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Transcranial Doppler
Introduction
Transcranial Doppler (TCD) is the use of Doppler technology to evaluate cerebrovascular blood flow within the basal arteries of the brain. The information from such an examination supplements that obtained from other modes of vascular imaging. The advantage however relies on its real time, noninvasive bedside use as it can be used to evaluate vascular changes in response to interventions performed during acute cerebrovascular events. Here are some examples of the conditions that can evaluated with TCD:
In blue, conditions that can be evaluated with point of care ultrasound TCD and that we will be exploring in this chapter. Please be advised that POCUS TCD is not intended to supplant an full TCD exam but be able to answer if the conditions are present or absent.
Principle: the Doppler effect
TCD uses the Doppler effect so its understanding is paramount in its clinical application. The Doppler effect is the measured change in frequency that corresponds to a change in velocity which in turn is related to a change in flow. Lets dig a bit deeper for better understanding.
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The ultrasound probe emits a frequency that travels to a vessel. This vessel contains moving red blood cells that interacts and reflect this sound wave. The reflected sound wave then returns towards the probe with a different frequency to that which was emitted. If the red blood cell is moving away from the probe, its wavelength is higher and has a lower frequency.
Let imagine we have an ambulance with a siren emitting the same frequency. If the vehicle remains stationary we perceive one unique frequency but if we hear and ambulance coming towards us and then moving away from us we hear a difference in frequency due to the movement of the vehicle. If its coming towards us the frequency appears higher since the wavelengths are compressed together. Once the ambulance moves away from us the wavelengths now are further and further away from each other and we perceive a lower frequency. The faster the moving object, the greater the perceived change in frequency. We can also display this information visually which is what the US machine would do for us. If this Doppler effect of an object moving away from us we would be displaying it blue and red if the contrary were true which is what happens when you turn on the Color Flow Doppler (CFD) feature of the machine.
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Schematic representation of the Doppler effect with the use of a an ambulance and a active siren. On the left, a human ear representing the ultrasound sensor. 1, stationary ambulance. 2, moving ambulance
This Doppler shift is thus directly proportional to the speed of moving red blood cells and ultrasound machine creates a spectral display of the different changes in velocity observed. It is important to note that to be able to measure this shift in frequency we need to be as parallel as we can to the flow and that at 90 degrees from flow we are unable to detect any doppler shift. An important feature of Pulsed Wave Doppler which is a technology that uses Doppler is that we can measure this shift in a particular point in space with the use of a gate.
This doppler change represents flow velocity with the following mathematical formula:
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This math formula is important since it describes the velocity as being directly proportional to the Doppler shift. Of the parameters, C is the speed of sound in the medium and corresponds to 1541m/s in soft tissue. Ft is the frequency of the probe and in order to penetrate to deeper tissues we need a lower frequency and thus this parameter does not change much. Theta (θ) is the angle between the emitted wave and the direction of flow. The larger this angle, the worse the error in measurement.
Doppler Shift x C
Flow velocity =
2 x Ft x Cos θ
The spectral information displayed from this doppler analysis (see image below) includes measures of blood flow velocities (y axis) across time (x axis). Parameters that can be measured from this include peak systolic velocity (Vs), end systolic velocity (Vd), acceleration time or systolic upstroke, time-averaged mean velocity (V mean) and pulsatility index (PI). Vmean is calculated by using the following Vmean = [Vs + (Vd x 2)]/3. The PI is a non invasive measure assessing vascular resistance and is thus used to assess downstream vascular resistance and is calculated as PI= (Vs-Vd)/Vmean.
Vs
Vd
At
Example of spectral Doppler frequency display of the middle cerebral artery. B-mode US with Color Flow Doppler sector overlaid. PWD sample box over the middle cerebral artery. Peak systolic velocity (Vs), end systolic velocity (Vd), acceleration time or systolic upstroke (At), pulsatility index (PI), time-averaged mean maximum velocity (Vmean) (traced in purple).
