Anesth Analg 2005;100:291-292
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000140816.04261.CE
LETTERS TO THE EDITOR
Perioperative Use of Transcranial Doppler
M. Sean Kincaid, MD,
Colleen M. Douville, RVT, and
Arthur M. Lam, MD
Cerebrovascular Laboratory, Harborview Medical Center, Departments of Anesthesiology and Neurological Surgery, University of Washington, Seattle, WA, artlam@u.washington.edu
To the Editor:
As avid proponents of the perioperative use of transcranial Doppler ultrasonography (TCD), we enjoyed reading the case report on intracranial arterial stenosis by Drs. Gundamraj and Lauer (1). However, we are concerned about several technical aspects in this article.
Transcranial Doppler, which is more accurately velocimetry, not flowmetry as stated in the report, is certainly useful in providing information regarding the nature of a stenotic lesion in the cerebral vasculature. Diagnosis of a middle cerebral artery stenosis, however, requires deliberate fulfillment of a number of criteria. A prerequisite for this task is accurate localization of the middle cerebral artery (MCA), a nontrivial process that was not described in the report. Given the displacement of the right MCA by tumor, a description of the depth of sample volume, relationship to MCA/anterior cerebral artery bifurcation, and waveform morphology would help establish the signal on the right side as MCA. If the MCA were displaced a sufficient distance, it would not be possible to obtain a signal with the TCD unless it were inadvertently directed at another artery. One aspect of the report that leads us to question the identification of both the right and left MCA are the flow velocities obtained. On the right, a velocity of 74 cm/s was found, which is not dramatically different from the normal range of 55 ± 12 cm/s. In contrast, on the left side, the side without tumor, the flow velocity was 34 cm/s, a velocity more appropriate for a geriatric patient than a 43 year old.
Following localization of the MCA on both sides, a velocity greater than 80 cm/s would be expected at the stenotic region of the MCA, with a side-to-side difference of at least 30 cm/s (2). This report nearly fulfills the first criterion and does fulfill the second, but to qualify as an MCA stenosis there would need to be demonstrated effects of turbulence and change in morphology of the TCD waveform from the stenosis, such as slowed acceleration and decreased pulsatility index distal to the stenosis. Should these stigmata of stenosis be found, this report would describe a mild MCA stenosis, not severe as it claims.
Without TCD flow velocity tracings to review, it is difficult to determine whether the hand-held technique for evaluating this patient’s flow velocity was adequate. Certainly for continuous evaluation of flow velocity during anesthesia induction, TCD probes should be fixed in place, not hand-held. Absence of signal, as is reported on the right side during the hypocapnia period, is more often than not a failure to find a signal or a loss of an established signal due to small hand movements. Although the arterial CO2 is not reported, no degree of hypocapnic vasoconstriction is able to drive cerebral blood flow to zero, as this report suggests. The inaccuracy of the hand-held technique for real-time evaluation of changes in flow velocity allows the findings at the time of induction to be overstated in their significance.
In fact, the changes in flow velocity are not far from what one would expect in a patient without intracranial pathology. An induction agent will decrease flow velocity due to flow-metabolism coupling, and subsequent hyperventilation will further decrease flow velocity by way of CO2 reactivity of the cerebral vasculature.
Where a TCD flow velocity tracing would be especially valuable is at the point where the diagnosis of intracranial hypertension was made. Increasing intracranial pressure (ICP) results in a progressive loss of diastolic flow velocity and eventually an oscillating pattern with diastolic flow reversal, not a loss of signal altogether (3). It is not clear from the case report whether such a well-established pattern of flow velocity change was the impetus for diagnosing and treating a high ICP.
In short, we believe the technology of TCD is currently underutilized in the perioperative setting, but this case report leaves one wondering whether a true crisis was averted, or whether expected findings from a TCD study were misinterpreted.
References
- Gundamraj RN, Lauer KK. Diagnosis of intracranial arterial stenosis using transcranial Doppler flowmetry. Anesth Analg 2004; 98: 1776–8.[Abstract/Free Full Text]
- Ley-Pozo J, Ringelstein EB. Noninvasive detection of occlusive disease of the carotid siphon and middle cerebral artery. Ann Neurol 1990; 28: 640–7.[Medline]
- Hassler W, Steinmetz H, Pirschel J. Transcranial Doppler study of intracranial circulatory arrest. J Neurosurg 1989; 71: 195–201.[Medline]
Response
Rao N. Gundamraj, MD, and
Kathryn K. Lauer, MD
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, klauer@mcw.edu
In Response:
We thank Drs. Kincaid and Lam and Ms. Douville for the remarks. We will try to reply to their concerns.
In our case, the Doppler recordings were obtained from a handheld probe utilizing the TC2000 Nicolet. Although neither of us personally performed the readings, an experienced transcranial ultrasonographer obtained them. The middle cerebral artery (MCA) M1 segment was identified by obtaining a signal, tracing the vessel to the bifurcation and identifying the anterior cerebral artery. The VMCA was recorded at 50, 52, and 54 mm depths, and the depth of maximum velocity was chosen for recordings. I regret that the flow velocity recorded tracings were not available to us for the purpose of this case report.
Although the initial recording on the nontumor side was low (43 cm/s), this patient had received some sedation, which could have accounted for the lower velocity. Cheng et al. (1) found a 17–21% decrease in flow velocity that recovered after administration of midazolam.
The measurements of flow velocity were done with an attempt made to maintain the signal during induction and hyperventilation, meaning the probe was held with an attempt to maintain the same angles. Clearly, the most appropriate and best studies are done with stationary probes that are fixed to patients’ heads during induction. However, other published studies have been done with handheld readings (2).
In this case, the drop of VMCA was surprising to us. Although Drs. Kincaid and Lam and Ms. Douville discussed the expected waveforms in patients with severe intracranial pressure, we did not see that type of pattern, not that we would have expected this to be the issue. In this case, hypotension and increased cerebrovascular resistance seem to have been the precipitating cause of the loss of VMCA. Could this been an overstatement of the VMCA decreases seen? Certainly, it would be have been more likely after induction, when airway manipulation may have altered the angle of insonation. But during hyperventilation, we were convinced that this was due to pathologic blood flow, as there was less head movement, and the probe was not appreciably moved by all accounts. We appreciate the comments made that slight changes in angles can lead to a loss of signal that may be misinterpreted. Was this the case in this patient? Although we could have been fooled, we did our best to follow the signal closely.
In the same vein, in the OR environment, where often the circumstances may not be ideal, there may also be flow changes that are underappreciated due to the lack of ability to monitor. We heartily agree that continued utilization of transcranial Doppler ultrasonography should carefully and conscientiously evolve into a more common monitor in the perioperative management of patients with intracranial risk.
References
- Cheng MA, Hoffman WE, Baughman VL, Albrecht RF. The effects of midazolam and sufentanil sedation on middle cerebral artery blood flow velocity in awake patients. J Neurosurg Anesthesiol 1993; 5: 232–6.[Web of Science][Medline]
- Brauer P, Kochs E, Werner C, et al. Correlation of transcranial Doppler sonography mean flow velocity with cerebral blood flow in patients with intracranial pathology. J Neurosurg Anesthesiol 1998; 10: 80–5.[Web of Science][Medline]
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