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Chapter 22
Transcranial Doppler inSubarachnoid
Hemorrhage: Usefulness intheDiagnosis
andMonitoring ofCerebral Vasospasm
FabiennePerren
Key Points
1. TCD/TCCS should be performed by experienced sonographers.
2. TCD/TCCS is a very useful noninvasive bedside tool allowing detection and
monitoring of vasospasm.
3. TCD/TCCS can be used to detect the onset of asymptomatic vasospasm and follow vasospasm progression.
4. TCD/TCCS can be used to facilitate treatment and to prevent the onset of DCI.
5. TCD/TCCS can be used to early select candidates for angioplasty.
6. TCD/TCCS can detect the resolution of vasospasm.
22.1 Introduction
After aneurysmal subarachnoid hemorrhage (SAH), a major complication and a
cause of poor outcome is the occurrence of vasospasm of the cerebral vessels (CVs).
Indeed, CVs, which lead to a progressive arterial narrowing, can result in cerebral
ischemia/infarction and delayed cerebral ischemia (DCI) signicantly increasing
disability and death [1–5].
Despite early treatment of ruptured cerebral aneurysms, postoperative vaso-
spasm with 2–20% of DCI remains a major complication [6, 7].
Cerebral vasospasm is seen in approximately 70% of SAH patients on digital
subtraction angiography (DSA) that although invasive, is still considered as the gold
standard for the diagnosis of CVS [8]. CT angiography (CTA) that tends to be more
F. Perren (*)
University Hospital and Medical Faculty, Department of Clinical Neurosciences, LUNIC
Laboratory, Neurocenter of Geneva, Geneva, Switzerland
Committee Member - ESNCH, Olso, Norway
e-mail: fabienneperren@yahoo.com
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_22
377© Springer Nature Switzerland AG 2022
378
F. P err en
widely used requires radiation exposure and contrast injection and thus cannot be
used to monitor clinical changes. Moreover, it does not allow cerebral blood ow
measurement [9, 10].
Transcranial Doppler (TCD) rst developed in Switzerland by Aaslid etal. in the
early 1980s to warn the development of CVs after SAH– and a decade later, using
color-coded duplex sonography (TCCS)– has been proved to be a safe, noninvasive,
bedside, dynamic monitoring technique widely used in neurosurgery to detect and
follow CVs [11–13]. TCD has been approved by the American Heart Association/
American Stroke Association (AHA/ASA), American Academy of Neurology
(AAN), and Neurocritical Care Society for daily noninvasive monitoring of mean
ow velocity (MFV) of the basal cerebral arteries to detect the onset of CVs after
SAH [14, 15]. Furthermore, TCD/TCCS can be applied as frequently as needed preand postoperatively and can guide the therapy of aneurysmal SAH [16]. Although
the scope of this chapter is limited to present transcranial ultrasound methods (TCD,
TCCS) for diagnosis and monitoring vasospasm assessment after SAH, the methods
would be similar in cerebral vasospasm as a complication of head trauma [17].
22.2 Aneurysmal Subarachnoid Hemorrhage (aSAH)
Subarachnoid hemorrhage (SAH) may commonly occur after head trauma. SAH
without preceding trauma occurs mainly in the setting of intracranial aneurysm rupture. Other causes have been identied including arteriovenous malformation and
vasculitis but it may also occur in the absence of vascular abnormality [18]. It refers
to extravasation of blood into the subarachnoid space situated between the pia and
arachnoid (Fig.22.1). Symptoms include generally acute severe headache “thunderclap headache,” neck pain/stiffness, vomiting, decrease of consciousness, and
sometimes seizures. Main complications of aneurysmal SAH include hydrocephalus, re-bleeding, vasospasm, DCI, and seizures.
Although clinically recognized since Hippocrates and cerebral aneurysmal rupture described by Bramwell in 1886, SAH symptoms were only fully described by
Symonds in 1924, who also introduced the use of lumbar puncture and xantochromia for its diagnosis [19–21]. A few years later, neurosurgical treatment of SAH
was rst introduced by Dott who also pioneered the use of angiograms [22]. In
1938, Dandy used the rst clips but it is only over 30years later that in Switzerland,
Krayenbühl, Yaşargil, etal. introduced microsurgical aneurysm therapy [23, 24].
The rst medical treatment, the so-called “triple H therapy” for delayed cerebral
ischemia due to vasospasm after SAH, was introduced in the 1980s, then followed
by transluminal balloon angioplasty and nally by endovascular coil treatment by
Guglielmi in 1991 [25–27].