Blood flow velocity indices and physiologic factors
There are physiologic variables that influence cerebral blood flow as measured by TCD so it is important to have them in mind. These include age, gender, blood pressure, temperature, carbon dioxide, hematocrit and mental or motor activity. Any measured differences in blood flow velocity should have these parameters in mind.
Age
Gender
BP
CO2.
Hematocrit
Blood flow velocities decline up to 0.5% per year from ages 20-70.
Women tend to have higher flow velocities than men between 20-60 years of age with a magnitude of difference of up to 15%. This difference no longer exists for those >70.
Measured velocities may be higher in patients with high blood pressure despite an intact autoregulatory system.
Partial pressure of carbon dioxide is directly proportional to cerebral blood flow.
Viscosity is inversely related to cerebral blood flow velocity. Approximately 20% increase in CBF occurs from decreasing hematocrit from 40 to 30%
Equipment and Technique:
We will be using a lower frequency probe that allows penetration through the thinnest portions of the skull. This corresponds to a 2Mhz probe.
TCD Windows
The acoustic windows that allow US transmission to evaluate the basal cerebral circulation are 4 (see diagram below). These are the transtemporal, suboccipital (transforaminal), transorbital, and submandibular (retromandibular). The transtemporal window is located above the zygomatic ridge between the lateral canthus of the eye and auricular pinna and has 4 interrogation zones (with a frontal [F], anterior [A], middle [M] and posterior [P] window) and is the most frequently used to interrogate the middle (MCA), anterior (ACA), posterior cerebral arteries (PCA), and terminal internal carotid artery (ICA). Bear in mind that in up to 20% of patients have inadequate transtemporal windows.
TCD Windows
F
A
M
P
Diagram showing the 4 TCD windows. In the trans-temporal window (F, A, M, P) notice the location of the red indicator which corresponds to the direction of the marker in the actual probe. See text for details.
The target artery is interrogated by selecting an appropriate acoustic window, probe angle and selecting a Color Flow Doppler window. The vessel is then recognized through flow direction, pulsatility, and velocity. Velocity is measured after turning continuous wave Doppler (CWD) and selecting an appropriate depth gate. We can also evaluate waveform changes induced by dynamic maneuvers such as proximal carotid artery compression.
During TCD examinations the sonographer should follow the blood flow in each major branch of the circle of Willis and attempt to identify 2 key points per artery. The MCA should be interrogated as proximal , mid and distal. The vertebral artery measured two distances apart. Basilar artery measurements taken as proximal mid and distal. There are age specific depth ranges and flow ranges for each major artery. In cases were it may not be possible to differentiate the anterior from a posterior circulation the blood response to carotid compression or vibration may be used. Bear in mind that our focus will be on the trans-temporal window since it will provide us with the highest yield when interrogating it as part of POCUS.
The following measurements for adults represent the location of the arteries in their corresponding window. We will be focusing on the trans-temporal window for the rest of this chapter :
Transtemporal window
Intracranial carotid artery (ICA) bifurcation
Simultaneous flow towards and away from probe
Middle cerebral artery (MCA)
Flow towards the probe
Anterior cerebral artery (ACA)
Flow away from the probe
Posterior cerebral artery (PCA)
2cm posterior to the ICA bifurcation. P1 segment has flow towards while the P2 has flow away from the probe.
Transorbital window
Opthalmic artery
Use under 10% max power to minimize subluxation of the lens. Probe directed towards the optic canal. Flow is in the direction of the probe.
Suboccipital window
Basilar artery
Flow away from the probe
Submandibular window
Distal ICA
Depth
55-65mm
35-55mm
60-70mm
60-70mm
55-70mm
60-70mm
40-60mm
Schematic diagram of the circle of Willis. Arrows depict direction of flow. The color in the arrows represent the resultant CFD in their respective window. Image by Rhcastihos.
Trans-temporal window and views.
Now that we have some idea of the structures and principles for TCD we will be exploring the trans-temporal window moving forward. We start with the probe orientation and the structures that should be seen and then start using color coded duplex sonography.
Probe position and 2D image for the trans-temporal window. The probe should be just above the zygomatic arch with the probe indicator pointing forward or towards the patient's forehead. Small adjustments with rotational movements of the probe will be of paramount importance for us to be able to identify structures within the cranium.
