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R. R. Gill et al.
particularly high risk [24, 25]. Black, Hispanic, Indian, and Asian populations have
the highest prevalence of ICA stenosis with risk of IAD-related stroke as high as
30–50% in Asian populations [28].
The gold standard evaluation of the intracranial vasculature remains catheter
angiography, but it is an invasive procedure which comes with risks. Clinicians
often turn to non-invasive alternatives such as magnetic resonance angiography
(MRA), computed tomographic angiography (CTA) and TCD, which are safer,
more practical, and cost effective. Angiographically veried severe stenosis of
70–99% portends an increased risk of stroke recurrence compared to moderate stenosis (50–69%). Robust collateral circulation mitigates this increased risk to some
degree [29]. This high risk was also profoundly reduced with aggressive medical
management, putting an emphasis on early non-invasive identication with the goal
of primary and secondary stroke prevention.
The validity of ultrasound in the evaluation of the extracranial carotid arteries as
both a screening and diagnostic tool is well established. The utility of TCD to evaluate for intracranial stenosis (Table 27.1) is less well described, particularly in the
vertebral-basilar circulation. Factors limiting the reliability of TCD include the
hemodynamic effects of coexisting stenotic lesions proximal to the region being
assessed (e.g., extracranial disease) or the effect of collateral circulation on TCD
velocities.
The Stroke Outcomes and Neuroimaging of Intracranial Atherosclerosis
(SONIA) study was a companion study to the Warfarin-Aspirin Symptomatic
Intracranial Disease (WASID) trial aimed to dene the ability of TCD and MRA to
diagnose and quantify the severity of intracranial atherosclerosis of 50–99% compared to cerebral angiography [28]. SONIA was a prospective multicenter study
utilizing standardized, reproducible ultrasound protocols and diagnostic criteria to
identify large vessel intracranial stenoses of 50–99%. The study demonstrated the
ability of TCD to reliably exclude the presence of moderate and severe intracranial
stenosis, utilizing a mean ow velocity (MFV) cutoff of 80cm/s in both the VA and
BA.By adjusting the cutoff MFV to 130cm/s, TCD maintains a strong NPV to
exclude severe intracranial stenosis in the VA and BA [29].
The vertebrobasilar circulation shows considerable variability in its size and
course limiting the sensitivity and specicity of TCD in detecting vertebrobasilar
stenotic lesions. A novel approach combining velocity cutoffs in conjunction with
the stenotic/pre-stenotic ratio for ≥70% stenosis demonstrated improved sensitivity
with good agreement with digital subtraction angiography [29, 30]. In the VA/BA,
Table 27.1 Mean TCD
velocities in the assessment of
intracranial atherosclerosis [30]
Mean velocity
Blood vessel
Vertebral 80cm/s 110cm/s
Basilar 80cm/s 130cm/s
MCA 100cm/s 240cm/s
ICA 90cm/s 120cm/s
≥50% Stenosis ≥80% Stenosis
27 Acute Neurologic Injury in the ICU: Role of Transcranial Doppler in Disorders…
469
a MFV>110cm/s or a stenotic/pre-stenotic ratio (SPR) of ≥3 had a sensitivity of
60% and specicity of 95% [30]. This approach shows good agreement with invasive angiography and may be a reasonable cost-effective alternative in resource limited settings. TCD may also supplement other forms of non-invasive imaging, with
concordant ndings potentially eliminating the need for conventional angiography.
27.7 TCD: Microembolus Detection
Transcranial Doppler is the only modality capable of detecting circulating cerebral
microemboli, both gaseous and solid (e.g., brinogen, cholesterol, platelets).
Diseases commonly associated with intracranial microemboli include carotid stenosis, arterial dissection, atrial brillation, patent foramen ovale, and mechanical cardiac valves as well as during vascular surgical procedures to address the
aforementioned conditions [7, 31]. These intracranial microthrombi can be detected
on TCD as microembolic signals (MES). The clinical signicance of MES in the
posterior circulation remains unclear; for example, the presence of intracranial arterial emboli on TCD in a case suspicious for dissection can aid in establishing a
diagnosis and prompt further evaluation, but in itself MES are not diagnostic.