The incidence of SAH has geographical variations. With 19–23 per 100’000, it
has been reported to be especially high in Japan and Finland [28, 29]. Mean age at
aneurysmal rupture is 55years and there is a slightly higher incidence of aneurysmal SAH in women [30, 31].
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
Fig. 22.1 Cerebral CT
scan showing extensive
SAH: There is
subarachnoid hemorrhage
located around the
brainstem, in the
supracellar cistern, and in
the right lateral ssure.
(Courtesy: Hov etal. [61])
379
Several risk factors have been associated with an increased risk of aneurysm
rupture including black race and Hispanics, hypertension, active smoking, alcohol
abuse, use of sympathomimetic drugs, and larger (>7mm) intracranial aneurysms
[32–34].
Cerebral aneurysms are related to hemodynamic stress due to pulsatile ow and
turbulences on the arterial walls at bends and bifurcations. Intracranial arteries lack
an external lamina and have a very thin adventitia. This predisposes to the formation
of saccular or berry aneurysms. However, acquired factors like atherosclerosis,
hypertension, smoking, advancing age, and hemodynamic stress are thought to be
associated with aneurysmal formation [35, 36]. Moreover, a number of diseases
leading to arterial wall weakness such as bromuscular dysplasia, polycystic kidney
disease, aortic coarctation, cerebral AVM, aplastic or hypoplastic contralateral vessel, SLE, Neurobromatosis type I, moya-moya disease, pseudoxanthoma elasticum, Marfan, Ehler-Danlos, and hereditary hemorrhagic telangiectasia syndromes
are associated with higher incidence of berry aneurysms [35, 37]. It has been
described that structural integrity damage of the arterial wall by shear stress causes
an inammatory response with the recruitment of T-, mast-cells, macrophages, and
inammatory mediators (IL-1β,-6,TNFα, MMP-1,-2,-9, complement system, and
380
Grade 0
Deep coma, decerebrate rigidity, moribund appearance
Grade 1
F. P err en
angiotensin II). Finally, it results in arterial wall brosis and abnormal collagen
synthesis leading to arterial wall thinning, formation of aneurysm, and risk of rupture [38].
22.3 Cerebral Vasospasm After aSAH
Subarachnoid hemorrhage, whether of aneurysmal origin or not, has been graded
according to the following grading scales:
1. The Hunt and Hess scale, created in 1968, is based on signs and symptoms.
2. The Modied Fisher Scale, which describes the severity of SAH according to CT.
3. The WFNS scale, developed in 1988 for patients suffering from SAH, is using
the Glasgow coma scale (GCS) combined with the presence or absence of focal
decits to determine severity of injury and to predict patient outcomes [39–41]
(Tables 22.1, 22.2, and 22.3).
Table 22.1 Hunt and Hess grading scale
Grade I
Grade Ia
Grade II
Grade III
Grade IV
Grade V
Unruptured aneurysm
Asymptomatic or mild headache and slight nuchal rigidity
Fixed neurologic deficit without acute meningeal/brain reaction
Cranial nerve palsy, moderate to severe headache, nuchal rigidity
Mild focal deficit, lethargy, or confusion
Stupor, moderate to severe hemiparesis, early decerebrate rigidity
Table 22.2 Modied Fisher grading scale (CT scan ndings)
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
No SAH and No IVH
Focal or diffuse, thin SAH (<5 mm thick); No IVH
Focal or diffuse, thin SAH; bilateral IVH
Focal or diffuse, thick SAH (>5 mm thick); No IVH
Focal or diffuse, thick SAH; bilateral IVH present
Table 22.3 WFNS grading scale
GCS of 15 Motor deficit absent
Grade 2
Grade 3
Grade 4
Grade 5
GCS of 13–14 Motor deficit absent
GCS of 13–14Motor deficit present
GCS of 7–13 Motor deficit absent/present
GCS of 3–6 Motor deficit absent/present
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
The Hunt & Hess and the WFNS grading systems have been shown to correlate
well with patient outcome, and in a recent study, the importance of neurological
decits in addition to level of consciousness has been shown for cut-off values–
suggesting unfavorable outcome for Hunt & Hess and WFNS – of 4–5 and 3–5,
respectively [2, 42]. The Fisher classication has been used successfully to predict
one major complication of SAH that is symptomatic cerebral vasospasm [43]. Both
Fisher Scale and Hunt & Hess Grade are related to the severity of aneurysmal SAH
and correlate with the incidence of cerebral vasospasm (CVS) [39, 40].