The following images have a side by side comparison of 2D ultrasound and anatomic landmarks that are necessary for TCD. The preset for these images is the cardiac preset (flipped images from a TCD preset). We first focus our attention to the middle of the field and look for 2 hypoechoic structures that look like a butterfly on its side (see image below). These structure represent either the thalami or the peduncles. The third ventricle lies anterior to the 'butterfly'. The third ventricle is an anechoic space with hyperechoic walls.
Probe position and 2D image for the trans-temporal window. Cardiac preset has been selected. The yellow structure represents the thalami or the peduncles. In white and in the near field the ipsilateral meninges. In the far field and in black, the contralateral temporal bone. The blue structure is the third ventricle and is an anechoic structure with hyperechoic walls. The white arrow points towards the far field border of the third ventricle.
Color-Coded Duplex Sonography: Trans-temporal window
Diagnostic TCD uses non-imaging probes set for measurement of spectral Doppler signs at specific distances to insonate target vessels. We can however take advantage of color-coded duplex sonography (CCDS) imaging probes with pulsed wave doppler (PWD) and angle correction to find and interrogate specific vessels. We start with trasntemporal window CCDS TCD window to access and serves as the main window to acquire in POCUS TCD. For optimal interrogation the Nyquist scale should be low to allow low flow velocities to be optimally interrogated. The probe should be placed with the index mark pointed towards the patient's front.
CCDS of the trans-temporal window. On the left, the third ventricle is seen in 2D. On the right, we have lower the distance to be able to see the near field and turned on Color Flow Doppler. Making small movements of the hand to visualize the vessels that make up the circle of Willis.
Right ICA
On these clips we used the right trans-temporal window. First, we start by turning CFD on and selecting the ICA and making adjustments on the probe.
Left MCA vs Right MCA
We can compare Right versus Left sided MCA by changing the probe location from the right to the left trans-temporal window.
Right trans-temporal window showing the right MCA
Left trans-temporal window showing the left MCA
Left MCA and ACA
Making adjustments to the sector CFD window to look at deeper structures we can visualize both right and left ACA as well as the left sided MCA
PCA
By using the left transtemporal window we can observe the posterior cerebral arteries. TCD preset was selected on these clips.
Left trans-temporal window showing the left PCA
Left trans-temporal window showing the left PCA with an overlay of the vessels of the circle of Willis.
Transorbital window
Left opthalmic artery
We have turned on CFD at the level of the optic nerve. This window is not part of the POCUS examination and here for illustration purposes.
PWD interrogation segments.
Now that we have identified the arteries lets take a look at their spectral analysis. While the CFD window is active, turn PWD and select the appropriate artery and its depth by moving the gate. The following are spectral doppler analysis clips thorugh the trans-temporal window (TTW)
Right TTW- Mid Right MCA
PWD with sample box over right mid MCA level at a distance of 39mm from the surface. Arrow in red depicting gate distance from skin. An overlay of the cerebral circulation appears for reference.
Right TTW- Prox Right MCA
PWD with sample box over right proximal MCA level at a distance of 50mm from the surface. Arrow in red showing the CFD sector and within it, the gate of PWD. An overlay of the cerebral circulation appears for reference.
Right TTW - Right ICA
PWD with sample box over ICA. An overlay of the cerebral circulation appears for reference.
Right TTW- Right ACA
PWD with sample box over right ACA. The baseline has been elevated to make room for the waveforms. Notice velocities below the baseline indicating flow away from the probe.
Left TTW- Left MCA
PWD with sample box over the left MCA using the left transtemporal window. An overlay of the cerebral circulation appears for reference.
Left TTW- Left PCA
PWD with sample box over left PCA. The baseline has been elevated to make room for the waveforms. However, the baseline still needs to higher since the waveform has been cut off. Notice velocities below the baseline indicating flow away from the probe. Notice the much lower velocities here as compared to the MCA spectral waveform.
