Transcranial Doppler ultrasonography (TCD) is a tool employed by the neurosurgeon and neurointensivist in the management of vasospasm in the intensive care unit after aneurysmal subarachnoid hemorrhage. A review of the current indications, monitoring parameters, indices, and relevance of modern TCD technology is provided, as well as algorithms for the use of TCD ultrasonography in the management of patients with subarachnoid hemorrhage. Other current uses of TCD ultrasonography are also discussed in the setting of neurocritical care.
Aneurysmal subarachnoid hemorrhage and its accompanying sequelae are management challenges for the neurosurgeon and neurointensivist. Transcranial Doppler ultrasonography (TCD) has emerged as a tool used extensively by many centers for the surveillance and monitoring of vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The overall management of the primary and secondary complications of SAH is complex, and the use of appropriate tools and diagnostic strategies is helpful. TCD has emerged as an inexpensive, noninvasive tool used not only for bedside monitoring of intracerebral hemodynamic changes seen with SAH. TCD can also be used to evaluate other neurologic conditions in the Neurosciences Critical Care Unit such as intra- and extracranial vascular stenosis, arteriovenous malformations, intraoperative emboli, venous sinus thrombosis, ischemic stroke, sickle cell disease, and brain death. This article provides a brief review of the pathophysiology of vasospasm, and other devices used to detect vasospasm. Also reviewed are the indices and technical aspects of TCD ultrasonography, the interpretation of data obtained from TCD studies, and TCD-based management algorithms for vasospasm.
Vasospasm after subarachnoid hemorrhage
The diminution of blood flow transiting through the cerebral vasculature seen after aneurysmal SAH due to vasoconstriction is referred to as vasospasm. Arterial spasm after SAH was originally described by Ecker, and has since been the subject of decades of laboratory research and clinical investigation. Various definitions of vasospasm are employed, including vasospasm seen on digital subtraction angiography or computed tomography angiography referred to as “angiographic vasospasm” and “clinical vasospasm,” which includes “delayed ischemic neurologic deficit” (DIND) and “delayed cerebral ischemia.” (DCI) DIND and DCI refer to clinical signs of transient or permanent neurologic deficits occurring remotely from the initial SAH or surgery, after other complications of SAH potentially causing neurologic deficits have been excluded. The exact cause of vasospasm is not clearly understood, but it is thought that extra-arterial blood products surrounding the arterial wall trigger a cascade of events at the cellular level, that culminate in vasoconstriction. Other factors involved include decreased vascular autoregulation, reversible vasculopathy, and relative hypovolemia. A further review of the current pathophysiology of vasospasm is presented in this edition of Neurosurgical Clinics . Vasospasm occurs most intensely adjacent to the subarachnoid clot, but can occur distantly from the majority of the subarachnoid blood, and is predicted by clot volume, age, location, and density of the SAH seen on the initial computed tomography (CT) scan. In the past, the most likely cause of mortality after SAH was from aneurysmal rerupture in the early period after SAH. Due to more aggressive early surgical and endovascular treatment of ruptured aneurysms, this has now been replaced by hydrocephalus and vasospasm.
The incidence of angiographic vasospasm after aneurysmal subarachnoid hemorrhage has been estimated to occur in 50% to 70% of patients with aneurysmal SAH, with approximately 50% of those exhibiting symptoms of clinical vasospasm. A review of angiography studies of more than 2700 cases of aneurysmal SAH found the average incidence to be approximately 67%, with the highest incidence occurring between days 10 and 17 after SAH. Vasospasm classically is reported to occur from days 4 to 14 after aneurysmal SAH, but variations on this rule abound. The incidence of early angiographic vasospasm, detected within 48 hours of aneurysm rupture, occurs in 10% to 13% of SAH patients and is associated with prior aneurysmal SAH, large aneurysms, intraventricular hemorrhage, and with reduced morbidity at 3 months. The impact of clinical vasospasms on outcome has been established, with both morbidity and mortality estimates ranging from 10% to 20%.