Cerebral vasospasm (CVS) is a progressive but reversible cerebral arterial narrowing and a major complication of aSAH that may signicantly increase disability
and mortality rates [44]. CVS may be clinically silent but it is a well-known complication that can occur at any time within the 3–4 weeks – generally within
3–7days– after aneurysmal SAH [45]. It is seen on angiography in as many as 70%
of patients and involves large and medium-sized cerebral arteries [44, 46]. The overall incidence of cerebral angiographic vasospasm after aneurysm rupture has been
estimated between 50% and 90% [45]. In the literature, its occurrence has been
estimated as follows: moderate or more severe vasospasm in at least one cerebral
artery will develop in two-thirds of patients with ruptured aneurysms, half of these
patients will become symptomatic as a result of ischemia, and a cerebral infarct will
develop in about half of these symptomatic patients [46].
381
22.4 Diagnosis ofCerebral Vasospasm andRole
ofTranscranial Ultrasound
Several imaging modalities are used to diagnose CVS after aSAH.Among the current techniques, DSA and CT angiography are invasive, and they require contrastdye injection, have radiation exposure, and do not allow dynamic monitoring of
vasospasm [31]. This implies that they are not used to detect subclinical vasospasm
prior onset of symptoms. They are frequently restricted to conrm vasospasm in
patients who are already symptomatic. A less invasive but not dynamic imaging
technique is magnetic resonance angiography (MRA) using time of ight (TOF)
sequences. However, this technology is less available and less used in this setting.
Currently, the primary screening imaging technique for asymptomatic vasospasm
is transcranial Doppler ultrasound [47, 48]. Besides its noninvasiveness, it has many
advantages such as its ability to measure in real-time cerebral hemodynamic
changes, its bedside availability that makes it ideal for monitoring, and its low cost.
Transcranial Doppler ultrasound has a high sensitivity, specicity, and positive
and negative predictive value and can, unlike other imaging techniques, early detect
and predict the development of symptomatic vasospasm with delayed cerebral ischemia [8, 49, 50]. Therefore, it has been approved and recommended by the American
Heart Association/American Stroke Association-AHA/ASA (Class IIA/Level B evidence) and by the American Academy of Neurology as a safe and effective modality
for noninvasive daily monitoring of the development of vasospasm after aSAH [47].
382
Factors CBFV
Moderate CVS Severe CVS
F. P err en
22.5 Transcranial Ultrasound Assessment
ofCerebral Vasospasm
Cerebral vasospasm typically affects the basal cerebral arteries of the circle of Willis
(MCA, ACA, PCA, ACoA, ACoP) which run through the basal cisterns where blood
accumulates after intracranial aneurysm rupture. Depending on the location of the
aneurysm rupture, CVS may occur in the proximal or more distal segments of the
basal cerebral arteries in which latter case it can be missed. CVS may affect one or
several intracranial arteries and is characterized by a segmental acceleration of the
CBFV uctuating over time and responding to therapy. This is why a baseline measurement of the velocities should always be performed.
Since Aaslid etal. developed TCD and demonstrated its ability to noninvasively
detect ow-velocity acceleration due to narrowing in the cerebral arterial segments
affected by CVS, transcranial ultrasound imaging has been used to monitor it after
aSAH [11, 12]. However, frequent factors (Table22.4) may inuence cerebral blood
ow velocities (CBFV) and should, therefore, be considered.