Submandibular window
This window will allows to compare flows with the spectral analysis obtained above. It can help us differentiate between a patient with hyperemia or vasospasm (see section below). The probe surface is positioned on the lateral aspect of the neck and tilted upwards and looking into the patient's skull. CFD is then turned on to interrogate the vessel.
Ultrasound probe position for the submandibular window. On the right, CFD sector on the area of the internal carotid. Blue hue indicating movement of blood away from the probe.
PWD with sample box over right internal carotid. The baseline has been elevated to make room for the waveforms. Notice velocities below the baseline indicating flow away from the probe.
Cerebral Vasospasm
Cerebral vasospasm is defined as a delayed and potentially reversible narrowing of the cerebral blood vessels that typically involves the proximal arteries that make up the Circle of Willis. Angiographic vasospasm (VSP) is strongly associated with cerebral infarction secondary to cerebral ischemia after an aneurysmal subarachnoid hemorrhage (SAH). VSP occurs in two-thirds of patients with SAH and there is a direct correlation between VSP severity after SAH and flow velocities in most cerebral arteries. TCD can be used as a screening tool to evaluate VSP since there is an inverse relation between the diameter of a cerebral vessel and TCD mean velocities. The decrease in vessel lumen diameter in VSP causes an increase in blood flow. Here we use spectral doppler profile to make these measurements. TCD is more sensitive in detecting proximal as opposed to distal VSP. VSP is seen as an increase in either segmental or diffuse elevation of mean flow velocities without an appropriate increase in flow of the corresponding vessel that feeds it.
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Flow criteria that can be derived from TCD are reliable to detect angiographic MCA VSP. These measurements are more useful if they are used to monitor the temporal course of VSP following a SAH and not as a single sporadic measurement.
Proximal VSP. Here we look at the middle cerebral artery (MCA) since it's interrogation is straightforward. We see an increased mean flow velocities across this vessel when interrogating it. However this increase in velocities could be due to hyperemia that can be seen as an increased flow throughout multiple vessels. The Lindegaard ratio (LR) is commonly used to compare the velocities of two vessels; it is the ratio between the time mean average velocity ([Vs + Vd x2]/3) of the MCA to ICA. This ratio helps differentiate hyperemia from VSP in that hyperemia would result on an increase of the velocities across both vessels and result in a LR ratio < 3. VSP on the other hand would result in higher velocities of the MCA as compared to the ICA and thus a LR >3. The severity of VSP can also be evaluated with this ratio as a LR between 3 to 6 is considered mild VSP and a LR>6 is an indication of severe VSP. Proposed LR for other intracranial vessels is not widely accepted.
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Distal VSP. Distal vessels are typically not well insonated and thus a surrogate measure is used. In this regard the Pulsatility Index (PI) is used. An increased PI implies increased resistance distal to the site of interrogation and could be due to either VSP or an increased intracranial pressure.
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Findings suggestive of MCA VSP include:
- Mean flow velocities > 120 cm/s. Normal mean velocities are <80cm/s. Mild VSP at mean velocities of 120-159cm/s, moderate VSP with mean velocities of 160-199cm/s and severe VSP with mean velocities >200 cm/s.
- Sudden rise in V mean >65 cm/s or 20% increase within a day during posthemorrhage days 3-7
- LR >6
- Abrupt increase in PI >1.5 in two or more vessels.
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Findings suggestive of basilar artery VSP include:
- V mean >70cm/s. Severe VSP with a mean flow velocity > 85cm/s
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The following images are a side by side comparison of normal MCA TCD PWD vs a patient with vasospasm. Notice the elevated velocities
Normal flow velocities across the left MCA using transtemporal window. Normal mean flow velocities are <80cm/s. In this example if we assume a Vs=100cm/s, Vd =60cm/s then Vmean= [100+(60 x2 )]/3 = 73cm/s
Elevated flow velocities across the left MCA using transtemporal window. In this example Vs is above 400cm/s.
TCD can thus be used as a non-invasive portable method to assess VSP and monitor the effectiveness of VSP therapy (hypertension, hemodilution and hypervolemia) as well as pharmacologic vasolidation or balloon angioplasty.
