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11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
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11.3.4 Autoregulation
Cerebral blood ow autoregulation refers to the intrinsic ability of the brain to
maintain a stable cerebral blood ow (CBF) despite uctuations in cerebral perfusion pressure [35]. In many neurological diseases (including TBI, stroke), an impairment of this autoregulatory response has been demonstrated [36, 37] and seems that
the degree of impairment is related to poor outcome.
Traditionally, assessment of cerebral autoregulation has been performed under
steady-state conditions, at constant baselines ABP and CBF, and then another
steady-state measurement was performed following manipulation of ABP.Many
authors adopted TCD as a static model for autoregulation assessment in patients
using the static autoregulatory index or static rate of regulation, dened as the net
change in cerebral blood ow following the manipulation of cerebral perfusion
pressure under steady state [38, 39].
Although for decades this classic static approach has been widely applied in
clinical practice, it does not take into account different factors including the different upper and lower limits of autoregulation or different slopes of the “autoregulatory zone” among different individuals [40]. Thus, the investigation of dynamic
cerebral autoregulation using TCD is an area of signicant research given the high
temporal resolution, which allows to measure the timing and the magnitude of the
changes of CBF to the CPP/ABP challenge. This “dynamic” approach uses the
induced or spontaneous rapid changes in ABP as an autoregulatory stimulus and
compares ABP and CBFV during the whole autoregulatory process (dynamic pressure autoregulation) [41].
In brain monitoring, TCD/TCCS can be useful to calculate an index of autoregulation called mean ow index (Mx) which is the correlation coefcient index
between MFV and CPP [42]. Zero or negative correlation indicates preserved autoregulation, whereas a positive correlation between CPP and CBFV indicates
impaired autoregulation. Mx index has shown to be strongly associated with poor
outcome at 6 months in patients with impaired autoregulation after severe head
injury [57]. More recently, Budohoski etal. [43] demonstrated in a cohort of 300
head-injured patients that a new autoregulation index, the Sx index (correlation
between PSV and CPP), shows a stronger association with the patient outcome
than Mx.
Despite the wide and generally accepted value of TCD in the assessment of cerebral autoregulation, this technique has some limitations. Measurements of CBFV
are frequently only taken from the MCA, and thus autoregulatory changes in the
posterior circulation may not be detected [44]. Moreover, TCD-based studies use
CBFV as a surrogate measure of CBF.However, CBFV is only proportional to CBF
when vessel cross-sectional area remains constant, as previously mentioned.
204
nICP ABPnCPP= –.
C. Robba and D. Cardim
11.3.5 Non-invasive ICP andCPP
ICP evaluation and management is crucial in many neurological diseases, and it is
commonly measured through intraventricular or intraparenchymal catheters which
are accurate, but their invasive nature and related complications preclude their use
in many conditions such as coagulopathy [45, 46]. TCD/TCCS waveform analysis
has been widely investigated as a technique for nICP estimation.
TCD-derived nICP methods are based on the relationship between ICP and indices derived from cerebral blood ow velocity. The correlation between PI and ICP
has been extensively studied. However, reports on its usefulness for predicting ICP
and CPP are discordant [47, 48]. Bellner etal. [25] found a signicant correlation
(R=0.94, P<0.0001) between invasively measured ICP and PI, with good sensitivity and specicity to detect ICP > 20 mmHg. Other authors found less positive
results; Zweifel et al. [26] in a cohort of 290 patients found a weak correlation
between PI and ICP (0.31; P<0.001), with a 95% prediction interval of ICP values
wider than ±15mmHg. In a recent study, Cardim etal. [12] demonstrated a nonsignicant correlation between nICP derived from PI and ICP measured invasively.
The role of PI in the assessment of ICP is not clear, and the variability of these
results can be explained by the fact that increase in PI is not specic to increase in
ICP.PI can increase following a decrease in CPP and ABP, or during decrease in
partial pressure of CO
Many authors have proposed mathematical models that simulate the cerebrovascular dynamics using simultaneous CBFV and ABP measurements. In a Black-Box
model for estimation of ICP, the intracranial compartment is considered a black-box
system, with ICP being a system response (output signal ICP) to the incoming signal ABP (input signal). Cardim etal. [12] evaluated the black-box method in a
cohort of 40 TBI patients, obtaining a moderate correlation with measured ICP
(R=0.39, P<0.05). Other mathematical models have also been proposed, such as
the cerebrovascular dynamics model for non-invasive estimation of ICP according
to Heldt [49].
