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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5813_Библиотеки_им_академика_М_И_Перельмана.pdf
98
C. B. Rynkowski and M. J. Aries
MCA-L Depth:45 2MHz PW
105.27 17.54
90-
45-
0-
-45
MCA-R Depth:50 2MHz PW
90-
45-
0-
-45
Peak
46.70
Mean
1.37
P.I.
118.2
Peak DV
48.83
Mean
2.15
P.I.
DV
13.85
Fig. 9.1 Bilateral transcranial Doppler (TCD) recordings
in middle cerebral arteries (MCA) showing high systolic,
low diastolic, and high pulsatility index (PI) values. This
vessel territory (Fig.9.3A). TCD can be used for
diagnosis and treatment of the postcarotid endarterectomy “hyperperfusion syndrome” which usually warrants aggressive ABP lowering [11].
9.3.4 Hypoperfusion
A reduced CBFV can be found in different conditions like severe TBI, severe intracranial hemorrhage, severe heart failure, and acute or chronic
large vessel stroke (Fig.9.3b). TCD might identify patients with initially asymptomatic vessel
stenosis who cannot tolerate hypotensive periods and may develop watershed infarctions [7].
In out-of-hospital cardiac arrest (OHCA) TCD
bilateral pattern can be seen with intracranial hypertension and low cerebral perfusion state
recordings may reveal individual cerebral hemodynamic patterns that are associated with worse
outcome. The critical closing pressure (CrCP,
mmHg) is high together with high PI and low
CBFV values in the rst 24 h after ictus. The
CrCP of the cerebral circulation indicates the
(“hypothetical”) value of ABP at which CBF
approaches zero and can be estimated with different TCD-based models [12]. Even short periods of hypoperfusion have been associated with
worse clinical outcome and this relationship is
much stronger for hypoperfusion in comparison
to hyperperfusion. This suggests that individual
ABP levels should be maintained at a sufciently
high level to avoid secondary ischemic brain
injury.
9 Cerebral Perfusion: Practical Contributions ofTranscranial Doppler atBedside
99
MCA L-L
180-
120-
60-
0-
Peak Mean P.I. HITS DV
192.9 137.6 0.6 109.8
ICA L-L
45-
0-
–45-
Peak Mean P.I. HITS DV
Depth:54 2MHz PW
Depth:50 2MHz PW
–56.8 –35.9 1.04 7.68
Fig. 9.2 Transcranial Doppler measurements in bilateral
middle cerebral arteries (MCA) and distal internal carotid
arteries (ICA). High mean CBFV values are found in the
9.3.5 Brain Death
When investigating brain death, TCD/TCCD
can show flow patterns that occur with cerebral circulatory arrest (Fig. 9.4). The most
important pattern is the disappearance (or even
negative appearance) of diastolic flow in both
MCA and vertebral arteries (VA). However,
these findings are only valid in patients with
a neurological exam that points towards brain
death [2]. TCD has a similar diagnostic power
to CT angiography and EEG for brain death
confirmation. In catastrophic brain injuries—
before herniation—flow patterns tend to mirror the cerebral circulatory arrest pattern.
left MCA with normal values in the other arteries. This is
suspicious for (mild) vasospasm of the left MCA
Generally, it resembles situations of extreme
intracranial hypertension, with an extremely
high systolic CBFV and a very low diastolic
CBFV.
9.4 Applications ofTCD
Evaluating Cerebral
Perfusion inCommon ICU
Pathologies
In this section we provide examples on how
TCD can be used in acute stroke, severe TBI,
OHCA, and hepatic encephalopathy to evaluate
cerebral perfusion or cerebral autoregulation.
100
a1
C. B. Rynkowski and M. J. Aries
However, as TCD is not incorporated in the different guidelines for management (except for
SAH spasm detection), its use is at present limited to research practice.
9.4.1 Acute Stroke
With TCD intracerebral arterial stenosis is
detected when vessel diameter reduction is higher
than 50%, which might be an essential information to guide individual ABP management in the
stroke unit [1, 2]. Nowadays, CT/MR angiogra-
MCA-R
135
90-
phy and perfusion imaging are advised to guide
acute stroke treatment, but these modalities are
not always available in low-income countries
or are limited to academic centers. TCD can be
used in a continuous monitoring mode—during
or after IV/IA thrombolysis—to conrm successful vessel recanalization, to detect reocclusion or
low-ow states, and to enhance clot brinolysis
[13]. TCCD can be used to identify brain shift
in the early phase of malignant MCA stroke and/
or hemorrhagic transformation of infarcted areas
and allow timely surgical decompression in eligible patients [13].
Depth:63 2MHz PW
115.13
Peak DV
107.73
84.3
45-
0-
a2
ICA-R Depth:50 2MHz PW
0-
–45
–90
Fig. 9.3 Transcranial Doppler (TCD) measurements in
patient with subarachnoid hemorrhage (SAH) (a) and
intracerebral hemorrhage (b). High cerebral blood ow
velocity (CBFV) values are found in the middle cerebral
artery (MCA) (a.1) and distal internal carotid artery
(dICA) (a.2) in SAH patient indicating hyperemia in the
anterior cerebral circulation. Low CBFV values are found
in both vessels (b.1 and b.2) in the intracerebral hemorrhage patient indicating low perfusion status which needs
(urgent) further evaluation of its cause
Mean
0.66
P.I.
