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23 Subarachnoid Hemorrhage (SAH) in the Neuro-ICU: Usefulness of Transcranial…
397
With the push to employ non-invasive technology within the NICU, given risk
reduction to the patient and wider accessibility to non-surgeon treating physicians,
TCD has been readily employed within the SAH population as a means of monitoring for the development of symptomatic and asymptomatic cerebral vasospasm. It
has even received support for its application in SAH patients from the Neurocritical
Care Society [9]. This chapter will focus on the application of TCD monitoring for
cerebral vasospasm in SAH, highlighting: technique, indices of vasospasm, autoregulation monitoring, intra-cranial pressure (ICP) monitoring, and newer/emerging TCD technologies.
23.2 TCD Assessment ofCerebral Vascular Territories
TCD employs the use of ultrasound technology for the assessment CBFV within a
vascular territory of interest. This typically involves the use of a Doppler transducer
with an emission frequency of 2.0–3.5MHz to assess, or “insonate,” a vessel of
interest [10–12]. Various areas of the skull, referred to as “windows,” have been
described for optimal assessment of various cerebral blood vessels, all at different
depths of ultrasound insonation. These areas are where the skull is the thinnest or
decient, allowing for a clear and direct path for insonation of the cerebral vessel.
Table23.1 describes the main windows for TCD, the vessel territory assessed, depth
Table 23.1 TCD acoustic windows
Window name Cranial location
Transorbital Over closed eyelid,
direct toward carotid
canal
Transtemporal Some literature
discusses an anterior,
middle, and posterior
sub-window
Located above root of
zygoma over squamous
temporal bone
Vessels assessed
(insonation depth) Limitations
Carotid siphon
(depth 55–50mm)
Ophthalmic artery
(depth 40–50mm)
ICA bifurcation
(depth ~65mm)
MCA (depth
35–55mm)
ACA (depth
60–70mm– with
ow away from the
a
probe)
PCA (1–2cm
posterior to ICA
bifurcation, depth
60–70mm)
Beam power must be kept
<10% to avoid subluxation of
lens
Difcult to obtain for long
durations
Most commonly utilized
window for TCD assessment
Not all patients have symmetric
windows
Not all patients have adequate
window
Long duration recording
difcult for ACA and PCA
(continued)
398
Table 23.1 (continued)
Window name Cranial location
Suboccipital Flexed neck, probe
directed through
foramen magnum
toward clivus and
posterior clinoid
processes
Submandibular At angle of jaw Distal cervical ICA
ACA anterior cerebral artery, cm centimeters, mm millimeters, MCA middle cerebral artery, PCA
posterior cerebral artery
Note: “a” denotes that these vascular territories will have ow directed away from the probe during
insonation, where all other vessels mentioned above typically have ow toward the probe
Purkayastha etal. [12]
Vessels assessed
(insonation depth) Limitations
Distal vertebral
arteries (depth
80–115mm just
lateral of midline)
Basilar artery (depth
60–100mm at
a
midline)
(depth 40–60mm)
F. A. Zeiler and J. Teitelbaum
Difcult to obtain longer
duration recordings
Uncomfortable for patient to
a
remain in this position for
extended periods
Limited to extracranial ICA
only
Requires operator to hold probe
in direction of vessel for
duration of recording (i.e., rigid
probe holders not readily
available)
of insonation, and some of the region-specic limitations. It should be noted that not
all patients have perfect cerebral vasculature, and not all patients have good windows for insonation at every vascular territory. Figure23.1 displays the position of
the window and ultrasound probe placement for the common windows of interest in
TCD assessment.
The overarching premise is that the Doppler probe assesses the Doppler frequency shift in ultrasound signal that occurs in response to cerebral blood ow. This
Doppler frequency shift is then utilized to calculate CBFV and other TCD indices.
In order to obtain the purest measure via TCD, ideally one would have the ultrasound probe in perfect line with the direction of CBF (i.e., 0-degree angle of
insonation). For sake of practicality, an insonation angle of 30 degrees or less is
considered acceptable for accurate measurements [10].
