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NEUROSURGICAL ANESTHESIOLOGY AND NEUROSCIENCE

Increased Oxygen Administration Improves Cerebral Oxygenation in Patients Undergoing Awake Carotid Surgery

From the Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, UK.

Address correspondence to Dr Mark Stoneham, Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford OX3 9DU, UK. Address e-mail to mark.stoneham{at}nda.ox.ac.uk.

Abstract

BACKGROUND: During regional anesthesia for carotid endarterectomy (CEA), 10% to 15% of patients develop signs of cerebral hypoxia after cross-clamping, manifested as changes in speech, cerebration or contralateral motor power. Reversal of such neurological deficits using administration of 100% O₂ has been described. We used near-infrared cerebral oximetry to assess whether 100% O₂ reliably improves regional cerebral oxygenation (rSO₂) during carotid cross-clamping.

METHODS: Sixteen patients undergoing awake CEA were studied. Bilateral rSO₂ optodes were applied before the initiation of sedation and the conduct of the regional blockade. Patients received 28% oxygen by Venturi facemask. Perioperative blood pressure was maintained at or within 10% above the patient’s normal limits during carotid cross-clamping. After cross-clamping, 100% O₂ was administered for 5 min by a close-fitting anesthetic facemask. The O₂ mask was then removed and the patient breathed room air. The effects on rSO₂ readings and arterial blood gases were observed after each intervention.

RESULTS: Data were analyzed for 15 patients. Ipsilateral rSO₂ values decreased by 7.4% ± 5% after carotid cross-clamping. Administration of 100% O₂ resulted in an increase in ipsilateral rSO₂ in all patients of 6.9% ± 3.3% (range, 1%–12%) (paired t-test, P < 0.001) over the cross-clamped value while receiving 28% O₂. Hemodynamic variables and arterial Paco₂ values were unaltered.

CONCLUSION: With the carotid cross-clamped, ipsilateral rSO₂ was reliably increased by the administration of 100% O₂ compared with 28% O₂. The etiology of this increase is unclear, but may relate to the associated increase in O₂ content of the blood or to an improvement in cerebral blood flow. Thus administration of 100% O₂ during carotid cross-clamping may be beneficial for all patients undergoing CEA.

Carotid endarterectomy (CEA), an operation proven to reduce the incidence of embolic stroke in symptomatic patients with >70% internal carotid artery stenosis, has an associated stroke rate of 1% to 5%.1 The pathogenesis of such strokes is multifactorial: embolic—during dissection or after clamp release; hypoperfusion—during cross-clamping; or hemorrhagic—usually associated with perioperative hypertension and postoperatively the hyperperfusion syndrome.

Advocates of regional anesthesia for carotid surgery cite direct monitoring of cerebral function during carotid cross-clamping as the principal advantage of the technique.2 With the patient awake, 10% to 15% of patients develop signs of cerebral hypoxia after cross-clamping, manifested as changes in speech, cerebration or contralateral motor power.3 Treatment of such cerebral hypoxia usually involves insertion of a bypass shunt into the internal carotid artery. However, shunting itself has disadvantages including: making the operation technically more difficult for the surgeon, prolonging the cross-clamp time and dislodging plaque material into the cerebral circulation which may itself cause embolic stroke.4,5 Thus many surgeons avoid shunting if possible.

A case report from our institution suggested that pharmacological increase of arterial blood pressure to, or above, preoperative values can reverse the developing neurological deficit in some patients, thereby avoiding the need for shunting.6 However, this is neither always successful nor without risks, as hypertension may itself precipitate myocardial ischemia in patients with coexisting cardiovascular disease.7

We described two other patients undergoing awake CEA who developed neurological deficits after carotid cross-clamping, but in whom the administration of 100% O₂ reversed the neurological impairment completely.8 We calculated from the oxygen content equation that, in this case, the O₂ content of arterial blood had been increased by a mere 4%, yet there appeared to be a causal relationship between the administration of 100% O₂ and the reversal of developing neurological symptoms and signs. This observation raised the possibility that giving 100% O₂ during the period of carotid cross-clamping could be an additional therapeutic option when anesthetizing patients undergoing CEA.