Detection of intracranial emboli makes the likelihood of an ischemic event much
higher [31]. High-intensity transient signals (HITS) are characteristic and are the
result of backscatter of ultrasound waves from gaseous or solid microemboli on
TCD [7]. Brief (<0.01–0.03second) unidirectional high intensity increases within
the Doppler frequency spectrum (>3dB) producing a characteristic “chirp,” “click,”
or “whistle” sound during TCD insonation occurring randomly characterize
HITS. Technical difculties of vessel insonation can be overcome by power M-mode
Doppler (PMD) which uses multiple sample gates placed with 2 mm spacing
increasing the ease of insonation through transcranial windows [31].
While the vast majority of MES are clinically silent, patients with microemboli
appear to have an increased macroembolic risk. TCD assessment for microemboli
can help tailor therapeutic interventions in this population such as antithrombotic
therapy or endovascular intervention [32, 33].
A Korean trial studied the utility of MES in patients with acute neurological
symptoms referable to posterior circulation ischemia [34]. The study protocol used
a 2-MHz transducer mounted to the head using a xed frame and required insonation
of the basilar artery for 30 consecutive minutes through a suboccipital window.
HITS were required at two insonation depths to conrm MES [34]. MES were
detected in 13% of patients and were strongly associated with intracranial, but not
extracranial, vertebrobasilar artery stenosis [34]. MES occurred more frequently in
patients with severe degree of V-BA stenosis and were more common in patients
with lesions on diffusion weighted MRI.An optimal timing of MES testing, relative
to stroke onset, has not been established for the posterior circulation. Quantication
and subsequent grading of MES in the posterior circulation has not been utilized as
470
R. R. Gill et al.
it has in the assessment of MES in right to left cardiac shunts with the International
Consensus Criteria (ICC) or Spencer’s Logarithmic Scale.
In stroke patients with posterior circulation symptoms, the presence of MES in
the vertebrobasilar circulation suggests the possibility of large artery vertebrobasilar disease, which may be atherosclerotic or due to dissection. The severity of stenosis appears to correlate with the likelihood of detecting MES. Autopsy studies
also suggest that extracranial atherosclerotic disease of the posterior circulation less
often embolizes to cause stroke than intracranial stenosis [34]. TCD for MES detection in the vertebrobasilar circulation can be a useful tool in guiding the management of patients with acute ischemia in the posterior circulation.
27.8 Intracardiac Right toLeft Shunt
Intracardiac right to left shunt (RLS) has been implicated in stroke (particularly in
patients <60years old and all patients with cryptogenic stroke), migraine and cluster headache, obstructive apnea, and hypoxemia and is most commonly caused by a
patent foramen ovale (PFO) [35]. A PFO is present in 20–25% of the general population as a remnant of the fetal circulation, and transcatheter closure has evolved
into a viable treatment for PFO in recent years. This necessitates accurate diagnosis
of PFO with transesophageal echocardiogram (TEE) remaining the gold standard
diagnostic approach. However, the invasive nature of TEE and the requirement for
sedative anesthesia make it less than ideal when screening populations with disease
states which implicate PFO as a potential etiological factor. In this light, the gaseous
contrast TCD (“bubble study”) has emerged as a practical and cost-effective
alternative.
During a contrast TCD study, a solution with microbubbles is injected peripherally during continuous TCD examination, ideally with power mode for increased
sensitivity. A Valsalva maneuver is performed 4–6 seconds after injection of the
gaseous contrast medium, causing an increase in right atrial pressure and an increase
in ow through a potential PFO.A signicant reduction in TCD mean ow velocity
of the insonated vessel indicates an adequate Valsalva maneuver. TCD monitoring
is continued for a further 16–20 seconds and the number of MES counted and
graded using the International Consensus Criteria (ICC) or Spencer’s Logarithmic
Scale [36]. A meta-analysis of 27 studies and 1968 patients compared gaseous contrast TCD with TEE and found the weighted mean sensitivity to be 97% and specicity to be 93% [37]. The vast majority of existing studies utilize the MCA as the
vessel insonated in their evaluation.
