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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5813_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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

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Part IX
Clinical Cases

Case 1: Vasospasm Treated
withIntra-Arterial Nimodipine
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
25
A 46-year-old woman was admitted to A&E for
poor-grade aSAH from ruptured left MCA aneurysm associated with intracranial haematoma
(ICH) and intraventricular haemorrhage (IVH)
(Fig.25.1a–c). After surgical clipping and EVD
positioning she was admitted to ICU.Between
days 7 and 10 after bleeding, TCCD examination
revealed increasing ow velocity in the left
MCA M1 (Fig.25.2a–h); therefore decision was
taken then to perform an angio-CT and CT perfusion. CT showed severe vasospasm in the left
MCA associated to prolonged mean transit time
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
(MTT) in left fronto-temporo-parietal regions
despite induced arterial hypertension (systolic
ABP >200 mmHg) (Fig. 25.3a–c). Digital
Subtraction Angiography (DSA) conrmed
severe vasospasm and the neuroradiologist
decided to start intra-arterial nimodipine infusion through the insertion of a catheter into the
left internal carotid artery (Fig. 25.4a–f). After
the treatment with intra-arterial vasodilators was
started both TCD ow velocities progressive
decrease and angiographic response were both
observed (Fig.25.5a–c).
© 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_25
285

286
R. Bertuetti et al.
ab c
Fig. 25.1 (a–c) In panel a on the left: CT head showing right fronto parietal heamatoma, SAH and IVH. In panels b
and c: CT angio points out aneurysm of the left MCA at its bifurcation
ab
cd
fgeh
Fig. 25.2 (a–h) Brain ultrasound in B mode in panel a
shows midbrain and basal cysterns, color doppler allows
visualization of the vessels of the circle of willis (panel b).
Application of pulsed doppler on left MCA (panels c–h)
allows measurement of increased blood ow velocity consistent with probable vasospasm
e

25 Case 1: Vasospasm Treated withIntra-Arterial Nimodipine
287
abc
Fig. 25.3 (a–c) CT perfusion after the coiling of the aneurysm conrms the narrowing of the left MCA (panel a) and
increased MTT (panels b and c) in the brain territories thereby supplied
ab c
de f
Fig. 25.4 (a–f) DSA frame images during the angiographic procedure for the insertion of a catheter in the left ICA for
intra arterial nimodipine infusion
ab c
Fig. 25.5 (a–c) TCCD of left MCA during and after intra arterial nimodipine infusion shows normalization of blood
ow velocity

Case 2: Vasospasm Treated
withBallooning Angioplasty
RitaBertuetti, MaurizioSaini, DavideSavo,
FrancescaSimonassi, KartikaChandrapatham,
andTarekSenussi
26
A 55-year-old woman was hospitalized for aSAH
from ruptured right posterior communicating
artery (PcomA) aneurysm (Fig.26.1a, b): GCS 8
on admission, Fisher grade 4 with a clot in the
fourth ventricle, and initial dilation of ventricle
temporal horns (Fig.26.2a–c). TCCD performed
after the initial CT head scan showed an increased
pulsatility index (PI) (Fig. 26.3a–c) conrming
that an obstructive hydrocephalus was inducing a
state of intracranial hypertension. After external
ventricular drain (EVD) insertion, TCCD ow
velocities improved and PI decreased: the patient
promptly recovered her neurology up to a GCS of
14 (Fig. 26.4a, b) and successfully underwent
aneurism coiling (Fig.26.5a, b). On day 6 after
bleeding, although completely asymptomatic 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
with normal brain CT perfusion, an increasing
trend in ow velocity in the right MCA was noted
(Figs.26.6a, b and 26.7a, b) at the TCCD examination. On day 10 acute left hemiparesis and VII
left cranial nerve palsy associated with a signicative increase in mean ow velocity in the right
MCA over 160cm/s with evidence of turbulent
ow (Fig.26.7a–d) were noted; this time, plain
CT head did not show hypodensity but CT perfusion was diagnostic for prolonged right frontotemporal MTT. Induced arterial hypertension
with vasopressors and hemodynamic optimization (SABP>200mmHg and MAP>100mmHg)
effectively restored perfusion in the suffering
frontotemporal regions—as demonstrated by
regression of neurological decits—until day 12
when a relapse of clinical symptoms prompted an
upgrading in the treatment strategy: the patient
underwent a new DSA conrming severe vasospasm in the right M1 segment that was immediately treated with balloon angioplasty and
intraprocedural arterial nimodipine infusion
(Fig.26.8a–c). After the angiographic procedure,
TCCD velocities and motor decits resolved
(Fig.26.9a–d).
© 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_26
289

290
ab
Fig. 26.1 (a, b) CT head angiography 3D rendering: the red arrow points out the aneurysm of the right PcomA, respon-
sible of the bleeding
R. Bertuetti et al.
ab c
Fig. 26.2 (a-c) CT head shows SAH sher grade 4: blood around sulcis (a), basal cisterns (b) and clot in the fourth
ventricle (c). In panel b. initial dilation o temporal horns of the lateral ventricles can also be appreciated
ab c
Fig. 26.3 (a-c) TCCD before EVD positioning: bilateral MCAs insonation demonstrates elevated PI and reduced
diastolic ow as in a state of intracranial hypertension

ab
26 Case 2: Vasospasm Treated withBallooning Angioplasty
Fig. 26.4 (a, b) TCCD of bilateral MCAs after EVD positioning: a normalization of the PI and a restored diastolic ow
can be appreciated
291
a b
Fig. 26.5 (a, b) DSA frame images during the coiling of the aneurysm

292
R. Bertuetti et al.
a
cd
e
b
Fig. 26.6 (a–e) TCCD of MCA (panels a. and b.) shows
a trending increase in mean ow velocity (97 cm/sec)
although not yet fully pathological, in fact CT perfusion
does not highlight any signicative perfusive decit consistent with vasospasm (c. and d.)
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