Modalities used for monitoring cerebral vasospasm
It should be emphasized that vasospasm is a clinical diagnosis, and radiographic studies and other markers of brain perfusion support this diagnosis through evidence of diminished vessel caliber. Left unchecked, patients with vasospasm may progress from diffuse neurologic signs such as confusion, increasing somnolence, and combativeness to focal neurologic deficits suggestive of infarction. Radiographic findings often precede such clinical deficits, and thus offer the opportunity to intervene to prevent neurologic injury. To this effect, in 1982 Aaslid and colleagues provided the first descriptions of the use of TCD for such purposes, by monitoring flow in intracranial arteries and later used TCD in the assessment of arterial vasospasm. Much work has been done on the use of this technology in the evaluation of cerebral blood flow, due to its relative inexpensiveness, bedside availability, and noninvasive nature. The gold standard for the diagnosis of cerebral vasospasm has remained digital subtraction angiography. Because of its expense, potential for severe complications, and the need to move the patient to the angiography suite, this test is impractical for use as a frequent monitor of vasospasm. The major advantage of angiography is the potential for both diagnosis and therapeutic intervention, discussed elsewhere in this issue. Computed tomography angiography (CTA) has emerged as a potentially helpful tool in the evaluation of vasospasm, with relatively good sensitivity and specificity for discovery of severe vasospasm in the proximal arteries of the circle of Willis, and with a high negative predictive value. Some have raised concern that sending a patient who has severe vasospasm to undergo CTA may delay definitive treatment with angioplasty or intra-arterial injection of antispasmodic agents. CTA is relatively insensitive for mild and moderate vasospasm, and ideally requires a baseline study early on in the course of SAH for purposes of comparison. Ionita and colleagues reported that with strongly positive or strongly negative TCD findings and a correlative neurologic examination, obtaining a CTA was not of added value in the management of such patients. These investigators suggested that CTA’s best role may be in a patient population with indeterminate TCD findings and an examination suggestive of vasospasm. Magnetic resonance angiography (MRA) has been used by some to assess for vasospasm after SAH, although it is a technology limited by logistics, acquisition time, motion, and hardware artifact. Other emerging technologies employ an altogether different approach to the detection of vasospasm. Perfusion imaging such as MR perfusion, CT perfusion (CTP), single photon emission computed tomography (SPECT), positron emission tomography (PET), and diffusion-weighted MR imaging are being studied for use with this indication. Of these technologies, a combination of CTA and CTP may be useful as a second-tier diagnostic study in cases where a high index of suspicion exists or TCDs are not reliable. Continuous electroencephalography (EEG) is also under investigation as a means to detect subclinical cortical dysfunction related to inadequate cerebral perfusion from vasospasm. A recent study has shown this to be a beneficial mode of monitoring SAH patients, allowing for detection of subsequent vasospasm days before the detection of abnormalities by TCD. Several logistical limitations to continuous EEG monitoring preclude widespread use of this technique currently, although further data correlating this technique to the development of vasospasm may make its use more widespread in the future.
TCD has become the most common screening tool for vasospasm monitoring due to its portability and noninvasive nature, and ease of repeat testing. Many advocate frequent TCD monitoring with schedules ranging from every other day to twice daily, usually starting on the first day after SAH onset, ending with resolution of vasospasm. TCD is also recommended for following the temporal course of angiographic vasospasm during its peak incidence.
The efficacy of TCD as a monitor for vasospasm is controversial. TCD is operator dependent, and limitations of insonation secondary to adequate acoustic windowing restrict its use in about 8% of patients. Other limiting factors include the rate of false-negative studies and variability between technicians performing examinations. These limitations may be overcome with new TCD techniques.
Many studies have established TCD threshold velocities for vasospasm diagnosis. These studies usually incorporate TCD and angiographic comparisons. In such work, a relationship has been demonstrated between intracerebral vessel diameter on angiography and velocities measured with TCDs. The underlying principle used for TCD estimations of cerebral blood velocity is based on variations of the Bernoulli equation. The velocity of blood flow in a conduit is inversely related to the diameter of that conduit. As the diameter of a blood vessel decreases, the blood velocity will increase. Although the vessel itself is not directly visualized with TCD ultrasonography, an indirect evaluation of the vessel diameter is achieved using the Doppler effect by calculating the Doppler shift, which is the difference between the frequencies of the transmitted and received ultrasound waves. The following equation allows for the calculation of vessel flow velocities and gives an indirect indication of vessel diameter.
where f 0 is transmitted ultrasound frequency (1.0–3.0 MHz in TCD)
c is velocity of sound in blood (approximately 1540 m/s)
v is velocity of blood flow.
