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18. Winn HR, Bryner C, Curnish RR, Rubio R, Berne RM.Changes in brain metabolites during
the rst 60 seconds of ischemia: adenosine production during hypotension. Trans Am Neurol
Assoc. 1978;103:59–61.
19. Reneman RS, Arts T.Dynamic capacitance of epicardial coronary arteries invivo. J Biomech
Eng. 1985;107(1):29–33.
20. Giller CA, Bowman G, Dyer H, Mootz L, Krippner W. Cerebral arterial diameters dur-
ing changes in blood pressure and carbon dioxide during craniotomy. Neurosurgery.
1993;32(5):737–41. discussion 41–2
21. Linfante I, Delgado-Mederos R, Andreone V, Gounis M, Hendricks L, Wakhloo
AK.Angiographic and hemodynamic effect of high concentration of intra-arterial nicardipine
in cerebral vasospasm. Neurosurgery. 2008;63(6):1080–6. discussion 6–7
22. Lindegaard KF, Lundar T, Wiberg J, Sjoberg D, Aaslid R, Nornes H.Variations in middle cere-
bral artery blood ow investigated with noninvasive transcranial blood velocity measurements.
Stroke. 1987;18(6):1025–30.
23. Ringelstein EB, Van Eyck S, Mertens I.Evaluation of cerebral vasomotor reactivity by vari-
ous vasodilating stimuli: comparison of CO2 to acetazolamide. J Cerebral Blood Flow Metab.
1992;12(1):162–8.
24. Schreiber SJ, Gottschalk S, Weih M, Villringer A, Valdueza JM. Assessment of blood ow
velocity and diameter of the middle cerebral artery during the acetazolamide provocation
test by use of transcranial Doppler sonography and MR imaging. AJNR Am J Neuroradiol.
2000;21(7):1207–11.
25. Markus HS, Harrison MJ.Estimation of cerebrovascular reactivity using transcranial Doppler,
including the use of breath-holding as the vasodilatory stimulus. Stroke. 1992;23(5):668–73.
26. Markwalder TM, Grolimund P, Seiler RW, Roth F, Aaslid R.Dependency of blood ow veloc-
ity in the middle cerebral artery on end-tidal carbon dioxide partial pressure--a transcranial
ultrasound Doppler study. J Cereb Blood Flow Metab. 1984;4(3):368–72.
27. Bernoulli D.Hydrodynamica, sive de viribus et motibus uidorum commentarii: opus aca-
demicum ab auctore, dum Petropoli ageret, congestum 1738.
28. Spencer MP, Reid JM.Quantitation of carotid stenosis with continuous-wave (C-W) Doppler
ultrasound. Stroke. 1979;10(3):326–30.
29. Spencer MP, Whisler D. Transorbital Doppler diagnosis of intracranial arterial stenosis.
Stroke. 1986;17(5):916–21.
30. Lindegaard KF, Bakke SJ, Aaslid R, Nornes H.Doppler diagnosis of intracranial artery occlu-
sive disorders. J Neurol Neurosurg Psychiatry. 1986;49(5):510–8.
31. Schneider PA, Rossman ME, Bernstein EF, Torem S, Ringelstein EB, Otis SM.Effect of inter-
nal carotid artery occlusion on intracranial hemodynamics. Transcranial Doppler evaluation
and clinical correlation. Stroke. 1988;19(5):589–93.
32. Koppl T, Schneider M, Pohl U, Wohlmuth B. The inuence of an unilateral carotid artery
stenosis on brain oxygenation. Med Eng Phys. 2014;36(7):905–14.
33. Telman G, Kouperberg E, Nitecki S, Karram T, Schwarz HA, Sprecher E, etal. Cerebral hemo-
dynamics in symptomatic and asymptomatic patients with severe unilateral carotid stenosis
before and after carotid endarterectomy. Eur J Vasc Endovasc Surg. 2006;32(4):375–8.
34. Lindegaard KF, Bakke SJ, Grolimund P, Aaslid R, Huber P, Nornes H.Assessment of intracra-
nial hemodynamics in carotid artery disease by transcranial Doppler ultrasound. J Neurosurg.
1985;63(6):890–8.
35. Calligaro KD, Dougherty MJ. Correlation of carotid artery stump pressure and neurologic
changes during 474 carotid endarterectomies performed in awake patients. J Vasc Surg.
