •9.3.5 Brain Death
- •9.4.1 Acute Stroke
- •9.4.2 Severe Traumatic Brain Injury
- •9.4.4 Acute Liver Failure
- •9.5 Conclusion
- •References
- •10.1 Introduction
- •References
- •11: Sepsis, Liver Failure
- •11.1 Introduction
- •11.2 Sepsis
- •11.3 Liver Failure
- •11.4 Conclusion
- •References
- •12: Stroke
- •12.1 Introduction
- •12.2 Acute Ischemic Stroke
- •12.2.4 Cerebral Autoregulation
- •12.2.5 Hemorrhagic Transformation
- •12.2.6 Midline Shift
- •12.2.7 Multimodal Neuromonitoring Approach
- •12.2.8 Sonothrombolysis
- •12.3 Conclusions
- •References
- •13: Cardiac Arrest
- •13.1 Introduction
- •13.4 Conclusions
- •References
- •14.1 Introduction
- •14.2 Brain Ultrasonography
- •14.2.2 Prone Positioning
- •14.2.3 ECMO
- •14.3 General Ultrasonography
- •14.3.1 Lung Ultrasound
- •14.3.2 Cardiac Ultrasound
- •14.4 Conclusion
- •References
- •15: Intracerebral Hematomas, Midline Shift, Hydrocephalus
- •15.1 Introduction
- •15.2 Cerebral Hemodynamics
- •15.3 Intracerebral Hematoma
- •15.4 Midline Shift
- •15.5.1 Hydrocephalus
- •15.5.2 Subdural Hematomas
- •15.5.3 Cerebral Venous Drainage Assessment
- •15.6 Conclusions
- •15.7 Future Directions
- •References
- •16: Vasospasm After Subarachnoid Hemorrhage
- •16.1 Introduction
- •16.8 Conclusions
- •References
- •17.1 Introduction
- •17.2 Pseudotumor Cerebri Syndrome
- •17.4 Posterior Reversible Encephalopathy Syndrome (PRES)
- •17.5 Acute Mountain Sickness (AMS)
- •17.7 Hydrocephalus
- •17.11 Conclusion
- •References
- •18: Brain Death
- •18.2 Diagnosis
- •18.3 TCD Procedure
- •18.3.2 Other Tests
- •18.3.2.1 Cervical Colour Doppler
- •References
- •19.1 Introduction
- •19.2.2 Possible Scenarios
- •19.2.3 Explanatory Cases
- •19.2.3.1 Case n. 1
- •19.2.3.2 Case n. 2
- •19.3 Future Perspectives
- •References
- •20.1 Introduction
- •20.4 Tuberculous Meningitis
- •20.5 Cryptococcal Meningitis
- •20.6 Neurocysticercosis
- •20.7 Cerebral Malaria
- •20.8.1 Sickle Cell Anaemia
- •20.8.2 Hydrocephalus
- •20.8.3 Traumatic Brain Injury
- •References
- •21.1 Introduction
- •21.2 Diagnostic Techniques
- •21.2.1 Transcranial Doppler Sonography (TCD)
- •21.2.2 Transorbital Imaging
- •21.2.3 Transcranial Imaging
- •21.4 Intraoperative Navigation
- •References
- •22.1 Introduction
- •22.2 Brain Ultrasound
- •22.4.2 Postpartum Angiopathy
- •22.4.3 Cerebral Venous Sinus Thrombosis
- •22.5 Conclusions
- •References
- •23.1 Introduction
- •23.2.3 Embolism Detection
- •23.3 Clinical Applications
- •References
- •24: Cardiac Surgery
- •24.1 Introduction
- •24.4.1 Preoperative Transcranial Doppler
- •Technique
- •24.7 Conclusions
- •References
- •28: Case 4: aSAH during Pregnancy
- •32: Case 8: Cerebral Circulatory Arrest
- •36: Case 12: Intracranial Hypertension after Ischemic Stroke

26 Case 2: Vasospasm Treated withBallooning Angioplasty
293
a
b
c
d
Fig. 26.7 (a–d) TCCD of MCA ags up a turbolent ow, in this case CT perfusion higlights hypoperfusion of the right
hemisphere as shown by a decreased CBF and an increased MTT on the colorimetric map

294
ab
cd
abc
Fig. 26.8 (a–c) DSA image frames during baloon angioplasty
R. Bertuetti et al.
Fig. 26.9 (a–d) TCCD of MCAs after baloon angioplasty and intra arterial nimodipine infusion shows normalization
of ow velocities

Case 3: Vasospasm Treated
withBallooning Angioplasty
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
27
A 40-year-old man presented to the emergency
department for severe headache; head CT scan
revealed aSAH from ruptured anterior communicating artery (ACA) aneurysm (Fig. 27.1a–c).
Aneurysm was secured with angiographic coiling
on day 1 (Fig.27.2a–c) and patient neurological
evolution was monitored by means of clinical
evaluation and daily TCCD examinations. Since
day 6 after coiling a progressive asymptomatic
R. Bertuetti (*)
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino– IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
increase in ow velocity (Fig. 27.3a–f) was
observed up to the eighth day when the patient
presented right hemiparesis and confusion associated with extremely high mean ow velocity
and turbulent ow in the left MCA (Fig.27.4a–l).
Severe vasospasm in left MCA was conrmed
with DSA and treated with balloon angioplasty
after which TCCD velocities started to normalize
as well as neurological decits disappeared.
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_27
295