To investigate this further, we examined whether cerebral oxygenation could be reliably improved by supplemental oxygenation for patients undergoing awake CEA. We used cerebral oximetry, a near-infrared spectroscopy technique, to estimate ipsilateral and contralateral cerebral oxygenation.9 Cerebral oximetry compares well with other monitoring modalities such as transcranial Doppler, stump pressure and somatosensory evoked potentials in detecting cerebral ischemia during CEA.10 Ipsilateral regional cerebral oxygen saturation (rSO₂) decreases by a variable amount after internal carotid artery cross-clamping, typically 8% to 17%, and returns to baseline after shunt insertion,9,11 However, this noninvasive technique has a low positive predictive value to predict reliably cerebral ischemia.12 There is considerable inter-patient variability in response to cerebral oximetry readings to carotid cross-clamping.13

If patients’ cerebral oxygenation reliably improves with supranormal oxygenation, then this could be an additional intraoperative treatment strategy for patients with impending cerebral ischemia.

METHODS

This study was approved by the Regional Ethics Committee and by the Medicines and Health Regulatory Agency. Patients undergoing elective CEA under regional anesthesia were invited to participate at the preoperative visit the day before surgery or in the preassessment clinic. Written informed consent was obtained from all participants. Exclusion criteria included: patient refusal to participate; unsuitability or refusal of regional anesthesia; non-English speaking, and patients with type 2 respiratory failure who may be at risk for respiratory depression if 100% O₂ is administered.

A standard anesthetic technique was used. Briefly, after appropriate sedation with midazolam, 0.5 to 1 mg with or without remifentanil infusion (up to 0.05 µg · kg^–1 · min^–1), deep and superficial cervical plexus blocks were placed using bupivacaine 0.5%, 20 mL.14,2

Perioperative monitoring consisted of pulse oximetry, contralateral invasive arterial blood pressure monitoring, 5-lead electrocardiography, respiratory rate by thoracic impedence measurement and arterial blood gas estimation.

Cerebral oxygenation was measured using the Invos 4100 cerebral oximeter (Tyco Healthcare, Portsmouth, UK) which uses near-infrared spatially-resolved spectroscopy technology to provide a measure of regional cerebral saturation. Cerebral oximeter optodes (Invos Monitor Adult Soma Sensor, Tyco Healthcare, Portsmouth, UK) were attached to the forehead on either side, immediately above the eyebrow, with a 1 cm gap between the two electrodes anteriorly. Careful attention was paid to optode placement as this can affect cerebral oximetry readings.15 The cerebral oximeter was connected before supplemental oxygenation, sedation or placement of regional blocks to establish a baseline and for the remainder of the operation. Data collected from each subject were downloaded to disk for subsequent analysis.

After baseline oximetry readings were recorded, 28% O₂ was administered by Venturi facemask. After any change in inspired O₂ concentration, 5 min were allowed to elapse before the cerebral oximetry readings were recorded. This time interval was reached after preliminary studies which showed that changes in rSO₂ readings after an intervention were complete within 5 min. Each change in oxygenation was recorded using the Invos 4100 event marker and the readings retrieved thereafter for subsequent analysis. Arterial blood gas analysis was performed after each intervention to ascertain the arterial partial pressures of O₂ (PAo₂) and carbon dioxide (PAco₂) together with the hematocrit.

Perioperatively, patients were closely monitored to maintain hemodynamic stability. Vasopressors, β-blockers or vasodilators were administered as appropriate to maintain the patient’s arterial blood pressure as normal for them immediately before carotid cross-clamping. After carotid cross-clamp application, the patient was closely monitored for neurological deterioration by assessing speech, cerebration, level of consciousness and contralateral hand strength. Cerebral oximetry values were recorded once they had stabilized. Ten minutes after carotid cross-clamping, 100% O₂ was administered by close-fitting anesthetic facemask and, again, the effects on neurological symptoms (if any) and cerebral oximetry readings noted. A second arterial blood gas sample was analyzed at this stage. After a further 5 min, to note the effects on cerebral oximetry recordings the O₂ mask was removed so that the patient breathed atmospheric air for 5 min. If at any stage the patient developed neurological symptoms or signs of cerebral ischemia, such as dysphasia, confusion, altered level of consciousness or decreased contralateral grip strength, 100% O₂ was administered by close-fitting anesthetic facemask.

Total blood loss was estimated during the operation from the suction bottle and surgical swabs. Hematocrit was recorded from analysis of the arterial blood gas samples taken perioperatively.

Statistical Analysis
Assuming a median decrease in cerebral oximetry reading after carotid cross-clamping of 12%,13 with an approximate standard deviation of 6%, with each patient acting as their own control, a power calculation shows that a study of 15 patients had a power of 0.8 to demonstrate an increase in cerebral oxygen saturation of 6% at P < 0.05.