2005;42(4):684–9.
36. Nornes H.The role of the circle of Willis in graded occlusion of the internal carotid artery in
man. Acta Neurochir. 1973;28(3):165–77.
37. Nornes H.Hemodynamic aspects in the management of carotid-cavernous stula. J Neurosurg.
1972;37(6):687–94.
L. L. P. Mejia et al.
17 Neuro-ICU: Cerebral Hemodynamics and Transcranial Doppler (TCD/TCCS…
38. Nornes H.Internal carotid artery blood ow during cerebral angiography. Neuroradiology.
1977;12(4):219–25.
39. Nornes H, Grip A, Wikeby P. Intraoperative evaluation of cerebral hemodynamics
using directional Doppler technique. Part 1: arteriovenous malformations. J Neurosurg.
1979;50(2):145–51.
40. Nornes H, Grip A, Wikeby P.Intraoperative evaluation of cerebral hemodynamics using direc-
tional Doppler technique. Part 2: saccular aneurysms. J Neurosurg. 1979;50(5):570–7.
41. Aaslid R, Markwalder TM, Nornes H.Noninvasive transcranial Doppler ultrasound recording
of ow velocity in basal cerebral arteries. J Neurosurg. 1982;57(6):769–74.
42. Sagawa K, Lie RK, Schaefer J.Translation of Otto Frank’s paper “Die Grundform des Arteriellen
Pulses” Zeitschrift fur Biologie 37: 483-526 (1899). J Mol Cell Cardiol. 1990;22(3):253–4.
43. Westerhof N, Lankhaar JW, Westerhof BE.The arterial Windkessel. Med Biol Eng Comput.
2009;47(2):131–41.
44. Frank O. The basic shape of the arterial pulse. First treatise: mathematical analysis. 1899. J
Mol Cell Cardiol. 1990;22(3):255–77.
45. Gosling RG, Dunbar G, King DH, Newman DL, Side CD, Woodcock JP, etal. The quantita-
tive analysis of occlusive peripheral arterial disease by a non-intrusive ultrasonic technique.
Angiology. 1971;22(1):52–5.
46. Greeneld JC Jr, Tindall GT.Effect of acute increase in intracranial pressure on blood ow in
thw internal carotid artery of man. J Clin Invest. 1965;44:1343–51.
47. Panerai RB.Assessment of cerebral pressure autoregulation in humans--a review of measure-
ment methods. Physiol Meas. 1998;19(3):305–38.
48. Zhang R, Zuckerman JH, Giller CA, Levine BD.Transfer function analysis of dynamic cere-
bral autoregulation in humans. Am J Phys. 1998;274(1 Pt 2):H233–41.
49. Panerai RB, Coughtrey H, Rennie JM, Evans DH. A model of the instantaneous pressure-
velocity relationships of the neonatal cerebral circulation. Physiol Meas. 1993;14(4):411–8.
50. Dahl A, Lindegaard KF, Russell D, Nyberg-Hansen R, Rootwelt K, Sorteberg W, etal. A com-
parison of transcranial Doppler and cerebral blood ow studies to assess cerebral vasoreactivity. Stroke. 1992;23(1):15–9.
51. Dahl A, Russell D, Nyberg-Hansen R, Rootwelt K, Bakke SJ.Cerebral vasoreactivity in uni-
lateral carotid artery disease. A comparison of blood ow velocity and regional cerebral blood
ow measurements. Stroke. 1994;25(3):621–6.
52. Ringelstein EB, Kahlscheuer B, Niggemeyer E, Otis SM. Transcranial Doppler sonography:
anatomical landmarks and normal velocity values. Ultrasound Med Biol. 1990;16(8):745–61.
53. Lohmann H, Ringelstein EB, Knecht S.Functional transcranial Doppler sonography. Front
Neurol Neurosci. 2006;21:251–60.
54. Miao J, Benkeser PJ, Nichols FT.A computer-based statistical pattern recognition for Doppler
spectral waveforms of intracranial blood ow. Comput Biol Med. 1996;26(1):53–63.
55. Gosling RG, King DH.Arterial assessment by Doppler-shift ultrasound. Proc R Soc Med.
1974;67(6 Pt 1):447–9.