Though each window and territory of interest has different positioning, the general technique for TCD is as follows: rst, identify the vascular territory of interest
and the desired window for insonation. Second, apply ultrasound gel to the skin
overlaying the window. Third, using a 2.0–3.5 MHz Doppler probe, attempt to
insonate the vessel of interest through the window. Fourth, using the pulse waveform CBFV window on the ultrasound machine, assess the shape of the CBFV
waveform, it should have the classic pulsatile shape as seen in Fig. 23.2a. Fifth,
23 Subarachnoid Hemorrhage (SAH) in the Neuro-ICU: Usefulness of Transcranial…
a
399
2
3
4
1
b
1
2
3
Fig. 23.1 TCD windows TCD transcranial Doppler. (Panel a): Sagittal view depicting various
TCD windows. #1=submandibular window, #2=transorbital, #3=transtemporal, #4=suboccipital. (Panel b): Axial view depictive circle of Willis and various TCD windows. #1=transorbital,
#2=transtemporal, #3=subocciptial. (Illustrations by Jon Stepaniuk)
400
F. A. Zeiler and J. Teitelbaum
a
b
Fig. 23.2 CBFV waveform and M-Mode via TCD of the MCA.CBFV cerebral blood ow velocity, MCA middle cerebral artery, TCD transcranial Doppler. Panel (a): Unilateral insonation of the
right MCA.Panel (b): Bilateral simultaneous insonation of the MCA, with the white circle highlighting the M-mode display
once an adequate CBFV waveform is obtained, use the M-mode (Power Motion
Doppler mode) window to assess the signal ow intensity over various depths in the
direction of insonation. This allows for the selection of the appropriate depth of
insonation, depending on the vascular territory of interest [13]. The M-mode display
can be seen in Fig.23.2b. Finally, once adequate CBFV waveform and depth of
AI
()
23 Subarachnoid Hemorrhage (SAH) in the Neuro-ICU: Usefulness of Transcranial…
401
insonation are obtained, one should obtain at least 30s of stable recording prior to
obtaining measurements for clinical purposes.
In order to obtain longer duration recordings, various companies have developed
frames or headbands, allowing for hands-free insonation. These are typically
designed for TCD of the middle cerebral artery (MCA) only. These devices still suffer from shifting and signal loss from patient movement and are thus not perfect,
requiring intermittent attention at the bedside for long recordings. Newer technology has been developed to potentially solve this issue and will be briey covered in
the “Future Directions” section of this chapter.
23.3 TCD forAssessment ofCerebral Vasospasm
23.3.1 Premise
Increase in cerebral vascular tone leads to the reduction in vessel caliber. This
reduction in luminal diameter leads to an increase in CBFV.Thus, in the setting of
cerebral vasospasm post-SAH, TCD can be utilized to follow the trend in CBFV
over time. As vessel spasm worsens, CBFV subsequently increases. Though the
values that indicate cerebral vasospasm are unclear, an increase by 30cm/s or more
in CBFV in a particular territory likely indicates vasospasm.
23.3.2 Literature inSAH
Given that the MCA is the most accessible artery for TCD and that it feeds a major
hemispheric territory, the majority of the literature on TCD for SAH focuses on
insonation of the MCA via a trans-temporal window. Within the MCA territory,
values indicative of cerebral vasospasm are as follows. CBFV below 100cm/s is
unlikely to be associated with spasm, whereas those between 120 and 200cm/s
indicate potential vasospasm. Finally, CBFV above 200cm/s are thought to clearly
indicate the presence of vasospasm [9]. One other metric of MCA TCD in SAH is
called the Lindegaard ratio. This is the ratio between the mean ow velocity of
MCA (MFV
) and extra-cranial internal cerebral artery (ICA) MFV
MCA
through the insonation of the ICA in the neck). This ratio is also trended over time
as a method of monitoring for cerebral vasospasm. A ratio less than 3 indicates, in
the absence of increased MCA CBFV, no vasospasm. A ratio less than 3 with
increased MCA CBFV potentially signals hyperemia. A ratio between 3 and 6 indicates mild to moderate vasospasm. Finally, a ratio greater than 6 indicates severe
cerebral vasospasm [1, 9, 14].