↓ increase, ↓ decrease
While there is no clear consensus for threshold velocity values of all the intracranial vessels, above which CVS should be considered, we propose to use cut-off
mean ow velocities (MFV): (Table22.5) and to combine these to additional criteria [51–53]. Indeed, in case of hyperemia, CBFV will also increase and therefore in
order to diagnose CVS, correction using following indices have been introduced:
Table 22.4 Examples of
factors inuencing cerebral
blood ow velocities
measured by transcranial
ultrasound
Table 22.5 Vasospasm: cut-off mean ow velocities
Anterior circulation: MCA
(ACA, ICA)
Posterior circulation: BA, VA,
MCA middle cerebral artery, ACA anterior cerebral artery, ICA internal carotid artery, BA
basilar artery, VA vertebral artery, PCA posterior cerebral artery, CVS cerebral vasospasm
PCA
Increasing age (>60 years)
Increased intracranial pressure (ICP)
Decreased hematocrit
Cerebral hyperperfusion
Hypercapnia/hypoventilation
Hypocapnia/hyperventilation
Hypertension
≥120 cm/s (≥3 KHz) ≥ 160 cm/s (≥4 KHz)
≥80 cm/s (≥2 KHz) ≥120 cm/s (≥3 KHz)
↓
↓
↑
↑
↑
↓
↑
ms
AI
()∗()
()
ms
()∗()
()
SR CVSSRsevereCVS>>23:; :
ms
AI
()∗()
()
SloanR CVS> 4:
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
383
1. The Lindegaard ratio: ratio between MCA and ICA mean ow velocities:
(Eq. (22.1))
LR MFVcms MFVc
=
LR hyperemiaLRCVS LR severe CVS236:;:;
MC
∗
Mean submandibular ICA
// /
‡
CA
(22.1)
2. The Soustiel ratio: ratio between BA and VA mean ow velocities: (Eq. (22.2))
SR MFVcms MFVc
=
∗
Mean of bothVAsegments3
// /
BA VA
(22.2)
3. The Sloan ratio: ratio between ACA and ICA mean ow velocities: (Eq. (22.3))
SloanR MFVcms MFVc
=
AC
∗
Mean submandibular ICA
// /
CA
(22.3)
As maximal acceleration of CBFV often occurs after neurological decits, a
close monitoring with transcranial ultrasound, allowing a comprehensive hemodynamic view, is mandatory. Indeed, according to our experience and as shown in a
few studies, CVS risk prone to clinical symptoms may be identied by the time
course of the CBFV in the MCA:
4. MFV increase >50cm/s per day.
5. MFV increase ≥50% per day within the 1st week after SAH onset.
Moreover, it has been also described that an asymmetry between mean MCA
CBFV with a ratio ipsi- vs contralateral side >1.5 may help to identify CVS “at
risk” of delayed cerebral ischemia (DCI) [50]. And a few studies have shown
that early impairment of cerebral autoregulation is associated with delayed cerebral ischemia and unfavorable outcome after SAH [54–59].
Finally, a vasospasm probability index for the MCA, taking into account Fisher
and Hunt and Hess grades, Lindegaard ratio, and spasm index (TCD velocities/
Xe-CT hemispheric CBF), has been also proposed to improve the detection of CVS
at risk of DCI [60].
384
F. P err en
22.5.1 TCD/TCCS: Examination Protocol
Since the introduction of noninvasive low-frequency (~2MHz) transcranial Doppler
(TCD) measuring “blindly” cerebral blood ow velocities, technical advances in
ultrasound imaging resolution and color-coding of blood ow (transcranial colorcoded duplex Sonography (TCCS) have allowed to additionally visualize brain
parenchyma (B-mode) (Fig.22.2) and the main basal cerebral arteries (color-coded
mode) (Fig.22.3). Both techniques can be used to detect and monitor CVS after
aSAH.Several “acoustic bone windows,” where ultrasound waves can be transmitted through thinner skull bone regions or foramina, are used for the insonation of the
cerebral arteries: the temporal (TW), orbital (OW), suboccipital/transforaminal
(OTW), and submandibular (MW) bone windows (Fig. 22.4a, b) [50]. In case of
insufcient ultrasound penetration, TCCS has the advantage over TCD to allow
cerebral vessel examination after the injection of an echocontrast agent. TCD,
depending on the length of the examination, consists of a 2MHz ultrasound probe
that can be xed in a headset (making bilateral monitoring possible) or applied
manually in the region of acoustic windows.
Fig. 22.2 Standard transtemporal axial examination plane using TCCS (B-mode) showing the
mesencephalon (dotted line)
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
385
Fig. 22.3 TCCS through the right temporal acoustic bone window showing color-coded duplex
imaging of the ipsilateral: middle cerebral artery (MCAr), anterior cerebral artery (ACAr) and
posterior cerebral artery (PCAr)
22.5.1.1 Transtemporal Window
It allows blood ow velocity, ow direction measurement, and visualization (TCCS)
(Fig.22.3) of the distal internal carotid artery (TICA), carotid siphon, the middle
cerebral (MCA, M1-2), anterior cerebral (ACA, A1-2), posterior cerebral arteries
(PCA, P1-2), and communicating arteries (ACoA, ACoP).
22.5.1.2 Orbital Window
It allows blood ow velocity, ow direction measurement, and visualization
(TCCS): the ophthalmic (OA) and internal carotid (ICA) siphon.
386
OW
MW
F. P err en
Fig. 22.4 (a) Human
skull, front view, showing
(in black): orbital (OW)
and temporal (TW)
acoustic bone windows.
(b) Human skull, lateral
view, showing (in black):
orbital (OW), temporal
(TW), sub-mandibular
(MW), and sub-occipital/
transforaminal (OTW)
acoustic bone windows
a
OW
TW
b
TW
OTW