56. Nicoletto HA, Burkman MH. Transcranial Doppler series part III: interpretation. Am J
Electroneurodiagnostic Technol. 2009;49(3):244–59.
57. Kidwell CS, el-Saden S, Livshits Z, Martin NA, Glenn TC, Saver JL.Transcranial Doppler pul-
satility indices as a measure of diffuse small-vessel disease. J Neuroimag. 2001;11(3):229–35.
58. Michel E, Zernikow B.Gosling's Doppler pulsatility index revisited. Ultrasound Med Biol.
1998;24(4):597–9.
59. Zweifel C, Czosnyka M, Carrera E, de Riva N, Pickard JD, Smielewski P.Reliability of the
blood ow velocity pulsatility index for assessment of intracranial and cerebral perfusion pressures in head-injured patients. Neurosurgery. 2012;71(4):853–61.
60. Ursino M, Giulioni M, Lodi CA.Relationships among cerebral perfusion pressure, autoregula-
tion, and transcranial Doppler waveform: a modeling study. J Neurosurg. 1998;89(2):255–66.
317
318
61. 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. 1988;42:81–4.
62. Schwartz A, Hennerici M.Noninvasive transcranial Doppler ultrasound in intracranial angio-
mas. Neurology. 1986;36(5):626–35.
63. Hennerici M, Rautenberg W, Sitzer G, Schwartz A.Transcranial Doppler ultrasound for the
assessment of intracranial arterial ow velocity–Part 1. Examination technique and normal
values. Surg Neurol. 1987;27(5):439–48.
64. Hennerici M, Rautenberg W, Schwartz A.Transcranial Doppler ultrasound for the assessment
of intracranial arterial ow velocity–Part 2. Evaluation of intracranial arterial disease. Surg
Neurol. 1987;27(6):523–32.
65. Arnolds BJ, von Reutern GM.Transcranial Doppler sonography. Examination technique and
normal reference values. Ultrasound Med Biol. 1986;12(2):115–23.
66. Martin PJ, Evans DH, Naylor AR.Transcranial color-coded sonography of the basal cerebral
circulation. Reference data from 115 volunteers. Stroke. 1994;25(2):390–6.
67. Rasulo FA, De Peri E, Lavinio A.Transcranial Doppler ultrasonography in intensive care. Eur
J Anaesthesiol Suppl. 2008;42:167–73.
68. Moppett IK, Mahajan RP.Transcranial Doppler ultrasonography in anaesthesia and intensive
care. Br J Anaesth. 2004;93(5):710–24.
69. Maeda H, Matsumoto M, Handa N, Hougaku H, Ogawa S, Itoh T, etal. Reactivity of cerebral
blood ow to carbon dioxide in various types of ischemic cerebrovascular disease: evaluation
by the transcranial Doppler method. Stroke. 1993;24(5):670–5.
70. Homburg AM, Jakobsen M, Enevoldsen E.Transcranial Doppler recordings in raised intracra-
nial pressure. Acta Neurol Scand. 1993;87(6):488–93.
71. Bellner J, Romner B, Reinstrup P, Kristiansson KA, Ryding E, Brandt L. Transcranial
Doppler sonography pulsatility index (PI) reects intracranial pressure (ICP). Surg Neurol.
2004;62(1):45–51; discussion.
72. Cardim D, Schmidt B, Robba C, Donnelly J, Puppo C, Czosnyka M, etal. Transcranial Doppler
monitoring of intracranial pressure plateau waves. Neurocrit Care. 2017;26(3):330–8.
L. L. P. Mejia et al.
Chapter 18
Non-invasive Multimodal Neuromonitoring
intheICU: TheRole ofTranscranial
Doppler (TCD/TCCS)
DemetriosJ.Kutsogiannis
Key Points
1. Multimodality neuromonitoring (MMM) is both static and dynamic, evaluating
cerebral structure, vasculature, and electrochemical function.
2. The various technologies included in MMM provide complementary informa-
tion with various degrees of inter-modality correlation.
3. The use of MMM permits earlier therapeutic interventions that may prevent
cerebral tissue hypoxia, metabolic stress, and irreversible cerebral damage.
4. The best method of monitoring, optimal physiological cutoffs, and threshold for
treatments must be individualized for every acutely brain-injured patient.
