Blood pressure manipulation during awake carotid surgery to reverse neurological deficit after carotid cross-clamping

M. D. Stoneham and O. Warner

Nuffield Department of Anaesthetics, Level 1, Oxford Radcliffe NHS Hospital, Headington, Oxford OX3 9DU, UK*Corresponding author

Accepted for publication: May 23, 2001


    Abstract
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 Abstract
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
We describe the management of three patients undergoing awake carotid surgery who developed signs of cerebral ischaemia after carotid cross-clamping. Drug treatment to increase arterial blood pressure above baseline reversed the neurological deficit and an internal carotid artery shunt was not needed. Shunt insertion is less frequent with regional rather than general anaesthesia, and blood pressure control can reduce this even more. Coincidentally, one of the patients, who gave a history of angina of effort after walking 100 m, complained of chest pain after cross-clamp release. This was treated successfully with sublingual nitroglycerin before ST segment changes became apparent on the ECG. These reports suggest that regional anaesthesia for carotid surgery allows potential complications to be identified earlier than under general anaesthesia using reports from the patient, so that treatment may be modified to prevent morbidity and even mortality.

Br J Anaesth 2001; 87: 641–4

Keywords: surgery, carotid endarterectomy; anaesthetic techniques, regional, cervical plexus block; arterial blood pressure, control


    Introduction
 Top
 Abstract
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
The choice of anaesthetic technique for carotid endarterectomy (CEA) is controversial.1 2 Proponents of general anaesthesia say the advantages are cerebral protection from general anaesthetic agents, control of the airway and ventilation, and patient comfort. Recently, regional anaesthesia has attracted considerable interest, with suggestions that it reduces per operative morbidity and mortality.3 4 Regional anaesthesia facilitates neurological monitoring during cross-clamping of the internal carotid artery (ICA), although there is also evidence of improved haemodynamic stability5 6 and, perhaps, less cardiovascular morbidity and mortality.7

Regional anaesthesia is associated with less use of ICA shunts8 than general anaesthesia, in which many surgeons routinely use a shunt on all patients. This may be of value, as shunting has inherent disadvantages.9 Signs of impending cerebral ischaemia in an awake patient are more sensitive and specific than the indirect indicators used during general anaesthesia, such as transcranial Doppler ultrasound, EEG processing and evoked potential monitoring.10 11 Thus, a shunt is only used if neurological deficit develops after ICA cross-clamping. Some surgeons prefer an awake patient because of the reassurance of being able to converse with the patient with the ICA cross-clamped.

The awake technique allows the anaesthetic management to be changed to treat ongoing problems by feedback from the awake patient. The following three case reports illustrate such dynamic management.


    Case 1
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 Abstract
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
A 65-yr-old ASA 3 male patient underwent left CEA under cervical plexus block. He had suffered a cerebrovascular accident 8 weeks previously in the form of hemiplegia and expressive dysphasia, from which he had made a full recovery. He had non-insulin-dependent diabetes mellitus and hypertension, controlled with amlodipine 10 mg once daily. He had 70–80% stenosis of the left ICA and <50% stenosis of the right ICA, assessed by carotid Duplex scan. His unpremedicated arterial blood pressure, recorded on the ward and in the anaesthetic room before sedation, was approximately 155/80 (mean 105 mm Hg). Perioperative monitoring consisted of five-lead ECG, invasive arterial blood pressure, oxygen saturation and end-tidal carbon dioxide estimation from within the oxygen facemask. No additional cerebral monitoring was used apart from the awake patient’s neurological state. The patient was sedated with a target-controlled infusion (TCI) of propofol administered via a Graseby 3500 Pump at up to 1.2 µg ml–1 predicted plasma concentration during placement of the regional blocks and intravascular lines and the dissection phase of the operation. This was switched off once dissection was complete.

Our usual practice during awake CEA is for the anaesthetist to administer heparin 50 unit kg–1, then the surgeons cross-clamp the ICA for 2 min while the anaesthetist observes the patient closely for signs of cerebral ischaemia, such as altered level of consciousness, confusion, dysphasia or altered contralateral grip strength. If there is no neurological change, then arteriotomy and endarterectomy proceed directly. If there is evidence of cerebral ischaemia, the clamp is released while a Pruitt–Isihara shunt is prepared and inserted electively.

In this case, within 30 s of trial cross-clamping, the patient developed subtle neurological changes. He was a few seconds slower in responding to questions and did not know which day of the week it was. We have seen previously that this may be the first or only sign of impending cerebral ischaemia. At this time, the TCI pump displayed a plasma propofol concentration of 0.1 µg ml–1; blood pressure was 140/75 (mean 97 mm Hg) and pulse 55 beats min–1. Because his mean blood pressure was marginally (7%) lower than baseline, we decided to increase this to see whether this could reverse the neurological effects. Two doses of ephedrine 3 mg were given, together with 0.9% NaCl 250 ml. Blood pressure rose to 190/90 and heart rate to 70 beats min–1. The patient’s neurological condition improved and the delay in response was reduced, and he was able to work out which day of the week it was (Thursday). After the patient had been reassured and after discussion with the surgeons, endarterectomy proceeded uneventfully without the use of a shunt. A Goretex patch angioplasty was performed before the clamps were released with a total cross-clamp time of 52 min. During this time, ephedrine and phenylephrine were given as required to maintain blood pressure at or above 165 systolic. A total of ephedrine 12 mg and phenylephrine 0.5 mg was administered during the cross-clamp period.