Limitations of TCD for VSP: The transorbital and transforaminal windows are less reliably insonated compared to the transtemporal window. In terms of vessels, the ACA and PCA are less sensitive and specific for VSP when compared to MCA. In fact the diagnostic accuracy of TCD for ACA or PCA VSP is limited to low. The fact that we have the highest likelihood to evaluate for VSP on the transtemporal window does not mean that we can exclude VSP if we cant find it there. We also have to be mindful on the myriad of factors that can make VSP challenging to find such as PaCO2, PaO2, age, blood viscosity as described above.
Intra-cranial Pressure (ICP) and Cerebral Circulatory Arrest
Flow across the circle of Willis follows cerebral autoregulation. As ICP increases a series of well defined changes occur in cerebral vessel flow: The first change that can be observed is an increase in the MCA peak systolic velocity (Vs) as ICP causes cerebral vessels to narrow from external pressure to this vessel. Then we see diastolic flow blunting as the pressure impairs diastolic filling as the pressure opposes forward flow. This finding worsens to the point that no forward flow happens during diastole and there is only forward flow on systole and even cause reversal of diastolic flow. As the ICP continues to increase we see lower and lower forward flow velocities during systole.
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The following illustration depicts the effect of progressively elevated ICP and its effect on cerebral blood flow as measured with spectral doppler on the MCA.
d
e
f
Progression of elevated intracranial pressure leading up to intra-cranial circulatory arrest. TCD spectral signal of MCA flows. a) Normal ICP with normal flows with a normal systolic upstroke and a normal step-down of diastolic flow. Progressively higher level of ICP is seen in b-e. b) Increased peak systolic flow with decreasing diastolic flow and eventual blunting of diastolic flow. c) Diastolic flow reversal progressively worsening. d) Biphasic flow with forward flow in systole is equal to the reversed diastolic flow. e) Isolated systolic flows of short duration with less than 200ms with an amplitude less than 50cm/s. f) No flow. Cerebral circulatory arrest represents stages d-f. Modified from Lau and Arntfield Crit Ultrasound (2017) 9:21
TCD cannot be used to accurately measure intracranial pressures (ICP). However it can be used to rule in high ICP.We can estimate ICP based on the Pulsatilty Index (PI) since the measurement obtained here reflects downstream resistance. A higher PI correlates to high ICP.
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ICP = (10.93 x PI ) -1.28
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A normal PI is <1.2 and corresponds to an ICP or 5-15mmHg. A PI > 2.13 correlates to an ICP > 22mmHg which is considered the cutoff for raised ICP. The above formula is one of many and some suggest to use TCD as a binary assessment for the absence of intracranial hypertension.
The following spectral doppler signals can be used to measure ICP based on this formula:
Normal flow velocities across the left MCA using transtemporal window. In this example if we assume a Vs=100cm/s, Vd =60cm/s then PI = 40 /([100+(60 x2 )]/3 = 73cm/s) or 0.5. ICP is thus less than 5mmHg
Elevated flow velocities across the left MCA using transtemporal window. In this example Vs=140cm/s, Vd= 150 then Vmean= 233 and a PI= 250/233 or 1.07. ICP approximately 10.5 mmHg.
Limitations of TCD for ICP: There is a wide confidence interval between PI derived ICP when compared directly to ICP monitors so caution should be exercised when this value is obtained form TCD. Physiologic factors can also influence PI derived ICP measurements such as decreased in PaCO2 or an increased arterial blood pressure independent of the actual ICP. A decrease in mean arterial pressure can increase PI measurements stemming from a low cerebral perfusion pressure. PI should be assumed to be directly proportional to mean arterial blood pressure and inversely related to cerebral perfusion pressure. Lack of pulsatile flow such as venous arterial extracorporeal membrane oxygenation or left ventricular assist devices make the ICP based on TCD measurements uninterpretable.
Cerebral Circulatory Arrest
Cerebral circulatory arrest is the permanent loss of capacity for consciousness and loss of all brainstem functions and occurs as a result of an arrest of circulation o the brain. We have explored some of this in the previous section on ICP. Step-wise changes are observed as part of the progression to circulatory arrest starting with blunted diastolic flow, reversal of diastolic flow followed then by quick, short amplitude (<50cm/s) systolic peak and then absence of flow.