Modalities used for monitoring cerebral vasospasm
It should be emphasized that vasospasm is a clinical diagnosis, and radiographic studies and other markers of brain perfusion support this diagnosis through evidence of diminished vessel caliber. Left unchecked, patients with vasospasm may progress from diffuse neurologic signs such as confusion, increasing somnolence, and combativeness to focal neurologic deficits suggestive of infarction. Radiographic findings often precede such clinical deficits, and thus offer the opportunity to intervene to prevent neurologic injury. To this effect, in 1982 Aaslid and colleagues provided the first descriptions of the use of TCD for such purposes, by monitoring flow in intracranial arteries and later used TCD in the assessment of arterial vasospasm. Much work has been done on the use of this technology in the evaluation of cerebral blood flow, due to its relative inexpensiveness, bedside availability, and noninvasive nature. The gold standard for the diagnosis of cerebral vasospasm has remained digital subtraction angiography. Because of its expense, potential for severe complications, and the need to move the patient to the angiography suite, this test is impractical for use as a frequent monitor of vasospasm. The major advantage of angiography is the potential for both diagnosis and therapeutic intervention, discussed elsewhere in this issue. Computed tomography angiography (CTA) has emerged as a potentially helpful tool in the evaluation of vasospasm, with relatively good sensitivity and specificity for discovery of severe vasospasm in the proximal arteries of the circle of Willis, and with a high negative predictive value. Some have raised concern that sending a patient who has severe vasospasm to undergo CTA may delay definitive treatment with angioplasty or intra-arterial injection of antispasmodic agents. CTA is relatively insensitive for mild and moderate vasospasm, and ideally requires a baseline study early on in the course of SAH for purposes of comparison. Ionita and colleagues reported that with strongly positive or strongly negative TCD findings and a correlative neurologic examination, obtaining a CTA was not of added value in the management of such patients. These investigators suggested that CTA’s best role may be in a patient population with indeterminate TCD findings and an examination suggestive of vasospasm. Magnetic resonance angiography (MRA) has been used by some to assess for vasospasm after SAH, although it is a technology limited by logistics, acquisition time, motion, and hardware artifact. Other emerging technologies employ an altogether different approach to the detection of vasospasm. Perfusion imaging such as MR perfusion, CT perfusion (CTP), single photon emission computed tomography (SPECT), positron emission tomography (PET), and diffusion-weighted MR imaging are being studied for use with this indication. Of these technologies, a combination of CTA and CTP may be useful as a second-tier diagnostic study in cases where a high index of suspicion exists or TCDs are not reliable. Continuous electroencephalography (EEG) is also under investigation as a means to detect subclinical cortical dysfunction related to inadequate cerebral perfusion from vasospasm. A recent study has shown this to be a beneficial mode of monitoring SAH patients, allowing for detection of subsequent vasospasm days before the detection of abnormalities by TCD. Several logistical limitations to continuous EEG monitoring preclude widespread use of this technique currently, although further data correlating this technique to the development of vasospasm may make its use more widespread in the future.
TCD has become the most common screening tool for vasospasm monitoring due to its portability and noninvasive nature, and ease of repeat testing. Many advocate frequent TCD monitoring with schedules ranging from every other day to twice daily, usually starting on the first day after SAH onset, ending with resolution of vasospasm. TCD is also recommended for following the temporal course of angiographic vasospasm during its peak incidence.
The efficacy of TCD as a monitor for vasospasm is controversial. TCD is operator dependent, and limitations of insonation secondary to adequate acoustic windowing restrict its use in about 8% of patients. Other limiting factors include the rate of false-negative studies and variability between technicians performing examinations. These limitations may be overcome with new TCD techniques.