Lindegaard Ratio LR MFVMFV
= /
MC
CA
(obtained
ICA
402
F. A. Zeiler and J. Teitelbaum
Numerous studies have been published linking the above MCA CBFV values
and Lindegaard ratio values to the risk of developing DCI. A recent systematic
review and meta-analysis have also been published in this context [14]. This review
found 17 unique manuscripts documenting objective TCD measures of CBFV and
the development of symptomatic cerebral vasospasm, or DCI, post-SAH.TCD evidence of vasospasm was dened as MFV
of 120cm/s or greater and a Lindegaard
MCA
ratio of 3 or greater. Overall, TCD-based assessment of the MCA in SAH patients
carried a 90% sensitivity (95% CI: 77–96) and 71% specicity (95% CI: 51–84) to
predict symptomatic cerebral vasospasm/DCI.However, this did not address the
association between TCD-based vasospasm and presence of angiographic conrmed spasm. Despite this oversight, the Neurocritical Care Society supports these
metrics, if one desires to employ TCD in for monitoring cerebral vasospasm in
SAH [9].
An algorithmic approach to standard TCD CBFV monitoring of the MCA in
aneurysmal SAH patients can be found at the end of this chapter, prior to the reference section (section 8.0). This provides a schematic for the approach to various
TCD-based CBFV recording values and Lindegaard ratio values, highlighting what
these values indicate and the potential risk for underlying cerebral vasospasm in the
SAH patient.
23.3.3 Limitations
There are clear limitations of this technique for monitoring DCI in SAH patients.
First, the reference ranges for MCA CBFV and the Lindegaard ratio are vague and
not entirely precise. Literature supports the potential for the presence of radiographic spasm in the absence of TCD abnormalities, thus highlighting its limitations. Second, the majority of the existing literature evaluates monitoring of the
MCA territory in SAH patients, and the reference ranges and quantitative ratio
measures described for the MCA are not readily described for other vascular territories. Both the anterior cerebral arteries (ACA) and posterior circulation are
difcult to insonate, not always being feasible for every patient. This does not
minimize the importance of being able to monitor them. Finally, the technique for
TCD is labor intensive and tedious, even with newer probe holding devices. Signal
is easily lost and sometimes difcult to re-obtain. Accurate measures require
trained staff. This all limits the duration of recording that is obtainable with current
commonly employed technology, leading to intermittent assessments of regional
cerebral vascular accessible through available patient TCD windows. Thus, longer
duration continuous recordings (i.e., over 30 min) are the exception, not the
expectation.
23 Subarachnoid Hemorrhage (SAH) in the Neuro-ICU: Usefulness of Transcranial…
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23.4 TCD forSemi-Intermittent Assessment ofCerebral
Autoregulation inSAH
23.4.1 Technical Requirements
Various techniques for cerebral autoregulation testing have been developed and are
described across the spectrum of neuro-pathologic conditions [11, 15–17]. A few
utilize TCD as a means of cranial monitoring. Most techniques employing TCD
refer to purely intermittent methods, either via thigh-cuff deation technique, transient hyperemic response, or orthostatic response testing [11, 15, 18]. All of these
intermittent techniques obtain spot measures of autoregulatory capacity either
through assessing direct changes in MCA CBFV or through the application of more
complex rst order differential equation modeling. These will not be cover in more
detail here, given they are intermittent and require direct manipulation of the
patient’s physiology.
Continuously updating measures of cerebral autoregulation are possible using
TCD, though we refer to them as “semi-intermittent” given the labor intensity of
TCD signal acquisition. These require either ofine or real-time complex CBFV
signal processing. With the advent of commercially available signal acquisition/
processing software, this signal manipulation is available for real-time application
within the NICU [19, 20]. The most widely described program for such application
in neurocritically ill patients is the software called intensive care monitoring plus
(ICM+) (Cambridge Enterprise Ltd., Cambridge, UK, http://www.neurosurg.cam.
ac.uk/icmplus). This software, like others, records physiologic signals from various
multi-modal monitoring devices employed within the NICU (including TCD), linking the high frequency digital signals (typically sampled at 100–200Hz) in timeseries, for further complex analysis techniques.