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The following illustration depicts the effect of progressively elevated ICP and its effect on cerebral blood flow as measured with spectral doppler on the MCA.
d
e
f
c
Progression of intra-cranial circulatory arrest. TCD spectral signal of MCA flows. c) Progressively worsening diastolic flow reversal. d) Biphasic flow with forward flow in systole is equal to the reversed diastolic flow. e) Isolated systolic flows of short duration with less than 200ms with an amplitude less than 50cm/s. f) No flow. Cerebral circulatory arrest represents stages d-f. Modified from Lau and Arntfield Crit Ultrasound (2017) 9:21
Serial TCD interrogations are necessary for the diagnosis of cerebral circulatory arrest and brain death including one preceding the onset of the arrest effectively demonstrating prior intra-cranial flow.
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TCD criteria for cerebral circulatory arrest include any one of the following taken at least twice, 30 minutes apart with a sensitivity of 88% and specificity of 98% :
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Disappearance of all previously seen intra-cranial flow with extra-cranial flow being present
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A biphasic (oscillating) waveform with net zero flow. This implies systolic forward flow is equal to diastolic flow reversal (waveform d on the image above).
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Small amplitude (<50cm/s) sharp systolic peaks of short duration (<200ms).
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Determination of brain death is typically a clinical diagnosis that includes brainstem reflex testing and apnea testing which may make determination of brain death difficult such as severe hypothermia. A TCD exam may rule in cerebral circulatory arrest by showing non-reassuring MCA flows. In this case ancillary testing such as cerebral angiography, brain perfusion scan and CT or MR cerebral blood flow angiography are necessary to confirm diagnosis. A reassuring TCD exam on the other hand may save these testing options for a later date and thus optimize the timing of these test in the presence of confounders to clinical determination of brain death.
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Limitations of TCD for cerebral circulatory arrest: Medical jurisdictions do not accept TCD as an ancillary test to confirm brain death. Even in the absence of cofounders and a clinical determination of brain death by clinical means, TCD may show reassuring spectral Doppler findings. This implies cerebral blood flow may be inadequate despite reassuring waveforms. On the other hand, non-reassuring waveforms TCD imply cerebral circulatory arrest but doesnot imply absent brainstem function.
Midline shift
Midline shift (MLS) is important to identify early as neurosurgical intervention can prevent further neurologic damage. Its identification also has prognostication implications. In addition to the clinical examination, computed tomography (CT) scan has become the standard of care for the diagnosis of MLS. In CT, the finding of > 0.5 cm of MLS has a positive predictive value (PPV) of 78% for predicting a poor outcome. In fact, this degree of MLS is one of the main CT criteria for the severity of traumatic brain injury and its presence coupled with compression of the third ventricle are both predictors of mortality within the first 15 days after injury. The Glasgow coma scale is correlates to CT derived MLS. MLS and coma are independent predictors of mortality at 15 days following an acute stroke.
Ultrasound can detect MLS with reasonable accuracy as compared to CT. Studies have shown only a small difference between the two measurements (up to 0.11 cm). A MLS> 0.35cm on ultrasound including in patients after decompressive craniectomy or with subcutaneous temporal hematomas can predict a MLS> 0.5 on CT.
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On ultrasound, detection of midline shift is based on measuring the distance from the skull to the middle of the third ventricle. This implies recognizing this structure on 2D B mode ultrasound. We do not rely on blood flow and thus Color Flow Doppler will not be used in this instance. The third ventricle is a narrow, laterally flattened region filled with cerebrospinal fluid (CSF) (purpule color structure labeled b in the diagram below). The thalamus represents the lateral limits of the third ventricle. The interface of thalamus with CSF is why we can differentiate this as a hyperechoic structure (see diagram below).
a
b
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c
Coronal section of the brain showing the lateral ventricles (labeled a and with blue color) and the third ventricle (labeled b and with purple color). The thalamus (label c) represents the lateral wall of the third ventricle and what we use in 2D ultrasound to identify the boundary of the third ventricle.