In situations where TCD of the MCA cannot be performed due to an insufcient
transtemporal window, insonation of the BA through a transoccipital window is a
viable and reliable alternative. In a study by Del Sette and colleagues (2007) comparing the right MCA to the vertebrobasilar circulation, the vertebrobasilar circulation achieved a sensitivity of 83.7% and a specicity of 100% [35]. This improved
to 100% sensitivity and specicity for only medium and large shunts. A similar
study by Guo etal. (2016) showed no signicant difference between the VA and
27 Acute Neurologic Injury in the ICU: Role of Transcranial Doppler in Disorders…
MCA, both achieving excellent sensitivity and specicity [38]. TCD of the vertebrobasilar circulation is thus a practical, cost-effective, and highly accurate means
of diagnosing a clinically signicant PFO.
471
27.9 Subclavian Steal Syndrome
Proximal high-grade steno-occlusive disease of the pre-vertebral subclavian artery
(SA), most commonly due to atherosclerotic vascular disease, can lead to a phenomenon known as subclavian steal syndrome. In subclavian steal syndrome (SSS),
exertion of the arm that is supplied by the stenotic SA results in a drop in SA pressure distal to the lesion. This results in redirecting ow from the contralateral VA via
the BA in a retrograde direction down the ipsilateral VA and away from the posterior
cerebral circulation. Occasionally, this ow pattern may even be seen at rest. Most
often SA stenosis is clinically silent and may be found incidentally with an observed
blood pressure difference in the upper extremities (the left SA is affected in a 4:1
ratio compared to the right). Clinical consequences of subclavian steal include arm
ischemia, which is most common, and vertebrobasilar ischemia which occurs more
often in patients with concurrent cerebrovascular lesions. Symptoms may include
dizziness and vertigo, ataxia, drop attacks, and decits associated with the cranial
nerves; however, symptoms often persist after correction of SA stenosis or improvement in retrograde VA ow, suggesting in many cases the steal is not the cause of
presenting symptoms [39].
Duplex ultrasonography can diagnose SA stenosis with a peak systolic velocity
>240cm/s being predictive of a >70% stenosis [40]. It can also assess the extracranial VA for ow reversal, which has been shown to be intermittent in 30% and permanent in 65% of patients with >80% SA stenosis. TCD can further evaluate the
direction of ow in the BA and this may be more predictive of symptoms as patients
who have antegrade ow in the BA are less likely to be symptomatic. Less than 25%
of patients with retrograde ow in the VA were found to have a corresponding reversal of ow in the BA [41]. If the symptomatic vertebral artery waveform appears
normal or shows only absent diastolic ow proceed with provocative maneuvers
such as raising the arm, squeezing a ball, or inating and deating a blood pressure
cuff on the affected side. In patients with conrmed symptoms attributable to SA
stenosis and demonstrable retrograde vertebral and basilar ow, therapeutic options
such as stenting or surgery can be considered.
27.10 TCD: Multimodal Monitoring
Multimodality monitoring has become an important tool in the management of critical ill patients in the Neuro ICU.Information gathered from intracranial pressure
(ICP) monitors, jugular bulb oximetry, brain tissue oximetry, cerebral microdialysis, near infrared spectroscopy, and electroencephalography often guides clinical
472
R. R. Gill et al.
management. TCD may be considered a component of multimodality monitoring in
the Neuro ICU, either supplementing information gleaned from these other monitors or serving as a surrogate for invasive neuromonitoring. TCD may provide noninvasive estimations of cerebral perfusion pressure (CPP) and ICP and can describe
cerebral hemodynamics including cerebrovascular reactivity and cerebral pressure
autoregulation [42]. These measurements are largely derived from anterior circulation TCD assessments and are beyond the scope of this chapter. Cerebral autoregulation and vasomotor reactivity are important parameters in severe brain injury and
are described briey.
Cerebral pressure autoregulation represents the relationship between CBF and
CPP. Autoregulation is a physiologic mechanism that serves to reduce the variation
in CBF when CPP varies between 50 and 150mmHg. The cerebral vessels take time
to react to spontaneous physiological perturbations (changes in CPP, PaCO2, PaO2)
or induced ones (breath holding, Valsalva maneuver). Fast responses reect
mechano- elastic properties of the cerebrovascular bed, such as cerebrovascular
resistance and compliance [42]. Slow responses reect cerebral autoregulation.