Oxygen content of blood at the various stages of the operation was calculated according to the formula:

Data analysis was performed using Microsoft Excel 2003 Spreadsheet Data Analysis ToolPack (Microsoft Corporation, CA) running on a personal computer. Paired t-testing and analysis of variance for repeated measures were used as appropriate. Correlation was used to relate changes in rSO₂ values and the degree of contralateral stenosis and to observe the relation between the decrease in rSO₂ values on cross-clamping and the increase after administration of 100% O₂.

RESULTS

Sixteen patients were recruited. Analysis was conducted on the 15 patients who completed the study protocol successfully. The remaining patient had moderately severe chronic obstructive pulmonary disease and was excluded because he developed a rapid perioperative increase in arterial CO₂ tension which may have been due to the remifentanil sedation.

Indications for CEA included: previous cerebrovascular accident (3); transient ischemic attacks (2); amaurosis fugax (3); blackouts (1); and asymptomatic patients with carotid stenoses awaiting cardiac surgery.6 A standard endarterectomy with patch angioplasty was used in all patients. Demographic, baseline hemodynamic and surgical details of the 15 patients are shown in Table 1.

After carotid cross-clamping, none of the patients displayed evidence of cerebral ischemia. However, one patient became nauseated during the cross-clamp period which was most likely related to vagal nerve stimulation.

Table 2 shows the changes in O₂ content during various stages of the operation. Administration of 100% O₂ to patients resulted in a mean 5.9% (range, 0.4%–11%) increase in O₂ content compared with when they were receiving 28% O₂.

Table 3 shows the effects of varying O₂ concentration and cross-clamping on rSO₂ readings at various stages of the surgery. Ipsilateral rSO₂ values decreased by 7.4% ± 5% after carotid cross-clamping whereas contralateral values were unchanged. Administration of 100% O₂ resulted in an increase in ipsilateral rSO₂ from 64.5% to 71.3%, an increase of 6.9% ± 3.3% (range, 1%–12%) over the cross-clamped value (paired t-test, P < 0.001). Figure 1 compares cerebral oximetry percentage changes from baseline on both contralateral and ipsilateral sides. Administration of 100% O₂ caused rSO₂ to increase on both sides, the increase was larger on the ipsilateral side (6.9% ± 3.3% vs 4.2% ± 4%) but this did not achieve statistical significance (P = 0.0571).

View larger version (8K): [in this window] [in a new window]   Figure 1. Change in regional cerebral oxygen saturation (rSO2) values from baseline with oxygen concentration.

There was no correlation between the degree of ipsilateral carotid stenosis and the decrease cerebral oxygenation after carotid cross-clamping (correlation factor = –0.1735). Similarly, there was no correlation between the decrease in rSO₂ after cross-clamping and the increase after administration of 100% O₂ (correlation factor = –0.037).

Paco₂, heart rate and arterial blood pressure were not significantly altered throughout the various interventions (Table 4).

DISCUSSION

The results of this study show that ipsilateral cerebral O₂ saturation is increased by the administration of 100% O₂ during the period of carotid cross-clamping. The increases in arterial blood O₂ content seen after the administration of 100% O₂ are similar to that seen in our previously published case report.8 This increased O₂ content is due to the increase in "dissolved" O₂, which is directly proportional to the Pao₂, and certainly contributes to the increases in rSO₂ seen in our study.

There is also experimental evidence that hyperoxia may increase cerebral blood flow.16 Administration of 100% O₂ to mice within 45 min of middle cerebral artery occlusion reduced the area of brain with low cerebral blood flow by 45%, suppressed peri-infarct depolarization and reduced the size of the infarct by 45%. Normobaric hyperoxia has also been used clinically as therapy for ischemic stroke, reducing cerebral ischemic injury and improving functional outcome.17

These two mechanisms are not mutually exclusive and both may be involved in the improved cerebral oxygenation seen in the current study.

Although our study results achieved statistical significance, it is difficult to know what a clinically significant increase in rSO₂ would be. After carotid cross-clamping, there is significant correlation between changes in middle cerebral artery flow and the decrease in rSO₂ value.18 We also know that 10% to 15% of patients develop neurological deficits after carotid cross-clamping.3 Such patients typically show a decrease in rSO₂ of 17% against only 8% for patients without neurological deficit.9 The threshold for cerebral ischemia is not entirely clear, but a decrease in rSO₂ of 13% has been identified as clinically significant.18 Thus, if 100% oxygenation causes a mean increase in rSO₂ of 7% (range, 1%–12%), this could just be enough to prevent neurones in the ipsilateral cerebral cortex from becoming ischemic. Given the tenuous nature of the blood supply to the ipsilateral cerebral cortex during the period of carotid cross-clamping, any intervention which improves oxygenation may be beneficial. It is certainly unlikely to do any harm for the duration of the cross-clamp period (up to 1 h).