Graphical representation of brain herniation. On red, intracerebral hemorrhage leading to an increased intracranial pressure causing displacement of the surrounding structures and brain herniation. Notice the displacement of the third ventricle from the mid line. Arrows depict the direction of movement of the structures. Image modified from RupertMillard.
How we measure MLS on US. There are currently two accepted methods of evaluating MLS that rely on identification of the third ventricle. The first method is to measure the distance from the ipsilateral temporal bone to middle of the third ventricle (black line, labeled A) and the distance from the contralateral temporal bone to the middle of the third ventricle (blue line labeled B). A positive result implies distance A is larger than B and thus MLS is away from the ipsilateral side.
MLS = ( Distance A- Distance B)/2
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A
B
C
Graphical representation of brain herniation. Transcranial ultrasound is used on the transtemporal window to measure the distance from the temporal bone to the middle of the third ventricle (distance A) and then the contralateral side (distance B). In this example we can see that distance B is larger than distance A and thus would result in a negative result. C corresponds to the distance from the ipsilateral to the contralateral temporal bone. Image modified from RupertMillard. See text for details.
This is what we see when we do the transtemporal window. We have placed a Color Flow Doppler window on the region of the internal catorid artery and MCA to help us guide where the third ventricle is located.
The clips above display the third ventricle (a blue arrow). On the left, 2D mode is set a a distance of 16cm and the probe is slightly adjusted to optimize the structures. On the right CFD is turned on to help locate the approximate depth of the thalamus and the corresponding depth of the third ventricle.
The second method is to measure the distances only from one side of the head. We measure the ipsilateral distance to the middle of the third ventricle (distance A on the diagram above) and to the contralateral temporal bone (distance D in the diagram above).
MLS = Distance A/ (distance C/2)
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Current recommendations is to use the first method mentioned above have 2 independent measures from each side to check for correct measurements which include Distance A+ Distance B should equal Distance D.
These still images display the the third ventricle and corresponding measurements. On the right the depth of 7.13cm corresponds to the A distance in the above diagram. Notice the + sign is located in the middle of the third ventricle. The left temporal to right temporal bone distance is measured at 14.2cm.
Limitations of Transcranial ultrasound for MLS: The transtemporal window may have significant bone attenuation and in up to 20% of patients we will not get any ultrasound data that can be used. This technique should only be considered as a screening tool and confirmation is necessary with the use of CT.
References
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Purkayastha S, Sorond F. Transcranial Doppler ultrasound: technique and application. Semin Neurol. 2012;32(4):411-420. doi:10.1055/s-0032-1331812
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Lau, V.I., Arntfield, R.T. Point-of-care transcranial Doppler by intensivists. Crit Ultrasound J 9, 21 (2017). https://doi.org/10.1186/s13089-017-0077-9
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Lau VI, Jaidka A, Wiskar K, Packer N, Tang JE, Koenig S, Millington SJ, Arntfield RT. Better With Ultrasound: Transcranial Doppler. Chest. 2020 Jan;157(1):142-150. doi: 10.1016/j.chest.2019.08.2204. Epub 2019 Sep 30. Erratum in: Chest. 2020 Oct;158(4):1797. PMID: 31580841.
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Alexandrov AV, Sloan MA, Wong LK, et al. American Society of Neuroimaging Practice Guidelines Committee. Practice standards for transcranial Doppler ultrasound: part I—test performance. J Neuroimaging. 2007;17(1):11–18.
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Samagh N, Bhagat H, Jangra K. Monitoring cerebral vasospasm: How much can we rely on transcranial Doppler. J Anaesthesiol Clin Pharmacol. 2019;35(1):12-18. doi:10.4103/joacp.JOACP_192_17
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Motuel J, Biette I, Srairi M, et al. Assessment of brain midline shift using sonography in neurosurgical ICU patients. Crit Care. 2014;18(6):676. Published 2014 Dec 9. doi:10.1186/s13054-014-0676-9