Anesth Analg 2006;102:896-899
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000195580.31382.38
NEUROSURGICAL ANESTHESIA
Cerebral Ischemia as an Apparent Complication of Anterior Cervical Discectomy in a Patient with an Incomplete Circle of Willis
John C. Drummond, MD,
Raymond N. Englander, MD, and
Catherine J. Gallo, MD
Department of Anesthesiology, The University of California, San Diego; VA Medical Center, San Diego; Department of Neurology, Department of Neurosurgery, Sacred Heart Medical Center, Eugene, Oregon
Address correspondence and reprint requests to John C. Drummond, MD, VA Medical Center, Anesthesia Service-125, 3350 La Jolla Village Drive, San Diego CA 92161. Address e-mail to jdrummond{at}ucsd.edu.
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Abstract
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A 58-yr-old patient sustained a cerebral ischemic injury in the distribution of the carotid artery ipsilateral to retraction during an anterior cervical discectomy. Relative hypotension was permitted during the anesthetic. Angiography revealed an anatomic variant of the circle of Willis that resulted in minimal collateralizaton of the left internal carotid artery territory. The combination of that vascular variant with relative hypotension and some degree of carotid compression appears to have resulted in clinically significant cerebral ischemia.
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Introduction
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Among the neurologic complications of anterior cervical discectomy with (ACD) or without (ACDF) fusion enumerated in standard surgical texts is stroke caused by retraction/compression of the carotid arteries (1). However, the electronically searchable literature gives no indication as to the incidence of this complication. In fact, the published literature contains only a single report of stroke that may have occurred as a consequence of reduction of cerebral blood flow (CBF) caused by retraction during ACD/ACDF (2). However, the authors have encountered at least three such cases in either clinical or medical-legal contexts and herewith submit a description of one for which complete information is accessible. Among the reasons for presenting this case report is that anomalies of the intracranial collateral blood supply of a type that was present in our patient, and that probably created a predisposition to his injury, are relatively common in the general population. This case report draws the attention of clinicians to a complication that may be inherent to this procedure but that may have been under-reported.
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Case Report
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A 58-yr-old male presented for C5-6 ACDF for progressive spondylosis with radiculopathy but without myelopathy. He took no medications and reported no chronic illnesses, including any form of vascular disease. He had undergone tonsillectomy and lumbar laminectomy, both uneventfully. Immediately preoperatively, arterial blood pressure was 136/80; mean arterial blood pressure (MAP) was 99, P 62, R 16. Induction of anesthesia was accomplished with propofol, fentanyl, and succinylcholine. The trachea was intubated uneventfully. Anesthesia was maintained with isoflurane, 0.75%–1.5% inspired and 50% nitrous oxide.
An incision was made on the left side of the neck. Exposure of the anterior surfaces of the C5 and C6 vertebral bodies was facilitated by a Caspar self-retaining retractor system. The tips of the retractor blades were anchored under the medial borders of the longus colli muscles. The presence of a palpable carotid pulsation cephalad to the lateral retractor blade was confirmed when the exposure was complete. The temporal pulse was not evaluated. Discectomy and fusion were performed without difficulty. The fusion used iliac crest graft and a SlimLoc plate. The procedure (induction of anesthesia to the conclusion of surgery) was accomplished in 1 h and 40 min. During that time, the ranges of physiologic values were as follows: Spo2 99–100, heart rate 40–68 bpm (sinus rhythm), MAP 48–68 mm Hg. The average MAP for the recorded 5-min intervals from induction to the beginning of emergence was 56 mm Hg, with a pressure nadir of 75/35 mm Hg. ETco2 was not recorded quantitatively.
At the conclusion of the procedure, the inhaled anesthetics were discontinued. Spontaneous ventilation and responsiveness to the endotracheal tube ensued and the trachea was extubated. However, the patient did not recover full consciousness and was bilaterally decerebrate with preserved pupillary responses and somewhat diminished corneal reflexes. The trachea was reintubated. Brain computed tomography and magnetic resonance imaging performed on the afternoon of surgery were normal. Echocardiogram, cervical arterial magnetic resonance angiogram (MRA) with contrast, a cervical venous duplex ultrasound of the jugular veins, chest radiograph, electrocardiogram, and all laboratory studies were normal. Repeat brain magnetic resonance imaging on postoperative day 13 demonstrated diffusely increased signal on diffusion weighted imaging (Fig. 1) and fluid attenuated inversion recovery sequences in cortical and deep gray matter in the distribution of the anterior and middle cerebral arteries on the left. There was minimal evidence of similar changes scattered in the cortex of the right hemisphere in a watershed distribution. An MRA of the aortic arch and cervical vessels revealed no abnormality. A time of flight MRA of the circle of Willis (CW) (Fig. 2) did not demonstrate either a left or right posterior communicating artery and revealed a hypoplastic anterior communicating artery.