To assess cerebral autoregulatory capacity, we require assessing the relationship
between a surrogate measure of pulsatile cerebral blood volume (CBV) or CBF
(i.e., CBFV) and a driving pressure, either mean arterial pressure (MAP) or cerebral
perfusion pressure (CPP). This is done through assessing the response in slow waves
(i.e., frequency range 0.05–0.005Hz) of TCD CBFV to slow wave uctuations in
MAP or CPP [21, 22].
In order to obtain this information, high frequency (i.e., 100–200 Hz) digital
signals from TCD MCA CBFV and MAP (from arterial line) or CPP (from ICP and
MAP monitoring) are recorded. A non-overlapping moving average lter is applied
to these high frequency signals, to decimate the signal to 0.1 Hz, allowing for
assessment of slow wave responses. This frequency range has been linked to cerebral autoregulatory capacity [21]. Then, using time-domain analysis techniques, we
derive continuously updating moving Pearson correlation coefcients between
mean CBFV (also denoted MFV) and either MAP or CPP, using 30 consecutive 10s
windows of data (i.e., 5min of data), typically updated every minute. The most
commonly described TCD index of cerebral autoregulation is called mean ow
index (Mx– correlation between MFV and CPP), with its MAP version denoted
404
Table 23.2 TCD-based autoregulation/cerebrovascular reactivity indices and calculation methods
Pearson correlation
Signals
Index
correlated
Mx MFV and CPP 10 5 60
Mx-a MFV and MAP 10 5 60
Sx PSV and CPP 10 5 60
Sx-a PSV and MAP 10 5 60
Dx EDV and CPP 10 5 60
Dx-a EDV and MAP 10 5 60
CBF cerebral blood ow, CPP cerebral perfusion pressure, Dx diastolic ow index, Dx-a diastolic
ow index based on MAP, EDV End-diastolic ow velocity, MFV mean ow velocity, PSV Peak
systolic ow velocity, MAP mean arterial pressure, min minute, sec seconds, Mx mean ow index,
Mx-a mean ow index derived from MAP, Sx systolic ow index, Sx-a systolic ow index based
on MAP, TCD transcranial Doppler. Note: FVs = calculated using maximum FV over 1.5s period,
updated every 1s; EDV = calculated using the minimum FV over 1.5s period, updated every 1s
Signal
averaging (sec)
coefcient calculation
window (min)
F. A. Zeiler and J. Teitelbaum
Index calculation
update frequency (sec)
Mx-a (correlation between MFV and MAP) [16, 22]. For all of the described continuous indices of cerebral autoregulation, positive values typically denote
“impaired” autoregulation, while negative values are believed to denote “intact”
autoregulation. Table 23.2 displays the various TCD-derived indices of cerebral
autoregulation and method of derivation.
Note that in the absence of either an external ventricular drain or parenchymal
ICP monitor, CPP cannot be utilized in the derivation of these indices. However, the
MAP versions can be derived through either continuous blood pressure obtained
invasively through an arterial line or non-invasively through nger-tip-based blood
pressure cuff technology (Finapres Medical Systems, Netherlands, http://www.na-
pres.com). This non-invasive version of MAP monitoring allows for a completely
non-invasive means of cerebral autoregulation assessment through applying TCD
assessment of CBFV.
23.4.2 Literature inSAH
Though the current literature body on TCD-based cerebral autoregulation monitoring in SAH patients is limited, the results to date are promising [17, 23, 24]. One
small study found a link between progressive worsening in TCD base Mx index and
the incidence of large vessel vasospasm (p= 0.007) [25]. Another study of 98
patients found increased odds of developing DCI post-SAH when early (i.e., within
rst 5days) impaired autoregulation was found, when using TCD-based systolic
ow index based on MAP (Sx-a) (OR 7.46; 95% CI: 3.03–18.40, p<0.000001).