5. Multimodality neuromonitoring technologies offer predictive value in prognos-
ticating neurological outcomes.
18.1 Introduction
The term multimodal monitoring (MMM) encompasses the various clinical and
technological modalities available to the contemporary physician caring for critically ill neurological patients. Injured patients include those with trauma, infections, and hemorrhagic or ischemic stroke. For many years, scoring systems
(Glasgow Coma Score, FOUR Score) utilizing the neurological examination were
used as the only stochastic method of following changes in neurological function.
However, it is well recognized that the neurological examination is limited in comatose patients and those under sedation and analgesia, and neurological changes may
D. J. Kutsogiannis (*)
Critical Care Medicine, Neurocritical Care (UCNS), Neurosciences ICU, The University of
Alberta, Royal Alexandra Hospital ICU, University of Alberta Hospital,
Edmonton, AB, Canada
e-mail: djk3@ualberta.ca
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_18
319© Springer Nature Switzerland AG 2022
320
not manifest or may lag important changes in cerebral vascular perfusion, electrophysiology, and metabolism. Two major acute brain injury diagnoses have been the
most informative in motivating the development of MMM techniques and research.
The rst being that of delayed neurological deterioration after subarachnoid hemorrhage (SAH), specically delayed cerebral ischemia (DCI). The second being the
identication of mechanisms for secondary brain injury after traumatic brain injury
(TBI) and the importance of abnormal cerebral autoregulation in worsening outcomes in TBI. Research utilizing transcranial Doppler and Transcranial ColorCoded duplex Sonography (TCCS) and other forms of MMM have DCI after SAH
is not specically related to catheter angiographically dened areas of proximal
vasospasm. Multidimensional and complex processes such as arteriolar constriction
and thrombosis, hypoxemic and non-hypoxemic mitochondrial metabolic failure,
and cortical spreading depolarization-related hypoperfusion are important etiological factors [1, 2]. In TBI, intracranial hypertension is an important secondary insult
after TBI, and its identication, prevention, and treatment are important in optimizing clinical outcomes [3]. The ability of the brain to regulate its blood ow despite
the level of cerebral perfusion pressure (CPP) is important in the prevention of secondary brain injury through its effect on intracranial hypertension, hypoxia, ischemia, and hyperemia. The loss of this cerebral autoregulation is detrimental to
patient outcomes. However, utilizing MMM techniques for the measurement of
dynamic cerebrovascular autoregulation assists in determining patient-specic optimal targets for CPP in order to mitigate the detrimental effects of poor intracranial
compliance. Such methods require the ability to calculate real-time moving correlation coefcients between intracranial pressure (ICP), or cerebral blood ow by
TCD/TCCS, and arterial blood pressure [4, 5].
D. J. Kutsogiannis
18.2 TCD/TCCS: Role andImportance intheNon-invasive
Multimodal Neuromonitoring intheICU
In the Consensus Summary Statement of the International Multidisciplinary
Consensus Conference on Multimodality Monitoring in Neurocritical Care [6], the
quality of the evidence was reviewed and recommendations were developed using
the GRADE system. Recommendations are classied as strong or weak based on a
consensus balance among benets, risks, burden, and costs according to the quality
of the evidence [7–9]. These recommendations are as follows.
1. High: Further research is very unlikely to change our condence in the estimate
of effect.
2. Moderate: Further research is likely to have an important impact on our con-
dence in the estimate of effect and may change the estimate.
3. Low: Further research is very likely to have an important impact on our con-
dence in the estimate of effect and is likely to change the estimate.
4. Very low: Any estimate of effect is very uncertain.
18 Non-invasive Multimodal Neuromonitoring in the ICU: The Role of Transcranial…
321
18.3 TCD/TCCS: Frequent Pathologies. What Do
WeMonitor?
18.3.1 Subarachnoid Hemorrhage (SAH)
18.3.1.1 Cerebral Autoregulation (CA)
Dysfunctional cerebral autoregulation is a component of risk for delayed cerebral
ischemia (DCI) in SAH.Otite assessed the relationship between cerebral autoregulation measured using dynamic transfer analysis (phase and gain) of the spontaneous blood pressure and blood ow velocities on days 2 to 4 after SAH.Multivariate
analysis indicated that a higher transfer function gain and a lower transfer function
phase were independently associated with angiographically conrmed vasospasm,
and computed tomography (CT) conrmed delayed cerebral ischemia (DCI) [10].