It would have been interesting to see whether the clinical benefits attributed to the administration of 100% O₂ in our earlier case reports would have been repeated in our current study. This was not possible since no patient in our study developed neurological deficit. This should not detract from the observation that, in every patient studied, ipsilateral cerebral oxygenation was increased by administration of 100% O₂.

In general, increasing fraction of inspired oxygen has less effect on tissue O₂ levels as perfusion decreases.19 One might therefore have predicted that there would be an inverse correlation between the decrease in rSO₂ after cross-clamping and the increase in rSO₂ after the administration of 100% O₂. Our results do not support this theory. In the same way, one might also expect there to be a larger increase in contralateral rSO₂ with 100% O₂ as this side of the brain is less ischemic. In fact, the ipsilateral increase was larger than the contralateral although this did not achieve statistical significance. Our study may be under-powered to detect this and further work is required to explore this interesting area.

If our study results are indeed true, then a logical extension would be to suggest that 100% O₂ should be administered to all patients undergoing CEA during the period of carotid cross-clamping, since the risk of administering 100% O₂ for an hour or less is low in this group of patients. However, other factors may have contributed to the increases in rSO₂ seen while there is also the question of inaccuracies in the near-infrared cerebral oximetry methodology.

As was mentioned, optode location can also affect rSO₂ values. Very careful attention was paid to positioning of the optodes in order to minimize this effect,15 and a consistent pattern of placement was used in all patients in the study. Furthermore, the close-fitting anesthetic facemask was very carefully applied so that it did not touch or affect optode position in any way.

Second, patient positioning can affect the cerebral blood volume and cerebral arterial-venous ratio.20 All patients in this study were anesthetized, and underwent surgery in the same position. Briefly, patients were positioned in a "deck chair" configuration on the operating table, with the chest and head inclined up and the knees flexed. A pillow was placed under the knees for comfort and the neck extended to facilitate surgical exposure. Thus, patient positioning was constant throughout the procedure and was unlikely to have affected perioperative cerebral oximetry values.

Third, cerebral oximetry values are directly correlated with hemoglobin concentration, increasing as the hemoglobin concentration increases and vice versa.15 However, despite there being a range of preoperative hematocrit values in our patients between 35 and 52, blood loss during this operation was minimal, with no patient losing more than 300 mL of blood. Therefore, this variability in preoperative hematocrit was not relevant since each patient acted as his or her own control.

Fourth, relatively small alterations in Paco₂ may cause significant alterations in cerebral blood flow, cerebral blood volume and therefore cerebral oximetry values.21 We measured Paco₂ directly after each intervention and, as Table 2 shows, there were only small changes in measured Paco₂ between the different phases of this study, which, therefore, minimized any such affect. The one exception was the patient with unsuspected chronic obstructive pulmonary disease who had a rapid increase in Paco₂, which necessitated exclusion of their data from analysis.

Fifth, extra-cranial oxygenation is also likely to be improved by O₂ administration, as there are a number of anatomical extra-cranial anastomoses between the left and right sides. There is conflicting evidence as to how much influence these extra-cranial tissues have on the total signal measured by noninvasive cerebral oximetry reading. However, spatially resolved spectroscopy which is the technology used by the Invos 4100 oximeter has relatively high sensitivity and specificity for intracerebral changes.22,23 This is not true for some other near-infrared technologies which have shown greater influence from extra-cranial sources.24,25

Further work is therefore needed to elucidate the mechanism of these changes which might involve studies of jugular bulb saturation26 or continuous conjunctival oxygen tension monitoring.27

In conclusion, we have shown that ipsilateral cerebral oxygenation is increased during carotid cross-clamping by the administration of 100% O₂. This intervention could therefore be added to the list of possible interventions available to anesthesiologists who are concerned about the adequacy of cerebral oxygenation in patients undergoing CEA.

Footnotes

*CaO₂ = oxygen content (ml · l^–1); Hb = hemoglobin concentration estimated from arterial blood gas analysis sample (ml · l^–1); 1.34 = Huffner constant; SaO₂ = hemoglobin-oxygen saturation (%); Pao₂ = arterial partial pressure of oxygen (kPa).

Accepted for publication June 5, 2008.

Funding to buy the disposable optodes for this study was provided by a research grant from the Vascular Anaesthetic Society of Great Britain and Ireland. The Invos 4100 cerebral oximeter was on loan from Tyco Medical, Portsmouth, UK.

Reprints will not be available from the author.

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