TCD allows non-invasive measurement of both the static and dynamic autoregulatory response. Static autoregulation is calculated by augmenting blood pressure,
typically with pressors, while recording MCA ow velocities and MAP. The estimated CVR is CVRe=MAP/FV [42]. The static rate of autoregulation (SRoR) is
the ratio of percent change in CVRe to MAP, or CPP if ICP is available [42]. An
SRoR of 100% suggests perfect autoregulation, while an SRoR of 0% connotes
complete failure of autoregulation [42]. Dynamic autoregulation is tested by measuring the time to recovery of ow velocities after a rapid but transient decrease in
mean blood pressure. This may be accomplished by the leg cuff test wherein a
modied blood pressure cuff is placed around one or both thighs and inated to
50mmHg above the systolic pressure for 3minutes. Deation produces an abrupt
drop in blood pressure. The time it takes for blood pressure and mean ow velocities
to normalize is measured and tted to a series of curves in a validated algorithm
[43]; this determines the rate of dynamic cerebral autoregulation or autoregulation
index (ARI). The threshold between good and disturbed autoregulation is an ARI
of 5 [44].
Vasomotor reactivity (VMR) represents the cerebrovascular response to uctuations in arterial CO
concentration with rapid adjustment of cerebrovascular resis-
2
tance. Hypercapnia or elevated arterial PaCO2 can be provoked in a number of ways
to evaluate the cerebral blood ow velocity response, the simplest being voluntary
breath holding, breathing CO2 or pharmacologically with the administration of acetazolamide in patients who cannot voluntarily breath-hold. Control of ventilation in
intubated patients can also be utilized in the ICU. Hypercapnia leads to cerebral
arteriolar vasodilation, via changes in extracellular pH, and subsequent increase in
MFV on TCD examination of the upstream larger cerebral arteries which can be
insonated with TCD [7]. Hypocapnia can conversely be triggered with induced
hyperventilation and has a vasoconstrictive cerebrovascular response. Vasomotor
reactivity may become impaired in arterial stenotic diseases and cerebral ischemia
and can be quantied as the percentage change in MFV.The breath holding index
27 Acute Neurologic Injury in the ICU: Role of Transcranial Doppler in Disorders…
473
(BHI) is the change associated with a timed breath hold and several studies have
shown a similar degree of reactivity in the anterior circulation (MCA) and the BA
following the same change in PaCO2 [45, 46]. Cerebrovascular reactivity can help
guide the management of patients who may require revascularization procedures
and has been shown to predict a higher rate of annual distal cerebral ischemic events
in patients with ICA stenosis and impaired VMR [47].
The application of vasomotor reactivity exclusively to the posterior circulation is
sparse. Park and colleagues evaluated a small cohort of patients with occlusive vascular disease in the anterior circulation and assessed the BA for VMR as it may
serve as a critical collateral supply to the impaired anterior circulation in these
patients. Patients with anterior circulation stenotic disease showed increased baseline MFV in the BA and impaired VMR [48]. This may represent a novel adjunctive
assessment, which may guide clinicians in the management of patients with intracranial and extracranial stenotic disease of the anterior circulation.
27.11 TCD: Traumatic Brain Injury
Traumatic brain injury (TBI) has been classied as a serious public health concern
by the Centers for Disease Control and Prevention. The mainstay of treatment in
TBI is pre-empting or mitigating secondary injury, as secondary ischemic brain
injuries are the major prognostic factors after severe TBI.Despite the fact that TBI
is a very heterogeneous disease, TCD shows considerably promise to guide management and predict outcomes in both mild and severe forms of injury. Similarly,
TCD appears useful in both pediatric and adult populations [49, 50].
In mild injury, TCD is largely used to identify patients without intact cerebral
autoregulation. Cerebral autoregulation denoted by the autoregulation index (ARI)
is dened as ARI=% ΔeCVR/% ΔMAPe, as noted above [41]. In sports related
concussion, TCD may demonstrate persistent impairment of autoregulation for up
to 5 days post-injury, despite a normal clinical exam as dened by the Glasgow
Coma Score (GCS) [51]. Disturbances of autoregulation may be more associated
with hemorrhagic lesions than other traumatic lesions [52]. TCD with tilt table testing may identify impairments of cerebral autoregulation in nearly 50% of pediatric
patients with complicated mild TBI [52]. The vast majority of disturbances are unilateral (70%) although over 30% of those patients with disturbed autoregulation
exhibit bilateral involvement [53]. In patients with complicated mild TBI (GCS
13–15), disturbances of autoregulation often persist until after hospital discharge
[51, 53].
