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INTRODUCTION

Transcranial doppler (TCD) is a bedside study of cerebral arterial hemodynamics that can be used as a monitoring tool in pediatric intensive care units. Uses of TCD include increased intracerebral pressure (mostly TBI), strokes, hypoxic-ischemic encephalopathy, vasospasm, extracorporeal membrane oxygenation and postcardiac surgery. Stages of brain death can also be monitor, however, TCD is not a recognized test to declare brain death. TCD is a diagnostic tool with a promising future, still needing further research and protocol development.

This chapter describes a simple and systematic technique to use transcranial doppler with duplex mode (colour and pulsatile doppler in the same monitor). Blinded transcranial doppler will not be described. Duplex TCD has a shorter learning curve; it permits to see the vessels (even if displaced due to pathology) and correct the insonation angle, making estimations of velocities more accurate.

EQUIPMENT

PROBE

Low frequencies even in small kids

(2-3MHz)

Alternative in neonates: lineal or microconvex

Through the fontanel

5-10Hz

PRESET

TCD

Need of 2D colour and pulsatile doppler

WINDOWS

Acoustic windows are find in those areas of the skull that are thinner and permit ultrasound penetration. The typical windows are transtemporal, suboccipital and supraorbital. In infants with open fontanel, transfonatealar view can be used to perform a cerebral blood flow study.

Image 1:

TRANSFONTANELAR: permits study of the internal carotid artery (ICA) and Willis Circle branches. Good for the anterior cerebral artery (ACA). Less useful for medial cerebral artery (MCA)
TRANSTEMPORAL (pterion): best window to study MCA. Also ACA and posterior cerebral artery (PCA). It is described in the next section.
SUPRAORBITAL: when unable to see through a transtemporal view. Both ultrasound output and insonation time need to be reduced to avoid eye damage. Study ophthalmic artery and internal carotid siphon.
SUBOCCIPITAL: study basilar artery and the intracranial portion of vertebral arteries.
Extra windows:

Posterolateral fontanel (rear mastoid) in neonates or infants are useful to evaluate the posterior circulation.
Transfrontal: newly described. Study the anterior cerebral artery.
Submandibular: distal cervical ICA, evaluating vasospasm in patients with subarachnoid hemorrhage.

HOW TO SCAN

TRANSTEMPORAL WINDOW: Studying MCA

Transtemporal window is the most used to study MCA, despite 10-20% of people not having a good window. We will send the ultrasounds through the pterion area. MCA flow comes towards us. We can study midline and Willis polygon

1. Position the probe above the zygomatic arch and anterior to the ear lobe. Marker towards the eye.

Image 1:

2. Adjust image depth to be able to visualize the contralateral temporal bone. Aproximately 10-11 cm for neonates, 14-16 for a child and 18-20 for an adult.

a. Localize the peduncles (butterly like image in the center of the brain)

b. Evaluate if there is midline shift.

c. Sometimes hemorrhages can be seen, pay attention.

3. Add color doppler in front of the peduncles. Circle of Willis will be seen (usually partial). Ipsilateral MCA will be shown in red because the flow is going towards the probe.

4. Decrease depth to optimize vessel view.

5. Pulsatile doppler study:

a. Adjust color scale for the velocities (cm/s). Try to visualize at least 5-7mm of the vessel.

b. Adjust sample volume to the width of the vessel (3-5mm). Place it on the MCA (where flow is red because the vessel has flow that is coming towards the probe).

c. Insonation angle: if MCA is measured just on the bifurcation with ICA (vessel is curved), insonation angle can be parallel to the vessel (towards 0º). In case of measuring d. MCA more distally where the vessel is straight, optimal insonation angle is 30 to 45º.

e. Activate doppler mode when vessel signal is stable for a few seconds. Repeat 3 measures and take the one who has higger velocities.

6. Measurements (further discussed in the next section)

CONCEPTS

CEREBRAL AUTOREGULATION: changes in blood pressure lead to changes in cerebral arteriols diameter in order to maintain a constant cerebral blood flow. Cerebral autoregulation helps maintaining a constant blood flow between 50 and 150mmHg of mean blood pressure. Out of these values, cerebral blood flow changes linearly with blood pressure.