Many studies have established TCD threshold velocities for vasospasm diagnosis. These studies usually incorporate TCD and angiographic comparisons. In such work, a relationship has been demonstrated between intracerebral vessel diameter on angiography and velocities measured with TCDs. The underlying principle used for TCD estimations of cerebral blood velocity is based on variations of the Bernoulli equation. The velocity of blood flow in a conduit is inversely related to the diameter of that conduit. As the diameter of a blood vessel decreases, the blood velocity will increase. Although the vessel itself is not directly visualized with TCD ultrasonography, an indirect evaluation of the vessel diameter is achieved using the Doppler effect by calculating the Doppler shift, which is the difference between the frequencies of the transmitted and received ultrasound waves. The following equation allows for the calculation of vessel flow velocities and gives an indirect indication of vessel diameter.
where f 0 is transmitted ultrasound frequency (1.0–3.0 MHz in TCD)
c is velocity of sound in blood (approximately 1540 m/s)
v is velocity of blood flow.
Indices and technical aspects TCD ultrasonography
TCD provides several indices that are useful when making clinical decisions regarding the management of vasospasm in SAH patients. The flow velocity (FV) is the most used metric and is further defined by the mean flow velocity (MFV), the peak systolic flow velocity ( V s ), and the end-diastolic flow velocity ( V d ). In clinical practice, the mean flow velocity (MFV = {V s − V d /3} + V d ) is typically reported, but additional information is used to calculate the resistance index (RI) and pulsatility index (PI). Both the RI and PI are presumptive measures of downstream vascular resistance, and serve as indicators of extravascular or intracranial pressure (equations 1, 2 ). Elevated RI and PI occur secondary to vascular stenosis, distal vasospasm, and elevated intracranial compliance.
The Lindegaard index (LI) is an important method of correcting for increases in hyperdynamic systemic flow velocities, either physiologic or induced, in patients with SAH. To calculate the LI, the MFV of the middle cerebral artery (MCA) is compared with an ipsilateral extracranial vessel, namely the proximal internal carotid artery (ICA). This ratio (equation 3 ) helps to distinguish global hyperemia from vasospasm, especially in the setting of triple-H therapy.
An understanding of normal TCD velocities is vital to understanding TCD findings of vasospasm, and it is recognized that each major cerebral artery has its own range of normal values. Data from a large study with normal volunteers has proposed normal values for mean velocity and pulsatility index in the anterior and posterior circulation ( Tables 1–3 ). The velocities are reported for men and women separately, as many of these differences were found to be statistically significant. FV may vary between technicians acquiring TCD indices by as much as 7.5% on the same day and 13.5% on different days. A combination of TCD velocities, Lindegaard ratios, clinical characteristics, and a spasm index (TCD velocities/hemispheric blood flow obtained from 133 Xe cerebral blood flow studies), called the Vasospasm probability index, has been proposed recently. The combination of Fisher grade, Hunt and Hess grade, and spasm index accurately detected clinical vasospasm in 92.9%. A model that included Fisher grade, Hunt and Hess grade, and Lindegaard ratio had an accuracy of 89.9% for detection of angiographic vasospasm. This study, along with others, suggests that the predictive value of TCD can be improved when used with other indicators. Another proposed “vasospasm risk index” found that a combination of high Fisher grade, early increase in the MCA MFV 110 cm/s or more recorded on or before post-SAH day 5, Glasgow Coma Scale score less than 14, and ruptured aneurysm of the anterior cerebral or internal carotid arteries translated into a high probability of identifying patients who would develop symptomatic vasospasm.
Related posts:
Epidemiology of Aneurysmal Subarachnoid Hemorrhage
Outcome and Cost of Aneurysmal Subarachnoid Hemorrhage
Endovascular Management of Cerebral Vasospasm
Medical Complications After Subarachnoid Hemorrhage
Cerebral Salt Wasting: Pathophysiology, Diagnosis, and Treatment
Risk Factors and Medical Management of Vasospasm After Subarachnoid Hemorrhage
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