–88.65
Peak DV
–62.79
Mean
0.66
P.I.
–49.84
b1
9 Cerebral Perfusion: Practical Contributions ofTranscranial Doppler atBedside
101
MCA L-L
0-
–45-
–90-
Peak Mean P.I. HITS DV
36.9 20.9 1.15 12.93
b2
ICA L-L Depth:65 2MHz PW
45-
0-
–45-
Peak Mean P.I. HITS DV
Depth:63 2MHz PW
–26.8 –23.1 0.76 –4.24
Fig. 9.3 (continued)
In combination with continuous (noninvasive or invasive) ABP recordings, TCD can
inform clinicians about cerebral autoregulation.
Most studies relied on linear (cross-spectral
or time correlation-based) methods to assess
the integrity of autoregulation. Time correlation methods use a moving linear correlation
between slow waves (10 s averages) of ABP
and CBFV (Mxa index). A positive correlation
is indicative of passive cerebral vasculature
and impaired autoregulation. Zero or negative
correlation is indicative of reactive vasculature
and intact autoregulation [14]. Dynamic autoregulation might be impaired during the acute,
subacute, and chronic stroke phase with altered
CA over the infarcted side, the contralateral,
or both. Impaired autoregulation is associated
with clinical deterioration and poor clinical
outcome [15]. Especially in comatose patients
with large infarcts, neurological worsening
might go unnoticed and intermittent neuromonitoring might ne-tune therapies for optimizing
CBF with augmentation of ABP or regulation of
CO2 levels [16]. An “optimal” ABP range likely
exists, but probably depends on an individual
autoregulation variability, temporal and spatial
heterogeneity of stroke pathophysiology, and
stroke subtype [14].
102
SD
SD
C. B. Rynkowski and M. J. Aries
MCA L-L
0-
–45-
–90-
Peak Mean P.I. HIT
25.6 9.2 2.7 0.92
VA R-R Depth:81 2MHz PW
0-
–45-
–90-
Peak Mean P.I. HIT
Depth:69 2MHz PW
V
V
–62.9 –21.6 2.8 0.72
Fig. 9.4 On the left side the transcranial Doppler (TCD)
spectrum shows a short systolic peak in the left middle
cerebral artery (MCA) without diastolic ow. On the right
side the same pattern is observed in the vertebral artery
9.4.2 Severe Traumatic Brain Injury
(VA). The pulsatility index (PI) is high in both vessels.
The absence of diastolic ow is characteristic of irreversible cerebral circulatory arrest
CBFV (dened as <20cm/s) and high PI (dened
as >1.4) are all associated with more aggressive
Although validated pharmacological interventions to treat TBI patients are still lacking, CBF
manipulations and optimization remain the mainstay of therapy. However, measuring of real-time
CBF changes during interventions cannot be
achieved by imaging techniques. Nowadays neuromonitoring is often limited to continuous invasive ICP/CPP recordings as estimates of CBF [7].
Different TCD ow patterns have been observed
during different phases after the trauma ictus.
Authors have reported cerebral hypoperfusion
(28%, mean CBFV < 35 cm/s), normal perfusion (45%), or vasospastic periods (27%) [17].
The abnormal patterns as well as low diastolic
treatments and unfavorable clinical outcome [10,
18]. Early TCD goal-directed therapy may restore
normal cerebral perfusion, can detect inadvertent
hypocapnia due to hyperventilation, and can limit
secondary injury. The autoregulation Mx index—
the moving correlation index between mean
CBFV and CPP—is lower than 0.05in patients
with impaired autoregulation, whereas values
greater than 0.3 reex high dependency of CBFV
on ABP [19]. Impaired cerebral autoregulation
has consistently been associated with unfavorable outcome [17]. Therefore, different research
groups have proposed to manipulate CPP cautiously to improve CBFV and limit secondary
9 Cerebral Perfusion: Practical Contributions ofTranscranial Doppler atBedside
103
injury in the initial hypoperfusion phase [5]. At
the moment a feasibility and effectiveness study
is undertaken to guide CPP—as the driving force
for CBF—by invasive autoregulation monitoring
(e.g., pressure reactivity index, PRx) results in
TBI patients with invasive ICP monitoring [20].
The PRx index is calculated as the moving correlation index between 10s values of ABP and
ICP.A positive phase II study might denitively
extend the options for intermittent TCD monitoring and goal-directed therapy at the bedside in
the near future [21]. Figure9.5 displays an example of a multimodal monitoring recording of 4h
in a severe TBI patient with robotic TCD probe
application (Fig. 9.5). An individual “optimal”
CPP (CPPopt) could be estimated using both
invasive ICP-derived autoregulation indices (i.e.,
PRx) and noninvasive TCD-derived autoregulation indices (e.g., Mx). The different autoregulation indices are plotted against 2.5mmHg bins of
CPP and with an automated curve tting method:
a CPP value with best preserved autoregulation
(most negative value using these indices) can be
determined and displayed at the bedside as the
CPPopt value [21, 22].