This was conrmed in multi-variate analysis (OR 12.66; 95%CI: 2.87–54.07,
p=0.001), including age, sex, WFNS grade, modied Fisher CT score, present of
23 Subarachnoid Hemorrhage (SAH) in the Neuro-ICU: Usefulness of Transcranial…
hydrocephalus, development of sepsis, metabolic derangements, and standard TCDbased assessment for cerebral vasospasm (i.e., MCA CBFV >120 cm/s and
Lindegaard ratio >3.0) [26]. Furthermore, the presence of bilateral impairment of
cerebral autoregulation, as measured by TCD-based Sx-a, was found to be linked to
worse outcome post-SAH, with those developing DCI having a larger interhemispheric difference in Sx-a measurements (p=0.035, 95%CI: 0.003–0.08) [27].
These results require validation in larger populations, but are promising for continuous cerebral autoregulation monitoring with TCD in SAH and its link to DCI.
405
23.4.3 Limitations
Despite the interesting application of complex signal processing and the promising
initial literature supporting its association with cerebral vasospasm post-SAH, there
are signicant limitations. First, it requires specialized software to record high frequency digital signals, later used for processing. It also requires integration of this
software with ICU monitoring devices, allowing for capture of digital physiologic
signals. Second, though recent software development has improved accessibility,
deriving these continuously updating indices requires some specialized knowledge
and training. Finally, the literature is currently limited and requires much further
validation before widespread application of this type of monitoring for clinical decision making in SAH patients.
23.5 Non-invasive Estimation ofICP
Though not indicative of cerebral vasospasm or DCI in SAH, elevations in ICP are
of interest to the treating physician, particularly in those SAH patients whom have
developed ischemic insults secondary to cerebral vasospasm. Current gold standard
ICP monitoring employs either the use of a ventricular catheter or parenchymal
pressure monitoring for the measurement of ICP.Both of these options are invasive
and require technical expertise for insertion, precluding their use by many physicians involved in the care of the SAH patients.
Recent literature suggests that through the application of TCD, one can potentially obtain a non-invasive estimation of ICP [28, 29]. This can be achieved through
three main methods: (A) use of TCD-based pulsatility index, (B) CPP estimation
method, and (C) mathematical modeling. Detailed exploration of these methods is
beyond the scope of this chapter, and we thus refer the reader to the referenced
articles for further information [28, 29]. Though promising, the future is still unclear
regarding this method of ICP estimation, but warrants mention in reference to
TCD in SAH.
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F. A. Zeiler and J. Teitelbaum
23.6 Future Directions
By exploring the above application of TCD in monitoring for cerebral vasospasm,
DCI, and their consequences in SAH, it can be seen that there exists a role for TCD
in this patient population. The main limitations of the above-mentioned monitoring
relate to the technical demands of TCD insonation and intermittent nature of recording. Recent advances in technology have led to the commercial availability of
robotic TCD devices, allowing for bilateral simultaneous insonation of the
MCA.These devices employ TCD sensor technology with an automatic algorithm
to aid with the set-up and acquisition of initial CBFV signal, followed by sensing
technology to correct for any shift in the head frame or signal loss during recording.
This automatic technology carries the potential to increase the speed and ease of
signal acquisition, followed by allowing for much long continuous recordings of
MCA CBFV.In addition, these devices are currently under evaluation and being
integrated with signal acquisition software, allowing for longer continuous assessment of cerebral autoregulatory capacity. Figure 23.3 displays an example of the
newer robotic TCD device (Delica EMS 9D System, Shenzen Delica Medical
Equipment Co. Ltd., China).
As these devices and technological advances like it become more available, the
role for TCD in SAH will surely expand and become more accessible to units where
expertise and staff availability for the application of TCD and prolonged recording
are limited. Furthermore, integration of TCD monitoring with other multi-modal
monitoring devices employed within the NICU (such as NIRS, cerebral microdialysis, CBF monitoring, and advanced neuro-imaging), and we will be able to gain
better understanding in the pathophysiologic process.
23.7 Conclusion
TCD monitoring in SAH for cerebral vasospasm and DCI is feasible and provides
potential for quick, non-invasive bedside monitoring. This currently requires assessing trends in TCD monitoring over time via region-specic transcutaneous cranial
windows. The technique caries limitations given its labor intensity, which may be
overcome with emerging technological advances in TCD monitoring.