TCD may be used to identify severe TBI patients with cerebral hypoperfusion, a
signicant predictor of long-term functional outcome. Hypoperfusion is typically
dened by a mean velocity (MFV
) of <35cm/s, end-diastolic velocity (EDV
MCA
<20cm/s, and/or pulsatility index (PI) >1.4 [52–54] In severe TBI, patients may
have cerebral hypoperfusion despite mean arterial pressures in target range [55]. In
one of the largest TCD studies of 255 severe TBI patients, TCD identied
MCA
)
474
R. R. Gill et al.
hypoperfusion in 28% of patients, of whom nearly all died [53]. Studies suggest that
TCD, albeit anterior circulation thresholds, may be used to guide early brain resuscitation and to dene optimal cerebral perfusion pressure targets [55].
Cerebral vasoreactivity (CVR), a measure of hemodynamic reserve, may also be
assessed by TCD after TBI.As previously mentioned, CVR is assessed by evaluating
the response to changes in the arterial content of carbon dioxide. Studies show that
CVR may be impaired as early as 4days and remain impaired for months after mild
or concussive injury despite symptom resolution [51]. Importantly, CVR impairment after TBI is associated with gray matter atrophy [55–57], headache [51–53]
and cognitive decits [58].
TCD may also be used to assess stroke risk in patients with TBI.Among patients
with blunt cerebrovascular injury, TCD with MES may be used to predict risk of
stroke [59]. Patients with known carotid artery dissection and MES by TCD are at
higher risk for embolism in a dose dependent manner. However, TCD with MES
appears to be ineffective at monitoring stroke risk from extracranial vertebral injuries [59]. TCD may also be used to assess the risk of arterial narrowing after
TBI.The incidence of arterial narrowing in the MCAs after TBI is near 30%; over
50% of patients with evidence of MCA vasospasm experience death or disability
[54]. BA vasospasm may be particularly important in the cause of secondary brain
injury in TBI [52].
27.12 TCD: Brain Death Determination
Brain death, or the nal clinical expression of complete and irreversible neurologic
coma, was rst described in 1959 and has gone through several iterations of denition, which vary from country to country, and even among hospitals within a nation.
The American Academy of Neurology (AAN) denes brain death as a complete
lack of evidence of responsiveness (coma) with a complete lack of brain stem
reexes on clinical assessment and an absent respiratory drive as demonstrated with
an apnea test [60].
However, in some situations, the exam nding may be inconclusive or ambiguous, or performing a clinical exam may be limited by factors such as facial trauma
or pre-existing conditions such as post-operative pupil dysfunction. In these cases,
ancillary testing such as cerebral angiography, electroencephalogram (EEG) and
transcranial Doppler (TCD) can be used. The AAN endorses TCD with Type A,
Class II level evidence supporting the modality for the assessment of cerebral circulatory arrest (CCA) in support of a clinical diagnosis of brain death. A pooled analysis of 22 studies found the sensitivity of TCD in assessing for CCA to be 90% and
specicity of 98%; these gures being consistent with published guidelines of the
American Academy of Neurology [61–63]. TCD as a conrmatory test of cerebral
circulatory arrest is a viable adjunctive test in the determination of brain death,
although in some retrospective analyses lower sensitivities have been reported and,
in that respect, serial testing has been shown to increase sensitivity [64].
27 Acute Neurologic Injury in the ICU: Role of Transcranial Doppler in Disorders…
ALTERNATING BIPHASIC FLOW SYSTOLIC SPIKES NO FLOW
Fig. 27.2 Typical waveform observed in the basilar artery conrming cerebral circulatory arrest.