296
R. Bertuetti et al.
abc
Fig. 27.1 (a–c) Head CT images showing thick aSAH and the ruptured aneurysm (panel c) of the ACA
abc
Fig. 27.2 (a–c) DSA image frames during the aneurysm coiling procedure: in panel a. and b. the aneurysm is recogniz-
able, in panel c. it is secured with coils
abc
def
Fig. 27.3 (a–f) Brain ultrasound and TCCD showing increasing velocity in the left MCA

27 Case 3: Vasospasm Treated withBallooning Angioplasty
ab c
de f
ghi
297
jkl
Fig. 27.4 In panels (a–f) TCCD of left MCA showing
elevated ow velocities consistent with vasospasm. In
panels (g–i) images frame of the DSA during baloon
angioplasty. In panels (j–l), normalization of ow velocities after baloon angioplasty

Case 4: aSAH during Pregnancy
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
28
A 36-year-old pregnant woman (25th week) presented to the emergency department after loss of
consciousness following severe headache and
vomiting; head CT scan and angio-CT showed
aSAH from ruptured right ICA aneurysm and
hydrocephalus (HCP) (Fig. 28.1a–f). Aneurysm
was then secured with coils (Fig.28.2a–c) on day
1 after the neurosurgeon had inserted an
EVD.Procedures were uneventful and the patient
woke up fully recovering (GCS 15) right after. In
R. Bertuetti (*)
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino– IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
the following day the young woman developed
upper left limb weakness associated with elevated
ow velocities detected in the right MCA
(Fig.28.3a–f). Induced arterial hypertension up to
a CPP over 100 mmHg using vasopressors and
uid boluses was initiated and titrated by means of
ultrasound monitoring of either placental vessel
ow velocities and fetal transcranial vessel ow
velocities in order to prevent blood ow impairment during vasopressor infusion (Fig.28.4a–f).
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_28
299

300
bc
ef
abc
R. Bertuetti et al.
a
d
Fig. 28.1 (a–f) Plain CT head (a. to c.) shows thick SAH in the basal cysterns and around sulcis and initial HCP. CT
angiography (d. to f.) points out (red arrow) the ruptured aneurysm (top of right ICA)
Fig. 28.2 (a–c) DSA frame images during the coiling of the aneurysm

ab
28 Case 4: aSAH during Pregnancy
abc
301
def
Fig. 28.3 (a–f) TCCD of the right MCA showing trending increasing velocities
abc
de f
Fig. 28.4 (a–f) Fetal transcranial blood ow velocities

Case 5: Intracranial Hypertension
andDecompressive Craniectomy
inSevere aSAH
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
29
A 33-year-old man, cocaine abuser, was admitted to ICU for loss of consciousness; head CT
and angio-CT showed aSAH Fisher 4 grade
from ruptured anterior communicating artery
aneurysm and lateral ventricles enlargement
(Fig. 29.1a–e). Despite urgent EVD insertion
and coiling of the ruptured aneurysm
(Fig. 29.2a–d), the patient developed untreatable intracranial hypertension secondary to diffuse brain swelling, and bilateral frontal lobe
infarctions. Neurosurgeons decided to perform
a decompressive bifrontotemporal craniectomy
in order to save the patient (Figs.29.3a–c and
R. Bertuetti (*)
Department of Anesthesiology, Critical Care
Medicine and Emergency, Division of Neurocritical
Care, ASST Spedali Civili di Brescia, University
Hospital, Brescia, Italy
M. Saini · D. Savo
Department of Emergency, Perioperative Medicine
and Intensive Care, Neuroanesthesia and
Neurointensive Care Unit, San Gerardo Hospital,
ASST-Monza, Monza, Italy
F. Simonassi · K. Chandrapatham
Anesthesia and Intensive Care, Ospedale Policlinico
San Martino– IRCCS for Oncology and
Neurosciences, Genoa, Italy
T. Senussi
Department of Surgical Sciences and Integrated
Diagnostics, University of Genoa, Genoa, Italy
29.4a–d). On day 7 (Fig.29.5), an increase in
ow velocities was bilaterally detected in both
ACAs and MCAs (Fig.29.6a–b) and conrmed
at the DSA as angiographic severe vasospasm
that was then treated with multiple ballooning
angioplasties (Figs. 29.7a–h and 29.8a–d).
Moreover, after decompressive craniectomy, we
were able to follow up the resolving hydrocephalus (HCP) and weaning from the EVD by
means of brain ultrasound: a good correlation
between ventricle sizes measured with the ultrasound and with the routine CT scans was
observed (Fig.29.9a–n).
© Springer Nature Switzerland AG 2021
C. Robba, G. Citerio (eds.), Echography and Doppler of the Brain,
https://doi.org/10.1007/978-3-030-48202-2_29
303

304
cd
R. Bertuetti et al.
abcde
Fig. 29.1 (a–e) Head CT and angio-CT showed aSAH Fisher 4 grade from ruptured anterior communicating artery and
lateral ventricle enlargement
ab
Fig. 29.2 (a–d) DSA (Digital subtraction angiography) images during aneurysm coiling
ab c
Fig. 29.3 (a–c) Head CT scan images before (left and middle panels) and after (right) decompressive craniectomy
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