Disturbed autoregulation within the rst 5 days after SAH, as measured by Sx
(TCD-derived autoregulatory index) and Tox (Near-infrared spectroscopy, NIRSderived autoregulatory index) signicantly increases the risk of DCI [11]. In another
study, neither cerebral autoregulation impairment as measured by TCD (Sx) nor
large artery vasospasm alone was associated with DCI.However, the combination
of large artery vasospasm with increasing loss of cerebral autoregulation within the
rst 7days from a SAH was signicantly associated with DCI [12].
18.3.1.2 Intraparenchymal Cerebral Oxygen Monitoring
A study of 46 patients representing 5424hours of PbtO
monitoring the number of
2
episodes of compromised PtbO2 (15–25 mmHg) and the number of episodes of
cerebral hypoxia (PtbO2<15mmHg) was independently associated with mortality
[13]. An important limitation of PbtO2 placement in SAH is that placement of the
probe must be congruent with the most probable site of cerebral vasospasm or
infarction. In one study, congruence was achieved in >88% of the insertions for
internal carotid artery and middle cerebral artery aneurysms but as low as 23% of
the insertions for vertebrobasilar arteries [14].
18.3.1.3 Cerebral Blood Flow
Using bedside xenon-enhanced computed tomography (XeCT), patients with poorgrade SAH and initial low CBF at day 0–3 post SAH who received hypertension,
hypervolemia, and hemodilution (HHH) therapy had a signicant increase in their
CBF at day 4–7 as compared to those not receiving HHH [15]. In a study performed
in 17 patients within 12hr. after SAH using XeCT, CBF was signicantly reduced in
all patients with SAH (mean 34ml/100g × min) as compared to controls (mean
67ml/100g × min) with signicantly worse CBF in patients with more severe SAH
322
D. J. Kutsogiannis
(Hunt Hess 4–5) versus Hunt Hess 1–3. This was attributable to acute peripheral
vasospasm of the microvasculature which is not detectable by conventional angiography or TCD/TCCS [16]. The coupling between cerebral blood ow (CBF) and
neuronal activity as measured by electroencephalogram (EEG) occurs within seconds [17]. As CBF falls below 30ml/100g/min, faster frequencies are lost, and a
progressive slowing of EEG activity occurs, and at CBF <10ml/100g/min all EEG
frequencies are suppressed [18]. EEG may complement neuroimaging as a continuous monitor of ongoing ischemia. Historically, middle cerebral artery (MCA) mean
ow velocities of <120cm/sec and >200cm/sec reliably predict the absence or presence of clinically signicant angiographic vasospasm with a high negative predictive
and positive predictive value, respectively [19]. More recently, a meta-analysis has
assisted in reconciling the complementary MMM information obtained from cerebral catheter angiography and TCD in predicting DCI in SAH.Synthesizing the
results from 15 studies, Kumar compiled the sensitivity, specicity, positive predictive value, and negative predictive value of cerebral catheter angiography for prediction of DCI as 57%, 68%, 32%, and 90%. For TCD, the respective measures were
better than those using cerebral catheter angiography, being 90%, 71%, 57%, and
92%, respectively [20].
18.3.1.4 Electrophysiology
Seizure Detection
In a systematic review of 18 studies which used continuous EEG (cEEG) to monitor
481 patients with SAH, the incidence of non-convulsive seizures (NCSz) was
7–18% and that of non-convulsive status epilepticus was 3–13%. The presence of
non-convulsive status epilepticus (NCSE) was associated with increasing age and
mortality [21]. In SAH patients undergoing continuous EEG (cEEG) monitoring in
the intensive care unit (ICU), up to 19% have non-convulsive seizures (NCSz) and
13% have NCSE.Using the GRADE system, the Neurointensive Care Section of
the European Society of Intensive Care Medicine (ESICM) recommends EEG monitoring to rule out NCSz in all SAH patients with unexplained and persistent altered
consciousness [22].
Ischemia Detection
The Neurointensive Care Section of the ESICM suggests EEG to detect DCI in
comatose patients in whom neurological physical examination is unreliable [22].
