Anesth Analg 2004;98:1776-1778
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000116926.28832.40
NEUROSURGICAL ANESTHESIA
Diagnosis of Intracranial Arterial Stenosis Using Transcranial Doppler Flowmetry
Rao N. Gundamraj, MD, and
Kathryn K. Lauer, MD
From the Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin
Address correspondence and reprint requests to Kathryn K. Lauer, MD, Associate Professor, Department of Anesthesiology, Medical College of Wisconsin, 9200 W. Wisconsin Avenue, Milwaukee, WI 53226. Address email to klauer{at}mcw.edu
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Abstract
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In this case report we describe the use of transcranial Doppler flowmetry during induction of anesthesia in a patient with a large pituitary tumor. In this patient, both IV anesthesia induction and onset hyperventilation were followed by severe decreases of flow velocity in the middle cerebral artery of the affected side.
Transcranial Doppler detected critical blood flow reduction in response to anesthesia induction and onset of hyperventilation in a brain tumor patient.
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Introduction
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Skull-base tumors can impinge on the intracranial internal carotid artery (ICA) (1). A preoperative asymptomatic stenosis may become critical during anesthetic manipulations. We describe a case in which transcranial Doppler (TCD) flowmetry signaled the danger of neurologic compromise during craniotomy in a patient with a large pituitary tumor.
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Case Report
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A 43-yr-old otherwise healthy woman presented with a history of right retro orbital pain for eight months, associated with blurred vision. Computed tomography (CT) scan and imaging demonstrated a mass in the clivosellar region extending into the cavernous sinus and the right mesiotemporal lobe; the mass displaced the right ICA and middle cerebral artery (MCA) (Fig. 1). A transnasal biopsy was performed and pathology demonstrated a nonsecretory pituitary adenoma. The patient was scheduled to undergo craniotomy and tumor resection.
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Figure 1. Magnetic resonance image coronal view T1 post-gadolinium contrast showing the pituitary tumor encasing the right internal carotid artery and extending to the cavernous sinus and hypothalamus.
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Before induction of anesthesia, MCA blood flow mean velocity (VMCA) was measured manually at the M1 segment through bilateral temporal windows with TCD. The TCD uses a 2 MHz probe (TC 2000; Nicolet Corp., Madison, WI) and was obtained by insonation at premarked temporal windows by a trained ultrasonographer with free-hand technique by measuring the maximum velocity at the same depth 3 times and recording the highest of the 3. Manual recordings were obtained, as our TCD flowmeter had only one probe, and bilateral recordings were desired. Baseline left VMCA was 34 cm/s whereas the right VMCA was 74 cm/s, suggesting possible right ICA or MCA stenosis by tumor encasement. After right VMCA reading, the right temporal window was continually manually monitored through anesthetic induction with an attempt to keep the angle of insonance constant.
With standard ASA monitors and a radial artery catheter, the anesthesia was induced with 300 mg of sodium thiopental, 8 mg of pancuronium, and 100 µg of fentanyl. Anesthesia was maintained with isoflurane in air and oxygen (fraction of inspired oxygen = 0.6). Immediately after induction, right VMCA decreased to undetectable levels. This flow decrease improved without intervention and stabilized over the 10 min postinduction. Hyperventilation was then instituted to decrease intracranial pressure (ICP), which resulted in a second critical decrease in VMCA (Table 1). With passive hypoventilation to resume normocapnia, right VMCA increased. Normocapnia was maintained during the rest of the case, and mean arterial blood pressure was supported with IV phenylephrine to maintain preoperative values. Because of the anticipated increased ICP, a lumbar drain was placed and the patient underwent craniotomy through a pterional approach. Surgeons confirmed the presence of a large tumor encasing the right ICA, which was resected subtotally. The patient emerged from anesthesia uneventfully and recovered without neurologic deficit.
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Discussion
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TCD is a noninvasive diagnostic tool that uses sound waves and the energy reflected to assess the flow characteristics of insonated cerebral arteries. The velocities measured by TCD directly reflect the hemodynamic changes in the vessel studied or the originating vessel. The relationship between velocity and cross-sectional area in a blood vessel can be determined by the formula Q = V x A, where Q is the flow, V is the velocity, and A is the cross-sectional area. If flow remains constant in the presence of stenosis, the velocity should increase (2).
Cerebral vascular flow changes to changes in arterial carbon dioxide concentration (PaCO2) are well known. This principle of cerebrovascular reactivity has been used in clinical trials to predict the outcome from carotid occlusive disease (3–7). It has been shown that cerebrovascular reactivity is preserved during general anesthesia (8–10). In cases of focal cerebral ischemia, the effect of hypocapnia has been mixed. Hypocapnia has demonstrated to both worsen and improve blood flow in the vulnerable brain (11–13).
In our case, the VMCA decreased to critical levels twice. The first was during induction of anesthesia with IV sodium thiopental. This was likely attributable to both the cerebral vasoconstriction and mild transient hypotension created by thiopental (14,15). Previous studies have shown that intracranial pathology can alter the blood flow response (as measured by TCD) to anesthesia induction. In areas with pathology, the correlation between blood flow as measured by TCD and xenon-CT is less than that in normal brain (18). In another study, patients with tumor (right or left) were found to have less blood flow in the right MCA territory (19).
Studies using carotid balloon occlusion have demonstrated a reduction in VMCA to about 40%–50% of baseline as a critical threshold, which would result in neurologic complications as revealed by electroencephalography (EEG) (16,17). However none of the studies have demonstrated a VMCA close to zero with hyperventilation in patients with carotid occlusion. The combination of severe stenosis from tumor encasement and normal cerebrovascular reactivity to hypocapnia may have contributed to VMCA reduction in our case. Concominant monitoring with another monitor for ischemia, such as EEG, may have been helpful in ascertaining the presence of ischemia.
Our case is the first to report such a critical reduction in VMCA with hypocapnia under anesthesia. Possibly because of early recognition, the patient did not develop any immediate postoperative or late neurologic sequelae from this event. This report underscores the potential benefit from TCD in the perioperative period, which in this case provided important physiologic information that may have avoided a cerebral ischemic insult.
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References
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Accepted for publication December 17, 2003.
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Abstract
Introduction