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Figure 1. Diffusion weighted b1000 magnetic resonance image recorded on postoperative day 13. There is diffusely increased signal intensity (diffusion restriction) in the basal ganglia and the cortex of the left hemisphere with sparing of the occipital lobe. Similar changes, of lesser signal intensity, are also evident in the cortex of the right hemisphere in watershed areas.
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Figure 2. Three-dimensional time of flight magnetic resonance angiogram of the circle of Willis. Note bilaterally absent posterior communicating arteries and a hypoplastic anterior communicating artery.
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The patient improved gradually during 9 wk in hospital. Significant motor aphasia, moderate spastic right hemiparesis, mild right-sided neglect, impulsivity, and significant cognitive deficits persisted. He was discharged to a rehabilitation facility.
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Discussion
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We strongly suspect that the cerebral ischemic insult was the product of a combination of some retraction-related compression of the carotid artery, moderate arterial blood pressure reduction and a CW that allowed for very little compensatory collateral flow.
Some degree of pressure on the carotid artery is probably an inescapable element of this surgical procedure. The performance of an ACD/ACDF requires that the surgeon achieve exposure of the anterior surface of the cervical vertebral column. This requires some lateral displacement of the carotid sheath and the strap muscles of the neck and medial displacement of the trachea and esophagus. For surgeons who perform the procedure, the principle that the tips of the retractor blades should be anchored under the medial edges of the longus colli muscles, which are the immediate anterior anatomic relation of the anterior surface of the cervical vertebrae, is a fundamental tenet of the conduct of ACD/ACDF (1). This placement minimizes the pressure brought to bear on the more superficial structures including the carotid sheath and the esophagus. This was the technique used by the surgeon in this instance. Many surgeons, including the surgeon in this procedure, also routinely palpate the carotid artery superior to the retractor. At best this maneuver is nonquantitative and, in addition, there is some possibility of false positive confirmation of adequate flow because of arterial pulsation transmitted through soft tissue.
Surprisingly, there has been little systematic study of the precise physiologic effects of the seemingly inevitable pressure on the carotid artery. The single relevant investigation was performed by Pollard and Little (3). Using Duplex ultrasonography, they observed average reductions in carotid cross-sectional area of 30% in a population of patients undergoing ACD/ACDF, with exposure achieved using Caspar self-retaining retractors (Aesculap, Tuttingen, Germany). The greatest degree of lumen reduction observed in an individual patient was 45%. Lumen reduction was greatest in younger patients, which the authors surmised was the result of the greater elasticity of younger vessels. However, they expressed the reasonable concern that lesser degrees of cross-sectional area reduction superimposed on an existing stenosis in atherosclerotic vessels could result in complete vessel occlusion.
Despite this demonstration of carotid compression, reports of ischemic injury related to this mechanism have been exceptionally rare. We could identify only one other published report of a cerebral ischemic injury attributed to retractor related flow reduction. Yeh et al. (2) described a patient who sustained an extensive ipsilateral hemispheric infarction immediately after a 5-hour ACD/F procedure. The extracranial vessels were examined by ultrasound, which revealed neither thrombus nor atheroma. No intracranial vascular examination was performed. Although specific arterial blood pressure data were not provided, the authors state that there was no intraoperative hypotension, hypoxia, or anemia. Carotid occlusion during the surgical procedure was inferred. However, unilateral carotid occlusion in a normotensive patient with a normal carotid system and an intact CW would not be expected to cause the severe pan-hemispheric hemodynamic ischemia in their patient. Accordingly, this case may also represent an instance of poor collateralization as a result of an incomplete CW. Chozik et al. (4) reported a major hemispheric infarction occurring 3 days after an anterior corpectomy and fusion. Angiography revealed a carotid occlusion, which they attributed to stasis-related thrombosis associated with sustained retraction and the neurologic event was attributed to delayed embolization rather than intraoperative ischemia.
The only other evidence for the occurrence of hemodynamic ischemia caused by carotid retraction resides in a report by Sloan et al. (5). Those authors recorded somatosensory evoked potentials (SSEPs) in 18 patients undergoing ACD/F. Three patients sustained loss of SSEP shortly after retractor placement. SSEPs, and the temporal pulse of two patients in whom it could be followed returned after release of the retractor. None of the patients sustained a neurologic injury.
