Transcranial Doppler: An Introduction for Primary Care Physicians

Sickle Cell Disease

This may be one of the most important TCD applications, and it is of very special interest for the primary care physician. Recent guidelines regard the use of TCD⁴ as a type A level of evidence (established as useful predictive for suspected condition), and class I (evidence provided by prospective studies in broad spectrum of persons with suspected condition) screening tool to assess stroke risk in children aged 2 to 16 years with sickle cell disease.

Sickle cell disease is associated with progressive occlusion of large intracranial arteries (most frequently the intracranial ICA and MCA). Total occlusion of any one of these arteries will lead to a massive stroke. These arteries are very accessible to TCD insonation and TCD can monitor FVs over time.

According to the TCD criteria for sickle cell disease, a MFV of up to 170 cm/s is considered normal and a MFV of 171 to 199 cm/s is called “conditional.” MFV of equal or greater than 200 cm/s is considered abnormal and require transfusion.⁵

A mean FV (MFV) of 200 cm/s or greater is accompanied by a stroke risk of 40% within the next 3 years. Transfusion, with reduction of hemoglobin S to less than 30% of total hemoglobin, will lower this risk by 70% compared with standard care alone.^5–8 An optimal timing to re-screen children with sickle cell disease and normal TCD is not set, but a repeat TCD examination every 6 months seems to be a reasonable objective.

Intracranial Vasospasm

Intracranial vasospasm is the constriction of cerebral blood vessels due to the presence of blood in the subarachnoid space after a trauma or rupture of cerebral aneurysm. The vasospasm—if severe—may result in ischemia to the brain and is associated with an increase in mortality of 1.5- to 3-fold during the first 2 weeks after subarachnoid hemorrhage (SAH).⁹ Vasospasm typically occurs within 3 to 21 days after SAH and may last for 12 to 16 days.¹⁰ Clinically this manifests a deterioration of the patient’s level of consciousness, new focal neurological signs, and headaches.

The pathophysiological changes that underlie vascular constriction after SAH is not completely known but may include changes within the vessel walls themselves, alteration of levels of vasoactive substances, and broader pathologic conditions such as immune responses, inflammation, and oxidative damage.

Subarachnoid hemorrhage occurs in an estimated 25,000 to 30,000 people in the United States each year.¹⁰ It could be identified by TCD up to 1 to 2 days before it becomes clinically symptomatic allowing for immediate initiation of triple H therapy.

Vasospasm that follows SAH causes increased FV inside intracranial vessels. This can be detected by TCD indicating the need for treatments before the onset of ischemia. TCD is already in use to diagnose and monitor management of vasospasm in emergency and critical settings according to established guidelines.^11–16 Usually a baseline TCD is performed at the earliest possible time (day 0); a daily TCD is then performed during days 3 to 10. A mean FV of 120 cm/s is considered a sign of mild spasm and a value above 180 cm/s is considered a sign of severe spasm. Mean FV obtained by TCD was found to correlate well with the angiographic residual lumen diameter of the MCA, and it was found to have excellent specificity (100%) but only good sensitivity (58.6%) in diagnosing vasospasm only due to the involvement of vessels that are not evaluated by TCD at times.¹³ The accuracy of TCD in the diagnosis of cerebral vasospasm can be increased by using the Lindegaard ratio (see Table 3). By calculating the MFV ratio between MCA, ACA, and the ipsilateral ICA (V_MCA/V_ICA or V_ACA/V_ICA), changes due to generalized hyperemia can be distinguished from vasospasm.¹⁷

Arterial Stenosis and Occlusion

TCD measurements that correlate with stenosis would be increase FV at the stenotic site.

1. Decrease FV downstream from a stenotic site.

2. Decrease FV proximal and increase PI proximal to the stenotic site.

3. Increase FV and/or reverse flow in collateral vessels (like the finding of reverse blood flow in the OA in case of ipsilateral carotid artery occlusion and the finding of increased FV of the first segment of contralateral ACA shunting blood through the anterior communicating artery to the contralateral hemisphere in the same scenario).