Many authors have also studied and proposed methods based on the primarily
intended calculation of non-invasive cerebral perfusion pressure (nCPP), and secondarily calculating non-invasive ICP based on the assumption that (Eq.11.5)
or increase in pulsatility of ABP waveform [5].
2
Aaslid etal. [50] rst developed a mathematical model for non-invasive estimation of CPP based on transcranial Doppler waveform analysis based on spectral
pulsatility index and the rst harmonic component of the arterial blood pressure, but
this method demonstrated low accuracy.
Czosnyka etal. [51] proposed a similar but modied formula, based on the waveform analysis of CBFV, which uses the EDV for the estimation of nCPP. In 96
patients suffering from head injury, the correlation between nCPP and measured
CPP was R=0.73 (P<0.001), with estimation error less than 15mmHg and in 84%
of the examinations.
(11.5)
11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
Varsos etal. used a method based on CrCP [52]. According to this method, nCPP
seems to be correlated with measured CPP (R=0.85, P<0.001), with a mean±SD
difference of 4.02±6.01mmHg, and 83.3% of the cases with an estimation error
below 10mmHg [52].
Considering the distinct categories for nICP estimation, there has been a considerable variability in the reported accuracy of these methods, and various methods
demonstrated wide condence intervals for prediction and remain to be fully validated [53]. Nevertheless, it is known that even the standard invasive techniques
might not comply with the specied limits for error [54–56]. Thus, it is debatable
whether these accuracy requirements are realistic for all sorts of ICP monitoring.
In view of this, an important concept that should be stressed is ICP not solely “as
a number,” once dynamical features of this parameter, such as its waveform and
relative changes in time, are fundamental for a proper assessment of the clinical
state of the patient [57]. Therefore, despite the intrinsic limitations and inaccuracy
to predict ICP mean absolute values, TCD-based nICP methods may have a potential clinical utility since this technique allows a non-invasive assessment of cerebral
circulation dynamics as ICP changes over the time domain.
These features also allow tracking nICP changes in real time in a variety of clinical settings (emergency rooms, ambulatories, operating theaters). This is one of the
advantages of transcranial Doppler ultrasonography and may become particularly
useful as a primary assessment tool in centers where ICP monitoring is not routinely
applied or unavailable. It may also suit patients in whom invasive ICP monitoring
may not be clearly indicated (mild closed head injury, for example) or contraindicated (coagulopathy, for instance).
205
11.4 Applications ofTCD/TCCS Monitoring
inClinical Practice
11.4.1 Traumatic Brain Injury
Traumatic brain injury (TBI) is a relevant cause of morbidity and mortality, and
several important disturbances of cerebral hemodynamics occur after TBI, including hyperemia, cerebral ischemia, and vasospasm.
Monitoring and targeted management of ICP and CPP are necessary for patients
with severe traumatic brain injury. Intracranial hypertension and low CPP are associated with poor outcome, and the literature is clear about the importance of a strict
neuromonitoring in order to avoid secondary brain insults [58].
TCD has been widely applied in TBI patients, in particular, for the assessment of
ICP and CPP in human and animal studies [12]; moreover, some authors showed
that impaired autoregulation, determined by TCD methods (Mx or Sx index), is
strongly associated with poor outcome at 6months [42, 43]. TCD demonstrated to
be useful in TBI patients as it is able to avoid the use of invasive techniques for the
measurement of CBF and provide similar prognostic information [43].
206
C. Robba and D. Cardim
TCD can be also useful in TBI patients for the assessment of cerebral dynamics
and cerebral swelling through the calculation of cerebral compliance. Hyperemia
may occur a few hours after TBI, lasting 2 to 4days, and also be assessed using
TCD patterns suggestive of high vascular resistance, consistent with elevated intracranial pressure [59], or following an ischemic event.
EDV and PI have been shown to have a role in the decision between “fast track”
and standard ICP monitoring at admission in patients with TBI [60]. In the emergency room, TCD might complement brain computed tomography scan and clinical
examination to screen patients at risk of further neurological deterioration after
TBI.In a recent study [61], transcranial Doppler parameters showed a strong negative predictive value (NPV) in TBI patients who did not undergo secondary neurologic deterioration, and patients with abnormal TCD patterns had greater disability
4weeks after TBI.