(Courtesy: Schreiber [69])
475
There are limiting factors however, and for TCD to be useful, a reliable signal
must be found. As part of a complete evaluation, the vertebrobasilar circulation is
assessed through a suboccipital transcranial window and at the time of TCD the
patient’s arterial blood pressure should be noted. Early ndings in elevated intracranial pressure include a mild decrease in the diastolic ow velocity and an increase in
the difference between peak-systolic and end-diastolic velocities. The characteristic
ndings of an oscillating ow pattern with a negative diastolic component represent
an increase in intracranial pressure above diastolic pressure during the process of
brain death and short systolic spikes are often seen as cerebral perfusion pressure
approaches zero. Figure27.2 outlines these ndings which are considered to be very
specic for cerebral circulatory arrest (CCA) [61, 65]. A complete absence of ow
may not in itself be reliable due to an inadequate window, and in this respect, it
should be noted that TCD is generally less reliable in patients with prior craniotomies [66]. TCD remains a viable ancillary investigation along with clinical examination in the determination of brain death but is not viable as the sole determinant.
Kuo and colleagues assessed the time-dependent validity in the diagnosis of brain
death using TCD.Specic diagnostic patterns described above increased in prevalence in the rst 24hours of conrmed brain death reaching a plateau at 36 hours
[67]. Additionally, the group found consistency of the BA and the middle cerebral
artery (MCA) in the diagnosis of brain death. However, it should be noted the BA
had a greater sensitivity, higher positive predictive value, and fewer false negatives,
lending further credence to the value of TCD of the vertebrobasilar circulation as a
part of a complete sonographic evaluation in the determination of brain death [67].
27.13 Conclusion
TCD is an important non-invasive tool to monitor cerebral hemodynamics, which is
an integral part of assessing patients in the Neuro ICU.Although treatment thresholds and outcome evaluations have been largely dened by anterior circulation
476
INTENSIVE CARE UNIT (ICU)
R. R. Gill et al.
criteria, evidence suggests that basilar artery assessments may provide important
additional and complementary information to complete the assessment. Not only do
patients with ischemic and hemorrhagic stroke subtypes benet from TCD assessment, but also patients with TBI, from mild to severe forms of injury and across the
age spectrum.
Algorithm 27.1 TCD/TCCS: Use ofPosterior Circulation
inDiagnosis ofAcute Brain injury
EMERGENCY DEPARTMENT (ED)
Clinical Status of the Patient
ABCD
Oxygenation (SpO2> 94%)?
CONCERN Hemodynamic Stability?
Subclavian Steal Syndrome ? CONCERN
GRADE 1
Pre-Subclavian Steal
I. Reduced antegrade VA Flow ACUTE BRAIN INJURY
GRADE 2
Intermittent / Partial
I. Alternating antegrade flow in
the diastolic phase
II. Retrograde flow in the
systolic phase
GRADE 3
Permanent / Advanced V. Nausea / Vomiting? I. Obtain Echocardiogram
I. Retrograde VA Flow
Normocapnia (PaCO235-45 mmHg)?
Right to Left Cardiac Shunt?
CRITICALLY ILL PATIENT
EXAMINE THE PATIENT
Posterior Circulation Ischemia ?
II. Depressed mental status? PERFORM
III. Cranial nerve abnormalities? I. Valsalva maneuver
IV. Dizziness / Ataxia? Does it augment HITS?
Transcranial Color-Coded duplex Sonography (TCCS)
Transcranial Doppler (TCD)
SUBOCCIPITAL ACOUSTIC WINDOW
I. Brief Unidirectional HITS
(< 0.01 –0.03 seconds)
within the Doppler frequency
spectrum (> 3dB) producing
a characteristic sound:
¨chirp¨, ¨Click¨ or ¨whistle¨ ?
and neurovascular imaging
to evaluate further.
CONCERN CONCERN
Posterior Circulation
arterial dissection?
DIRECT SIGNS INDIRECT SIGNS
I. Increased CBFV (> 120 cm/s) I. Severely reduced or
II. > 50% Increase compared
with an unaffected segment
or I. VA (80 cm/s)
or diminished PI in PCAs
absent CBFV
II. Increased PI II. BA (80 cm/s)
III. Increased contralateral
VA CBFV
CONFIRM WITH VESSEL IMAGING AND MRI
Posterior Circulation
arterial Stenosis ?