CEREBRAL BLOOD FLOW (CBF): depends on

Cerebral perfusion pressure: mean blood pressure minus intracranial pressure

CPP= MAP-ICP

2. Cerebrovascular resistance (CVR)

REMEMBER

F= P1-P2/R  Flow = Change in pressure over resistance.

In the brain: CBF = CPP/CVR = MAP-ICP/R

F= v x A  Flow = velocity times area (sometimes easier to frame it v = F/A)

For a constant flow in autoregulation: velocity will increase with a decrease on area.

If area is maintained, flow and velocity will be directly proportional.

Other factors influencing CBF and velocities:

PaCO2: linear proportion. For every extra mmHg there is a 4% increase in velocity in autoregulation. Lack of CO2 reactivity has poor prognosis in TBI.
PaO2: hypoxemia causes cerebral vasodilatation, increasing CBF.
Hematocrite: anemia increases cardiac output and, therefore, velocity but decreases viscosity and intracranial resistance.

THINK ABOUT IT !

Lose of autoregulation in traumatic brain injury: any change on blood pressure will significantly change cerebral blood flow.

In order to evaluate autoregulatory capacity, early and continuous or often TCD could be a good tool to measure cerebral perfusion pressure. This is an ongoing are of research.

MEASUREMENTS

Doppler waveforms are not different from any other arterial doppler. Once the waveform trace is obtained, we’ will quantify blood flow velocities (peak systolic, end dyastolic and mean) and

VELOCITIES
- Peak Systolic Velocity (PSV or Vsv, cm/s): maximal systolic velocity during a cardiac cicle.
- End Dyastolic Velocity (EDV or Ved, cm/s): falls about 20-50% of PSV. Low resistance.
- Mean Velocity or Time Average Mean maXimal velocities (Vm or TAMX, cm/s): automatic or manual outlining a wave in a cardiac cycle that calculates the average value of the maximal velocity over one cardiac cicle. Calculated as:
  - Vm (cm/s) = (PSV+2EDV)/3 or EDV + 1/3 (PSV-EDV)

REMEMBER

In TCD estimated velocities will be equal to real or underestimated but can never be overestimated.

INDEXS: both of them pretty similar. They are a measure of resistance.

Pulsatility Index (PI): PI: (VS-VD)/TAMX.

Normal values 0.7 to 1.1. High values  resistance to flow.

Most used, independent of insonation angle.

Resistive Index (RI):RI = (VS-VD)/ VS.

Normal values postneonatal age 0.45 to 0.6.

Preferred index due to its narrower normal range values.

Lindegaard’s Ratio: LR = Vm (MCA)/ Vm ICA (ipsilateral proximal ICA).

Index that corrects for a diffused systemic increase in flow velocities in hyperdynamic circulatory state. Used to differentiate between hyperemia and vasospasm.

LR normal 1.1-2.3
LR = 3-6 mild/moderate vasospasm
LR > 6 severe vasospasm.

THINK ABOUT IT !

Let’s do a physiologic experiment. In this first image, we have a person at baseline, eupneic. We do a TCD in the MCA and we calculate the velocities and RI:

In this second picture, we asked this same person to hyperventilate until she starts to feel a little bit dizzy. Subsequently, paCO2 will decrease. Observe what happens with flow velocities and RI:

Explanation: A decrease in paCO2 will prompt to have vasoconstriction, decrease velocities and decreased flow (this is why whe hyperventilate in increased ICP. Remember that the cerebral blood flow is regulated regarding MAP (constant flow for MAP between 50-150) but this mechanism doesn’t apply to change in flow related to change in paCO2. As per the drawing above, paCO2 and CBF have a linear relationship in the CO2 reactivity zone.

INTERPRETATION AND PATTERNS

TRAUMATIC BRAIN INJURY: TBI can alter cerebral hemodynamics in different ways. Usually we will found a patter of hyperemia, ischemia or vasospasm. It is important to consider TCD a reproducible tool that can be repeated over time, used as monitoring and not just as a single measure. MCA is the easiest artery to localize, offering a greater reproducibility.