11.4.2 Aneurysmal Subarachnoid Hemorrhage
Aneurysmal subarachnoid hemorrhage (aSAH) has an incidence of 6–10 per
100,000 people per year [62], with a 6-month mortality rate ranging from 32 to
67%, and 30% of survivors harbor permanent neurological impairment [63].
In 20 to 40% of patients, new ischemic neurological decits that were not present
on hospital admission become apparent in the days and weeks following the ictus
and are mainly associated with vasospasm consequent to aSAH.Vasospasm usually
occurs 3 to 14days following aneurysmal subarachnoid hemorrhage (aSAH), and it
is known to be one of the causes leading to delayed cerebral ischemia (DCI) and
poor outcomes [64].
Angiography is considered the gold standard for the detection of vasospasm;
however, TCD has been extensively used for monitoring patients with aSAH, and it
has been demonstrated to be able to assess vasospasm and monitor and guide the
clinical treatment (triple-H therapy, angioplasty, etc.) [65].
TCD for the detection of vasospasm, usually performed on the MCA, has been
studied by several authors. TCD is able to detect vasospasm as the constriction of
the cerebral vessels leads to an increase of cerebral blood ow velocities [65].
According to a recent meta-analysis [66] including 2870 patients, TCD was
found to be highly predictive of evidence of vasospasm in patients with aSAH with
sensitivity of 90% (95% condence interval (CI) 77%–96%), specicity of 71%
(95% CI 51%–84%), positive predictive value (PPV) of 57% (95% CI 38%–71%),
and NPV of 92% (95% CI 83%–96%) at pooled estimates for TCD diagnosis of
vasospasm.
Vora etal. [66] in a retrospective study of 101 patients found that MCA means
ow velocity higher than 120cm/s had a specicity of 72% and sensitivity of 88%
for ≥33% of angiographic vasospasm with a NPV of 94% for MFV< 120 cm/s.
Moreover, MFV>200cm/s was 98% specic and 27% sensitive with a PPV of 87%
for angiographic vasospasm of ≥33%.
11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
207
To differentiate an increase of the CBFV related to systemic hyperdynamic ow
and vasospasm, the Lindegaard ratio (LR) [67] is normally used, which is dened as
MFV on the MCA divided for the extracranial ICA MFV.LR<3 indicates hyperdynamic ow (hyperemia) and >3 indicates vasospasm. Mild vasospasm is dened
as MFV > 120 and <149 cm/s (LR = 3–6); moderate vasospasm is dened as
MFV > 150 and <199 (LR = 3–6) and severe vasospasm as MFV > 200 cm/s
with LR>6.
TCD has been extensively used for the detection of cerebral vasospasm showing
good sensitivity and specicity, but TCD can also have a role in the detection of
cerebral autoregulation after aSAH.Late detection of impaired cerebral autoregulation in these patients [68] is associated with increased risk to develop DCI independently of the incidence of vasospasm [69], and it is associated with poorer
outcome [70].
11.4.3 Stroke
In patients affected by internal carotid artery (ICA) stenosis, impaired autoregulation assessed by signicant increases in Mx and decreases in dynamic autoregulation index observed in the pathological stenoocclusive arteries have shown to
correlate with the degree of stenosis and is considered a tool to identify patients at
risk of stroke and for need of surgical decompression [71]. For instance, in a cohort
of 48 patients with angiographic occlusion, TCD showed an overall sensitivity of
83% and specicity of 94%, especially in the anterior circulation [72].
TCD can also be a reliable prognostic indicator in MCA occlusive stroke [73],
and its role in the assessment of cerebral autoregulation after stroke has been extensively studied. Some authors have consistently shown an impairment in ipsilateral
cerebral autoregulation and an association with the need for decompressive surgery,
neurological decline, and poor outcome [44].
TCD may also have a role in the prediction of outcome in patients with stroke,
according to the site and severity of occlusion observed. In a study of 335 patients
with acute stroke who received thrombolytic treatment, distal MCA occlusions
assessed through TCD were associated with the greatest chance of early recanalization (44%), compared with 30% in the proximal MCA, 30% in the basilar artery,
and <10% in the terminal ICA [74].
Despite the important role of TCD in patients with ischemic stroke, CTA and
MRI are still considered rst-line imaging techniques due to the operator dependency and poor ability of TCD to access the posterior cerebral circulation [6].
208
C. Robba and D. Cardim
11.4.4 Other Clinical Scenarios
TCD presents a wide range of clinical applications in the context of anesthesiology,
neurology, neurosurgery, and neurointensive care settings (Table11.2).