In the event of some reduction of flow caused by carotid compression, the impact on cerebral perfusion will be, in large part, a function of the potential for collateral flow to the territory perfused by that carotid. That will in turn be a function of two variables: the status of the CW and the MAP. When complete, the CW (Fig. 3) provides two alternative pathways for blood delivery in the event of unilateral carotid flow reduction. The first, and physiologically more important (6), occurs from the contralateral carotid via the pre-communicating (A1) segment of the anterior cerebral artery, the anterior communicating artery and then retrogradely through the ipsilateral A1. The second is from the posterior circulation via the pre-communicating (P1) segment of the posterior cerebral artery and the ipsilateral posterior communicating artery. However, the CW is complete in only 42%–52% of neurologically normal adults (7–9). Alpers et al. (9) reported the presence of a complete CW in 52% of neurologically normal adults at autopsy. Using MRA, Macchi et al. (8) identified a complete CW in only 47% of a series of 118 older patients (mean age, 76 years) in good health. In that study, 25% of patients (30/118) had no apparent functional collateral pathway from the posterior to the anterior circulation, i.e., 25% had some combination of bilaterally hypoplastic or absent PComs and/or P1 segments. The frequency of an incomplete CW has been even greater in series comprised of patients with ischemic neurologic disease (10,11).
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Figure 3. Normal Circle of Willis. ACA = anterior cerebral artery; ACom = anterior communicating artery; ICA = internal carotid artery; A1 = the first segment of the ACA (between the ICA and the ACom); MCA = middle cerebral artery; PCom = posterior communicating artery; PCA = posterior communicating artery; Basilar = basilar artery; P1 indicates the first segment of the PCA (between the basilar and the PCom); Vertebral = vertebral artery.
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In all studies, abnormalities of the anterior collateral pathway, i.e., absent or hypoplastic anterior communicating artery or A1 segments occur at an incidence, i.e., 3%–6%, that is much less than that observed for posterior circulation anomalies (6,10,12). However, in two surveys performed by Macchi et al. (8,12), combinations of anterior and posterior CW anomalies resulting in functional isolation of one carotid distribution from the remainder of the CW (as occurred in our patient) were observed in 7%–8% of healthy subjects studied using MRA. Although MRA may fail to identify some functional pathways, these latter data suggest that a significant percentage of patients may be at risk in the event of unrecognized carotid compression. An incidental observation of these investigations is that CW abnormalities appear to occur more frequently on the left side (the side of the surgical approach in our patient) than on the right. In 16 of the 17 observed instances of an isolated carotid distribution in the studies of Macchi et al. (8,12), the isolated vessel was the left carotid.
The other probable determinant of collateral flow is the MAP during the time of carotid compression. Arterial blood pressure recorded immediately preoperatively in our patient was 136/80 (calculated MAP = 99 mm Hg). MAPs intraoperatively were between 48 and 68 mm Hg with an average value of 56 mm Hg during the 80-minute procedure. The anesthetic management was arguably within standards of care that have prevailed in North American practice. Relative degrees of induced hypotension (although it was not deliberately undertaken in the present instance) have been used as adjuncts to surgery on the vertebral column. Furthermore, the lower limit of CBF autoregulation has often been cited as 50 mm Hg (although one of the authors has argued that the actual limit for adult humans is considerably higher) (13,14). It seems likely that in the present instance the confluence of a relatively rare pattern of CW anatomy that resulted in limited potential for collateral blood delivery with some degree of carotid compression and MAPs that were relatively low resulted in an intraoperative ischemic insult predominantly in the distribution of the left carotid artery.
Our experience with a single case cannot justify a recommendation for broad changes in management practices. However, our experience provides evidence strongly suggestive of a risk of cerebral ischemia related to carotid compression during ACD/ACDF, a risk that may be exaggerated by unknowable patient characteristics. Our experience leads us, first, to reaffirm the importance of established protective strategies, including attention to retractor placement to minimize pressure on the carotid sheath, postretraction palpation of the carotid distal to the retractor, and confirmation of persistent and unchanged temporal pulsation after retractor placement. In addition, we strongly suggest that avoidance of hypotension not essential to the conduct of the surgical procedure is a practice habit that should entail minimal hazard to the patient and that may be relevant to the prevention of cerebral ischemic injury during ACD/ACDF.
Clinicians widely accept the concept that CBF autoregulation provides CBF preservation in the face of hypotension. However, it should be appreciated that that mechanism may not be applicable in situations in which the cerebral vessels proximal to those that mediate autoregulation have been compressed, as may occur during ACD (3). In addition to the preceding recommendations regarding physiologic management, it is possible, but unproven, that electrophysiologic monitoring may also be appropriate in some instances. Where equipment and anesthesia personnel with the relevant experience are available, monitoring of the electroencephalogram (raw or processed) or SSEP may be considered (5). Cerebral oximetry or transcranial Doppler ultrasonography might also provide warning of cerebral ischemia. These precautions and/or additional monitoring techniques might have most relevance in patients in whom any degree of deliberate arterial blood pressure reduction is intended.
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Footnotes
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Accepted for publication October 6, 2005.
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References
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- Yeh YC, Sun WZ, Lin CP, et al. Prolonged retraction on the normal common carotid artery induced lethal stroke after cervical spine surgery. Spine 2004;29:E431–4.[Medline]
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Abstract
Introduction