Automated quantitative EEG (QEEG) algorithms using predetermined thresholds
for the decrease in alpha band power and increase in theta band power have also
been demonstrated to precede the angiographic detection of vasospasm or DCI by
2.3days [23]. In a systematic review of cEEG in SAH, Kondziella concluded that a
QEEG pattern of a decreased alpha/delta ratio, decrease in relative alpha variability,
and total power had a weak association with the development of DCI.However, all
the included studies were subject to a high risk of methodological bias [21].
18 Non-invasive Multimodal Neuromonitoring in the ICU: The Role of Transcranial…
323
A poor prognosis, dened as modied Rankin score of 4–6 (dead or moderately
to severely disabled), was independently associated with cEEG evidence of the
absence of sleep architecture, the presence of periodic or generalized periodic lateralized epileptiform discharges, the absence of EEG reactivity, and the presence of
NCSE [24, 25].
18.3.1.5 Cerebral Metabolism
Cerebral microdialysis (CMD) abnormalities are dened as increases in lactate/glucose (L/G) and lactate/pyruvate (L/P) levels of greater than 20% followed by a 20%
increase in glycerol concentration dened ischemia of the cerebral territory of the
microdialysis probe. Delayed cerebral ischemia was identied in 17 of 18 patients
with this degree of elevation, 14 of whom had cerebral CT evidence of infarction
[26]. Using CMD in comatose SAH patients, Oddo characterized elevated CMD
lactate (>4mmol/L) as either hypoxic, dened as PbtO2<20mmHg, or as hyperglycolytic, dened as having a CMD pyruvate of >119μmol/L.A pattern of hypoxic
lactate elevations was associated with a high mortality versus a pattern of increased
cerebral hyperglycolytic lactate which was associated with good long-term recovery [27]. Cerebral microdialysis probes should be placed in the vascular territories
with the highest infarct risk in relation to the aneurysm location. These territories
being the anterior cerebral arteries for anterior communicating artery aneurysms
and the ipsilateral middle cerebral artery territory for internal carotid artery, middle
cerebral artery, and posterior communicating artery aneurysms [28]. The Consensus
Statement from the 2014 International Microdialysis Forum recommends the use of
CMD in mechanically ventilated poor-grade SAH patients and those with secondary neurological deterioration. As a primary monitoring device, the probe location
recommended is in the frontal lobe in the watershed anterior cerebral–middle cerebral artery territory. In SAH patients with secondary deterioration, the recommended probe location should be in brain regions at risk for ischemia guided by
TCD/TCCS or CT perfusion scanning [29].
18.3.2 Intracerebral Hemorrhage (ICH)
18.3.2.1 Intraparenchymal Cerebral Oxygen Monitoring
There is little experience with the use of intraparenchymal oxygen monitoring in
ICH. Hemphill described the use of the LICOX® catheter in swine and seven
patients with ICH.Tissue hypoxia, dened as the area under the curve with tissue
PbtO
<15mmHg, was common with increasing FiO2, mean arterial pressure, and
2
CPP predicting increasing PbtO2 [30]. Invasively monitoring perihematomal brain
tissue oxygenation has also demonstrated a signicant increase in the risk of brain
tissue hypoxia (PbtO2<15mmHg) in those patients with a CPP<80mmHg [31].
324
D. J. Kutsogiannis
Targeting CPP in these patients to their optimal CPP (CPPopt) guided by their pressure reactivity index (PRx) has the potential to improve clinical outcomes in
ICH. However, larger studies utilizing this MMM interventional approach are
required to more rmly determine this [32].