After cross-clamp release, the remainder of the operation proceeded uneventfully. The patient was kept in recovery for 2 h for close neurological and haemodynamic assessment, after which he was sent to the ward. He was discharged home on the second post-operative day.


    Case 2
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 Case 2
 Case 3
 Discussion
 References
 
A 73-yr-old female underwent left CEA under deep cervical plexus block. She gave a history of angina of effort after 100 m, orthopnoea and hypertension. Medications included isosorbide mononitrate, captopril 12.5 mg and bendrofluazide 10 mg daily. She had sustained a non Q-wave myocardial infarction 10 yr previously. She had 95% stenosis of the left ICA and 30% stenosis of the right ICA, as assessed by carotid Duplex scan. Baseline arterial blood pressure was 175/95 (mean 122 mm Hg) and pulse was 65 beats min–1. TCI propofol was given at up to 1.0 µg ml–1 predicted plasma concentration during regional block insertion but was switched off once dissection was complete.

In this case, the 2 min trial cross-clamp was uneventful, but 25 min after arteriotomy the patient became dysphasic and confused. Arterial blood pressure at this time was 155/75 (mean 108 mm Hg) and pulse 72 beats min–1. Metaraminol 0.25 mg was given, which increased the pressure to 195/95. The patient’s symptoms resolved completely and endarterectomy proceeded uneventfully without shunt insertion being needed. Because the internal carotid artery was of sufficient calibre, the patch angioplasty was not done and so the cross-clamp time was only 29 min. A total of five boluses of metaraminol 0.25 mg were given to maintain blood pressure until the end of the operation. After release of the cross-clamp, the patient complained of discomfort in her left chest and arm similar to her angina, although there was no change in the ST segment in leads II and V5. This pain resolved rapidly with sublingual nitroglycerin spray and reassurance. The patient was kept in recovery for 2 h for close observation as before. A 12-lead electrocardiogram was unchanged from before surgery. Her recovery was uneventful and she was discharged home on the third post-operative day.


    Case 3
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 Case 2
 Case 3
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A 68-yr-old man with a dilated cardiomyopathy underwent left carotid endarterectomy under cervical plexus block. He had >90% stenosis of the left ICA and 25% stenosis of the right ICA, as assessed by carotid Duplex scan. Unpremedicated baseline arterial pressure in the anaesthetic room was 135/75 (mean 95 mm Hg). The trial cross-clamp period was uneventful, but 5 min after arteriotomy the patient became dysphasic and confused. Arterial blood pressure at this time was 125/65 (mean 85 mm Hg) and pulse 83 beats min–1. Phenylephrine 0.25 mg was administered, which elevated the pressure to 160/95. The patient’s speech improved transiently. However, when arterial pressure fell to 140 systolic, dysphasia and confusion developed again and, in addition, right arm weakness. Incremental increases in the systolic blood pressure to 165 mmHg with phenylephrine reversed these deficits and enabled completion of the endarterectomy without need for the ICA shunt. A total of 2.5 mg phenylephrine was administered. The patient was kept in recovery for 2 h for close observation as before and discharged on the second post-operative day.


    Discussion
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 Abstract
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
The crucial feature in these three cases was the fact that none of the patients was hypotensive by conventional criteria when they demonstrated features of cerebral ischaemia. However, increasing and keeping blood pressure to normal or above normal improved cerebral circulation, so that shunting was not required during carotid cross-clamping. The mechanism is presumably an increase in the pressure gradient across the circle of Willis and collateral cerebral circulation. Treatment to increase blood pressure, by as much as 25% above baseline for all patients, has been described during CEA under general anaesthesia previously.12 13 This has some cardiovascular risk and increases the risk of myocardial ischaemia in patients under general anaesthesia,14 15 as the incidence of ischaemic heart disease is great in this population. Regional anaesthesia certainly does not abolish the risk of myocardial ischaemia,16 but it may perhaps reduce it.5 7 It is more logical to augment blood pressure only when required.15 The dose of vasopressor/inotrope may be titrated against the patient’s blood pressure until the neurological deficit is reversed, while at the same time the patient’s cardiovascular condition is monitored closely.

The choice of vasopressor depends on pre-existing disease and previous medication. Ephedrine could be used if the patient is already bradycardic, for example with ß-blockers; phenylephrine or metaraminol could be used otherwise.