In a case of total occlusion, there should be no flow signal from the occluded site. Increased velocity and/or reversed flow in the collateral vessels may also be seen. Other vessels in the same window should be accessible for insonation. A decrease in blood FV proximal to the site of the occlusion may also be seen. The presence of multiple findings described above increase the likelihood of the presence of stenosis or occlusion in a given vessel.¹⁸

Similar TCD approaches are already utilized in some centers for the detection of occluded vessels in acute and subacute stroke. It is the noninvasive test of choice to evaluate the cerebrovascular tree when a contraindication exists to the use of MRI and CT and cerebral angiography. TCD testing has a high positive predictive value of >80%¹⁹ making TCD an attractive tool for assessing the cerebrovascular tree in low risk patients.

In the Midwestern region of the United States, Medicare pays $62.31 for the professional component and $465.30 for the technical component of MRA of the intracranial vessels and pays additional and a similar amount for MRA of the cervical vessels. It only pays $51.99 for the professional component and $245.47 for a complete TCD study (for both intracranial and extracranial vessels). Since TCD is a noninvasive^20,21 and inexpensive technique with no known risks or side effects, it can be an excellent tool for frequent follow-up of vascular lesions to assess effectiveness of a therapy without the concern of subjecting the patient to frequent radiation and the increasing costs of diagnostic testing like MRI.

TCD can also be used to observe the effectiveness of thrombolytic treatment in stroke patients. If the vessel is not recannulized, other treatments can be considered.²¹

Monitoring for Sources of Emboli and Heart Shunts during Procedures

Microemboli traveling along an insonated vessel will appear as high intensity transient signals (HITS) on the TCD spectrum. Although the exact clinical relevance of these findings remains uncertain, it may identify high-risk status for clinical stroke offering an opportunity to localize the source in patients with multiple potential sources and providing a possible monitoring tool for the efficacy of a chosen treatment.

TCD can also be used as a quality control, training, and monitoring tool inside operation rooms for surgeries with risk of embolization^22–24 their contribution to the postoperative neurobehavioral changes.

TCD can detect the presence of right-to-left shunts such as patent foramen ovale (PFO) in patients with contraindications to transesophageal echo (TEE) with similar sensitivity and specificity^25–28. This clinic use requires the administration of agitated saline after which the patient performs a valsalva maneuver²⁸. The test is positive for right-to-left shunt if a shower of high signal material (air) is detected in the MCA by TCD 5 to 10 seconds after the intravenous injection of 10 mL of agitated saline²⁶. If this shower of air emboli is detected after a minute of injection, it might indicate the presence of a pulmonary shunt; a diagnosis that cannot be obtained by TEE.

Brain Death (cerebral circulatory arrest)

TCD evaluation of a brain death patient yields a “reverberating or oscillating” pattern of flow (normal arterial blood flow in systole and reversed flow in diastole secondary to the very high distal brain resistant in the brain dead patients) leading to absence of net flow per unit of time.^29–32 The reverberating pattern may progress to “no flow” in the advanced stages of brain death. Although it is not a common practice to get a TCD as part of a brain death examination, it can, however, be used as a useful adjunct test.³³

Testing for Cerebrovascular Autoregulation

Cerebral autoregulation is the ability to maintain the cerebral blood flow despite minute-to-minute variation in cerebral perfusion rate. In a normal physiologic state, this can be achieved by the arteriolar control over the cerebral peripheral vascular resistance. People with impaired cerebral autoregulation might have a variety of presentations such as headache, dizziness, and syncope.

TCD measurements of FV and PI before and during pharmacological or mechanical manipulation of autoregulation and systemic blood pressure can be used to monitor the reactivity of the intracranial vasculature tree. Breath-holding and acetazolamide administration are two of the most used maneuvers to manipulate cerebral autoregulation.^34–36

The breath-holding test is used to assess cerebrovascular reactivity to hypercapnia as calculated by means of the breath-holding index (BHI). The index is calculated by dividing the percent increase in mean FV (MFV) during breath-holding by the breath-holding time (in seconds) that subjects held their breath after a normal inspiration: BHI = {[MFV at the end of breath-holding − resting MFV]/resting MFV} × (100/seconds of breath-holding).

This technique can be useful in testing the candidacy of asymptomatic patients with internal carotid artery stenosis for endarterectomy surgery. Recent data³⁷ showed increased risk of ischemic strokes in patients with severe (>70%) carotid stenosis and impaired autoregulation as tested by TCD. TCD can also assess the potential risk of cerebral ischemia in patients with carotid stenosis going for major anesthesia and surgery. TCD might also be a useful investigation in work up of a patient with vasovagal syncope^38–41.