Besides the common previously described applications in neurointensive care
settings (TBI, SAH, stroke), it has been successfully applied in the diagnosis of
brainstem death [75] in central nervous system infections and in many ischemic
cerebrovascular diseases (sickle cell disease, right to left cardiac shunt, venous
thrombosis) in adult and pediatric populations [6, 76, 77].
Moreover, TCD is gaining interest even in the intraoperative settings. It has been
successfully applied in order to assess nCPP and nICP in surgical procedures at risk
of intracranial hypertension [78, 79], such as laparoscopic procedures with pneumoperitoneum and Trendelenburg position [80]. It has been also successfully used for
neuromonitoring during carotid endarterectomy or during cardiopulmonary
bypass [81].
Growing and recent evidences support the use of TCD even in metabolic coma
(such as during liver transplant or hepatic encephalopathy) or in pregnant patients to
assess autoregulation and cerebrovascular changes as prognostic factor for preeclampsia and cerebrovascular events during pregnancy [82].
Finally, TCD has been recently applied in septic patients to assess nCPP and
PI.Some authors found higher values of PI and cerebral vascular constriction in
septic patients compared to control group, suggesting a possible role of TCD in the
assessment of the mechanisms underlying the pathogenesis of sepsis-related
encephalopathy [83].
11.5 Conclusion
The non-invasiveness, repeatability, portability, and high temporal resolution of
TCD have promoted the wide use of this technique, especially for bedside monitoring of CBF in the neurocritical care settings.
Invasive techniques still appear to remain the gold standard across most of the
clinical applications; moreover, operator dependency and the need for an appropriate temporal window are signicant limitations to TCD clinical utility.
However, despite some limitations including operator dependency and 10–20%
of patients having inadequate transtemporal acoustic windows, TCD remains a
valuable tool for the assessment of cerebral hemodynamics in critically ill patients.
Its wide utility as a diagnostic tool makes it a useful “stethoscope for the brain.”
INTENSIVE CARE UNIT (ICU)
11 Neurocritical Patient in ICU: Transcranial Doppler (TCD/TCCS) as the Brain…
Algorithm
EMERGENCY DEPARTMENT (ED)
Clinical Status of Patient
ABCD
Level of consciousness (Glasgow)
Bilateral Pupillary reactivity
Hemodynamic stability?
Oxigenation?
DIAGNOSIS
Subarachnoid Hemorrhage (SAH) Ischemic Stroke Traumatic Brain Injury (TBI)
CNS infection (Meningitis/Encephalitis) Intracerebral Hemorrhage (ICH) Acute Liver Failure (ALF)
Brain Tumors Preeclampsia Neurosurgery Peri-operative
Brain Death Sickle Cell Disease Sepsis - Delirium
Cerebral Venous Thrombosis Right to Left cardiac shunt
Multimodal Monitoring (MMM)
Transcranial Color-Coded duplex Sonography (TCCS)
Transcranial Doppler (TCD)
209
Flow Velocity (FV) Pulasatility Index (PI) Autoregulation (AR) CrCP & Wall Tension (WT)
Spectral Waveform
Qualitatives – Quantitatives
Changes
(Trends)
PSV / MFV / EDV Spectral Waveform Changes? Zero or negative value
Cerebral arterial Compliance (Ca) Cerebrovascular Time Non-invasive ICP/ CPP
Compliance of Intracranial space (Ci)
Cerebral Compliance
Ca→ABP ⇔ CaBV
Ci
BASIC SIGNALS ADVANCED SIGNALS
ICP
PI: (PSV – EDV) / MFV
0.5 – 1.1
Cerebral vascular resistance
TCD/TCCS – based index
CaBV
TAU = Ca x CVR (sec.)
Constant (TAU) (nICP) / (nCPP)
Time → Changes→
Dynamic AR
Indexes Measurement
MFV & CPP (Mx)
PSV & CPP (Sx)
(AR is preserved)
Positive value
(Impaired AR)
Pressure (mmHg)
Measurements
CrCP (mmHg)
DCM (mmHg)
ESTIMATE
ICP
CPP
Pressure (mmHg)
nICP = ABP - nCPP
ABCD Airway-breathing-circulation-disability, CPP Cerebral Perfusion Pressure, ICP Intracranial
Pressure/MFV Mean ow velocity, EDV diastolic ow Velocity, PSV Peak systolic ow velocity,
Ca Cerebral arterial compliance, Ci Compliance of intracranial space, CVR Cerebrovascular
resistance
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