≥ 50% STENOSIS
MFV Cutoff:
≥ 80% STENOSIS
MFV Cutoff:
I. VA (110 cm/s)
II. BA (130 cm/s)
ABCD Airway-breathing-circulation-disability, CBFV Blood ow velocity, MFV Mean ow veloc-
ity, VA Vertebral artery, BA Basilar artery, PI Pulsatility index, PCA Posterior cerebral artery
Serial TCD/TCCS assessment
INTENSIVE CARE UNIT (ICU)
27 Acute Neurologic Injury in the ICU: Role of Transcranial Doppler in Disorders…
Algorithm 27.2 Monitoring disease states withposterior
circulation TCD/TCCS
EMERGENCY DEPARTMENT (ED)
477
PERFORM
Serial TCD / TCCS ABCD
Suboccipital Acoustic window Oxygenation (SpO2> 94%)?
ASSESS Normocapnia (PaCO235-45 mmHg)?
CBFV and PI Hemodynamic Stability?
CONSIDER
CA and VMRto: CLINICAL FEATURES
Guide Management I. Depressed mental Status?
CONSIDER
MMM IV. Hyperemia ?
I. ICP EXAMINE THE PATIENT V. Tissue metabolic dysfunction?
II. PbtO
2
III. CBF II. Depressed mental status?
IV. SjvO
2
V. CMD IV. Dizziness / Ataxia? TCD / TCCS if:
VI. cEEG V. Nausea / Vomiting? I. Posterior circulation
VII. NIRS / BIS
Transcranial Color-Coded duplex Sonography (TCCS)
SUBARACHNOID
HEMORRHAGE (SAH)
PERFORM CONCERN ASSESS
TCD / TCCS
Suboccipital acoustic window CONSIDER
I. CBFV
II. BA / VA Ratio I. Assess PI
VASOSPASM ? II. CBFV
Sonographic Vasospasm INTERPRET
I. CBFV > 60 cm/s
(60% specificity and 100%
sensitivity for BA Vasospasm)
II. BA / VA ratio > 2.5
(66% Sensitivity and 97%
specificity for decrease 25% in
BA diameter)
III. BA / VA ratio > 3
(92% sensitivity and 97%
specificity for decrease 50% in
BA diameter)
Transcranial Doppler (TCD) Serial TCD/TCCS assessment
Vertebro-Basilar Circulation
Clinical Status of the Patient
CRITICALLY ILL PATIENT
ACUTE BRAIN INJURY
Posterior Circulation Ischemia ?
III. Cranial nerve abnormalities? CONSIDER ON ADMISSION
TRAUMATIC BRAIN
INJURY (TBI)
Elevated ICP ? I. Mechanism of Injury likely to
TCD / TCCS
I. High PI with normal CBFV may
suggest early elevations in ICP
Blunt Cerebrovascular injury to the
Posterior circulation Vasospasm
IF CONCERN II. Record ABP
Posterior circulation
CONSIDER I. Oscillating doppler waveforms
TCD/TCCS with MES II. PSV forward flow / EDV reversed flow
IF CONCERN
CONSIDER
II. Cranial nerve abnormalities
with concern of high ICP ?
III. Brain Ischemia ?
hypoperfusion
CONSIDER
BRAIN DEATH
DETERMINATION
Cause Brain Death?
II. Clinical exam consistent
With Brain Death?
CONSIDER
TCD / TCCS
Suboccipital acoustic Window
I. CBFV
ASSESS
STAGE 1
STAGE 2
I. Systolic spikes
II. Absence of diastolic flow
I. Disappearance of intracranial Flow
STAGE 3
ABCD Airway-breathing-circulation-disability, CBFV cerebral Blood ow velocity, PI Pulsatility
index, PSV Peak systolic velocity, EDV End-diastolic velocity, MES microemboli signal, BA
Basilar artery, VA vertebral artery, ABP arterial blood pressure, ICP intracranial pressure, CPP
cerebral perfusion pressure, CMD cerebral micro-dialysis, CA cerebral autoregulation, VMR vasomotor reactivity, CBF cerebral blood ow
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in evaluating vertebral arteries. J Ultrasound Med. 1989;8(5):229–35.