9.4.3 Post-out-of-hospital Cardiac
Arrest Syndrome
Despite recent improvements in the management
of OHCA, the survival at hospital discharge is
still below 10%. Neurological injury is not only
the result of the anoxic period of cardiac arrest,
but can also be exacerbated during the postresuscitation phase due to changes in CBF [12].
Recently, it has been demonstrated with TCD and
noninvasive optic nerve sheath diameter (ONSD)
measurements that some patients might experience periods of intracranial hypertension that
probably contributes to the low CBF state and
poor outcome [23]. In that way TCD should be
able to identify in advance patients under risk of
generalized cerebral edema that might benet
from longer or more aggressive sedation or targeted temperature management.
Recent studies have divided the rst 72h of
return after spontaneous circulation (ROSC) in
three phases. Immediately after ROSC, CBFV is
characterized by hyperemia for 30min, followed
by a hypoperfused phase lasting 6–12h. The third
period, from 12 to 72h after ROSC, shows restoration of normal CBFV, increased CBFV, or persistent decreased CBF [12]. Ra et al. reported
that patients with poor neurological outcome had
a lower diastolic CBFV and higher PI (CBFV
17cm/s, PI 1.49) compared to patients with good
outcome (CBFV 26 cm/s, PI 1.12), despite the
absence of differences in systemic ABP.Patients
who died prematurely from multiorgan failure
were excluded from the outcome analysis [24].
Cerebral autoregulation status might be seen as
an important explanation for the observed phases
with general impairment in the initial phase and
recovery in some patients in a 24–72-h period
after ROSC. However, autoregulation measurements are hampered by the fact that ABP is kept
very stable and therefore not able to challenge the
autoregulation process.
9.4.4 Acute Liver Failure
Around half of comatose patients with acute
liver failure (ALF) and hepatic encephalopathy develop intracranial hypertension with
high (around 25%) mortality rates. In 80% of
the patients with ALF, the brain ultrasonography will demonstrate initially hyperemia that
probably precedes and/or contributes to the
dangerous cerebral edema. With progressing
encephalopathy low perfusion states and higher
PI values dominate. Multiple mechanisms contribute to the pathogenesis, including circulating
neurotoxins, systemic inammation, and loss of
cerebral autoregulation [25]. Global impaired
cerebral autoregulation was found with intermittent TCD measurements in ALF patients, which
recovered after hepatic function improvement or
transplantation. In patients with ALF invasive
ICP/CPP monitoring is not advised mainly due
to lack of evidence, the associated coagulopathy, and the bad clinical condition not allowing
most available ICP-lowering therapies. Recently,
noninvasive ICP assessment has gained interest
with intermittent estimation of ICP/CPP using
104
C. B. Rynkowski and M. J. Aries
Fig. 9.5 Patient example of “optimal” CPP (CPPopt)
estimation using intracranial pressure (ICP)- and transcranial Doppler (TCD)-based indices. Top 3 panels display
raw (high frequency) signals for arterial blood pressure
(ABP), ICP, and cerebral blood ow velocity (CBFV)
over 4-h monitoring period, demonstrating stable continuous TCD recordings. The bottom ve panels display
CPPopt plots for (1) invasive ICP-derived autoregulation
indices PRx, PAx, and RAC and (2) noninvasive TCDderived autoregulation indices Mx and Sx. All the differ-
ent autoregulation indices seem to indicate that the
CPPopt is probably around 61mmHg. Mx is calculated as
the moving correlation between mean CBFV and CPP; Sx
as the correlation between systolic CBFV and CPP; PAx
as the moving correlation between amplitude of ICP and
ABP; PRx as the moving correlation between ICP and
ABP; RAC as the correlation between amplitude of ICP
and CPP. TCD assessment of middle cerebral artery
(MCA) CBFV was conducted via a robotic TCD system
[21]
9 Cerebral Perfusion: Practical Contributions ofTranscranial Doppler atBedside
105
TCD parameters. The authors were able to show
good negative predictive value with the applied
methodology to exclude intracranial hypertension. The noninvasive measurements could be an
important future bedside tool to identify intracranial hypertensive ALF patients and test out brainprotective therapies [25].
9.5 Conclusion
Both TDC and TCCD are useful to assess noninvasively individual cerebral hemodynamics in
critical care patients at the bedside. Innovations
like robotic probe vessel tracking might guarantee reliable measurements for longer periods
and will extend the bedside applications to alarm
the clinical team for hypo- and hyperperfusion
periods and complications like vasospasm or
autoregulation impairment. Neurological complications in critically ill patients are very common
and focused assessment with TCD/TCCD is an
attractive option to improve clinical management
and improve clinical outcome.
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Part III
Pathology and Clinical Applications:
Emergency Department