18.3.2.2 Intracerebral Volume, Midline Shift, andPulsatility Index
Measurements by TCCS
ICH is a dynamic process with the advantage provided by TCCS being its availability to provide rapid repeated assessments at the bedside. In a cohort of patients suffering from spontaneous ICH, TCCS measurements of hematoma volume (HV) and
midline shift demonstrated a strong correlation with brain CT measurements. The
optimal threshold to predict mortality at 1month was an HV of 47.62mL measured
by CT (85.7% sensitivity, 85.7% specicity) and an HV of 30.36mL measured by
TCCS (85.7% sensitivity, 82.2% specicity). TCCS tended to overestimate the volume of smaller ICHs and to underestimate the volumes of larger ICHs. In previous
univariate analysis, an increased pulsatility index (PI) from the ipsilateral MCA was
associated with higher mortality. In separate multivariable analysis, both CT and
TCCS measurements of HV size were the only independent predictors of 1-month
mortality with an equal magnitude of effect [33]. For real-time bedside monitoring,
the use of serial TCD/TCCS monitoring has been proven to be reliable in determining the extent of early hematoma expansion. Prior studies have demonstrated that
the initial size of the ICH, percentage of hematoma growth, Glasgow Coma Score,
hypertension, the presence of intraventricular hemorrhage (IVH), and age are predictive of mortality and poor functional outcome [34, 35]. Serial TCD examinations
every 30minutes for 6hours have demonstrated good volume estimation compared
to cerebral CT, and this early hematoma expansion appears to be exclusive to spot
sign positive patients [36–38]. This information may be used at the bedside to predict early hematoma expansion and clinical worsening so as to allocate these
patients to higher levels of neurocritical care monitoring.
18.3.2.3 Electrophysiology
Electrographic seizures found on cEEG and periodic epileptiform discharges are
common in ICH, occurring in up to one-third of patients [39, 40]. The Consensus
Statement from the Neurointensivist Section of the ESICM recommends EEG to
rule out NCSz in all ICH patients with altered levels of consciousness [22].
18 Non-invasive Multimodal Neuromonitoring in the ICU: The Role of Transcranial…
325
18.3.3 Traumatic Brain Injury (TBI)
18.3.3.1 Intracranial Pressure andCerebral Perfusion Pressure
When intracranial pressure increases, cerebral vascular autoregulation is gradually
lost, and cerebral arterioles and veins are compressed reducing blood return and
increasing vascular resistance. The consequence is a reduced MFV and a reduced or
reversed (negative) end-diastolic velocity. Collectively, this increases the numerator
and lowers the denominator of the equation for the pulsatility index, PI= (Peaksystolic velocity– End-diastolic velocity)/ Mean ow velocity (MFV). The MCA PI
has been demonstrated to have a strong positive correlation with ICP measurements
in various etiologies of cerebral brain injury with one study indicating an estimated
ICP=10.93 × PI– 1.28 [41]. Other investigators have determined that a resistive
index and PI cutoff value of 0.705 and 1.335, respectively, predicted ICP>15mmHg
with a sensitivity of 0.885 and a specicity of 0.970 [42]. Likewise, in a cohort of
365 TBI patients with mild TBI, an abnormal TCD examination dened as a PI
>1.25 and an end-diastolic ow velocity <25 had an 80% sensitivity and a 79%
specicity in predicting neurological worsening [43]. These ndings may enable
clinicians to risk stratify patients into higher risk groups requiring an increased level
of monitoring. At present, the current edition of the Guidelines for the Management
of Severe Traumatic Brain injury does not offer any guidance for the use of TCD/
TCCS in the management of severe TBI.The guidelines do, however, recommend,
treating ICP>22mm Hg and maintaining a CPP between 60 and 70mm Hg with
the ideal CCP target depending on the autoregulatory status of the patient [3].
18.3.3.2 Cerebral Autoregulation
Static and dynamic autoregulation measure the amount and rapidity with which
associated with poor outcomes in TBI and other neurological injuries. Measurements
from TCD (Mx), ICP (PRx) brain tissue oxygenation PbtO
(ORx), and near-
2
infrared spectroscopy (THx) have been utilized dynamically and correlated with
CPP in order to determine the range within which CPP is optimal (CPPopt). Patients
with TBI whose CPP is targeted in the CPPopt range have been demonstrated to
have improved outcomes. The most validated approach uses a correlation coefcient method between ICP and CPP to determine a pressure reactivity index (PRx)
for which a recent systematic review has offered a weak recommendation using the
GRADE system [4]. In retrospective studies, optimizing cerebral autoregulation
(CPPopt) to maximize cerebrovascular reactivity reduces neurological disability
and mortality [44, 45]. Current MCA TCD-based methods of determining cerebral
autoregulation appear to have a good correlation with the more commonly used
pressure reactivity index (PRx) [46]. However, more research is required to dene
the role of TCD/TCCS-based measures of cerebral autoregulation in the management of TBI.