1. HIGH VELOCITIES PATTERN will be found in hyperemia and vasospasm.

HYPEREMIA: bilateral velocity increase (>2 times normal) with a normal Lindegaard ratio. Indexs are diminished (low resistance pattern). A mild increase in ICP can give a hyperemic pattern with augmented velocities in both MCA.

VASOSPASM: increased velocities + increased Lindegaard ratio. Adult criteria for vasospasm is Vm in MCA >120 cm/s with LR >3. Severe vasospasm when Vm >200 cm/s and LR >6. Bad prognosis when Vm accelerates >50-65 cm/s in les than 24h (more ischemia).

HELPFUL TIP

When vasospasm is suspected, please measure MCA velocities and calculate Lindegaard ratio in every segment, vasospam could be localized!

DRAWING MCA segments

REMEMBER

Difference about hyperemia and vasospasm

Both will have high velocities with increased cerebral blood flow.
Hyperemia will present with bilateral increased ICA velocities. Normal Lindegaard ratio.
Vasospasm usually unilateral with a higher Lindergaard ratio (usually above 3)

2. HIGH RESISTANCE PATTERN

ISCHEMIA: usually presented as low velocities with high resistive index. Understanding that F= v x A, when A is decreased due to vasospasm, velocities will be high. Very high velocities present more risk of ischemia.

INCREASED ICP: ow flow with high RI. When ICP increases, CPP decreases and flow decreases (it is more difficult to provide blood to the brain). There will be sequencial changes starting with a decrease in EDV with progressive increase of PI and RI. After that, Vm and PSV will decrease as PI and RI keep on increasing.

1) ↓ EDV  ↑ PI and RI

2) ↓ Vm and ↓Vs  ↑↑ PI and RI

BE CAREFUL

Low velocities exclude vasospasm only if increased ICP is excluded!! In severe increased ICP cases, velocities are reduced so a vessel narrowing can be missed!

3. TRAUMATIC BRAIN INJURY: TBI can alter cerebral hemodynamics in different ways. The most typical pattern is increased resistance due to increased ICP. We can also find patterns of hyperemia (early phases), ischemia or vasospasm (later as a complication). It is important to consider TCD a reproducible tool that can be repeated over time, used as monitoring and not just as a single measure. TCD can help optimizing CPP, hyperventilation treatment and decision making (eg. Proceed to brain death exam when no flow or systolic spikes pattern is stablished. MCA is the easiest artery to localize, offering a greater reproducibility.

Literature is mostly based in adults.

If Vm < 28 cm/s 80% Likelihood premature death.

IP >1.31 fairly correlates with ICP>20mmHg in first 24h after TBI.

EDV < 25 cm/s and PI> 1.31 after correcting hypotension, anemia, hypoxemia and hypoventilation predicts bad prognosis.

TCD could be use to optimize MAP and monitor the decrease in PI and increase in EDV and Vm.

High sensitivity in detecting increased ICP if PI>1.31 and EDV<25 in the abscense of dyastolic flow or with reversed dyastolic flow.

High NPV to identify normal ICP.

Literature in pediatrics

Bad prognosis if first 24h EDV<25cm/s and PI>1.3

Increased ICP if first 24h Vm<40 and PI>1.5

If autoregulation is lost: high CBF with high velocities, normal PI.

4. BRAIN DEATH: High resistance pattern. Visualize MCA through transtemporal window, if not posible, use transorbitary window to find carotid sifon. Four phases can be observed when ICP is super increased:

EDV decreases, PSV stable. PI and RI increase (High resistance pattern)
High systolic spikes. When ICP = MAP the dyastolic flow is 0. Reversible situation.
Oscilant pattern: short positive sytole with longer negative dyastole or systolic spikes with PSV < 40-50 cm/s with a duration >200ms without dyastole and Vm<10 cm/s.
Absence of flow. Needs of previous TCD with flow to comfirm abscense of flow.

BE CAREFUL

To think about brain death, flow abnormalities need to be bilateral, invariable and >30min.

Reverse dyastolic flow in ICA can suggest brain death but be careful with COFOUNDING FACTORS:

Absent dyastolic flow o retrograd dyastole can we seen in portosystemic shunts, aortic insufficiency or persistent ductus arteriosus.
Craniectomy or extracranial/VP shunts can present with normal flows despite being in the context of brain death.