Of the potential benefits of awake carotid artery surgery, reducing the requirement for ICA shunt insertion is the best proven. Under general anaesthesia, shunt rates vary considerably from 0 to 100%,17 but the mean rate is greater than the 10–15% reported for awake carotid surgery.18 19 Manipulation of blood pressure can reduce the requirement for shunting still further, which may be beneficial because of the risks of shunt insertion.9 These include prolongation of the cross-clamp time; cerebral ischaemia during shunt insertion and removal; risk of embolic stroke by dislodgement of plaque material during shunt insertion; and sudden profound blood loss and hypotension as a result of accidental dislodgement of the shunt. Finally, patch angioplasty is technically more difficult for the surgeon when suturing around a shunt.

In our second case, the patient developed angina as well as neurological impairment during the operation and the patient’s conscious state alerted us to her myocardial ischaemia. Treatment was given and the problem reversed before changes in the ECG or the patient’s haemodynamic status became apparent.

We consider that, with an awake patient, the anaesthetist has more options and more information to make perioperative decisions about a patient’s management when they develop cerebral or myocardial ischaemia after carotid cross-clamping. In high-risk patients, such as those undergoing carotid surgery, this could contribute to differences in morbidity and mortality between regional and general anaesthesia.


    References
 Top
 Abstract
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
1 Lineberger CK, Lubarsky DA. Con: general anesthesia and regional anesthesia are equally acceptable choices for carotid endarterectomy. J Cardiothorac Vasc Anesth 1998; 12: 115–7[ISI][Medline]

2 Zvara DA. Pro: regional anesthesia is the best technique for carotid endarterectomy. J Cardiothorac Vasc Anesth 1998; 12: 111–4[ISI][Medline]

3 Forssell C, Takolander R, Bergqvist D, Johansson A, Persson NH. Local versus general anaesthesia in carotid surgery. A prospective, randomised study. Eur J Vasc Surg 1989; 3: 503–9[Medline]

4 Papavasiliou AK, Magnadottir HB, Gonda T, Franz D, Harbaugh RE. Clinical outcomes after carotid endarterectomy: comparison of the use of regional and general anesthetics. J Neurosurg 2000; 92: 291–6[ISI][Medline]

5 Sbarigia E, DarioVizza C, Antonini M, et al. Locoregional versus general anesthesia in carotid surgery: is there an impact on perioperative myocardial ischemia? Results of a prospective monocentric randomized trial. J Vasc Surg 1999; 30: 131–8[ISI][Medline]

6 Eibes TA, Gross WS. The influence of anesthetic technique on perioperative blood pressure control after carotid endarterectomy. Am Surg 2000; 66: 641–7[ISI][Medline]

7 Tangkanakul C, Counsell CE, Warlow CP. Local versus general anaesthesia in carotid endarterectomy: a systematic review of the evidence. Eur J Vasc Endovasc Surg 1997; 13: 491–9[ISI][Medline]

8 Counsell CE, Salinas R, Naylor R, Warlow CP. Routine or selective carotid artery shunting during carotid endarterectomy and the different methods of monitoring in selective shunting. Issue 4. Oxford: Update Software: Stroke Module of the Cochrane Database of Systematic Reviews [updated 01 December 2000]

9 Salvian AJ, Taylor DC, Hsiang YN, et al. Selective shunting with EEG monitoring is safer than routine shunting for carotid endarterectomy. Cardiovasc Surg 1997; 5: 481–5[Medline]

10 Ackerstaff RG, van de Vlasakker CJ. Monitoring of brain function during carotid endarterectomy: an analysis of contemporary methods. J Cardiothorac Vasc Anesth 1998; 12: 341–7[ISI][Medline]

11 Silbert BS, Koumoundouros E, Davies MJ, Cronin KD. Comparison of the processed electroencephalogram and awake neurological assessment during carotid endarterectomy. Anaesth Intensive Care 1989; 17: 298–304[ISI][Medline]

12 Smith JS, Roizen MF, Cahalan MK, et al. Does anesthetic technique make a difference? Augmentation of systolic blood pressure during carotid endarterectomy: effects of phenylephrine versus light anesthesia and of isoflurane versus halothane on the incidence of myocardial ischemia [see comments]. Anesthesiology 1988; 69: 846–53[ISI][Medline]

13 Umbrain V, Keeris J, D’Haese J, et al. Isoflurane, desflurane and sevoflurane for carotid endarterectomy. Anaesthesia 2000; 55: 1052–7[ISI][Medline]

14 Riles TS, Kopelman I, Imparato AM. Myocardial infarction following carotid endarterectomy: a review of 683 operations. Surgery 1979; 85: 249–52[ISI][Medline]

15 Modica PA, Tempelhoff R, Rich KM, Grubb RL Jr. Computerized electroencephalographic monitoring and selective shunting: influence on intraoperative administration of phenylephrine and myocardial infarction after general anesthesia for carotid endarterectomy. Neurosurgery 1992; 30: 842–6[ISI][Medline]

16 Prough DS, Scuderi PE, Stullken E, Davis CH Jr. Myocardial infarction following regional anaesthesia for carotid endarterectomy. Can Anaesth Soc J 1984; 31: 192–6[ISI][Medline]

17 Knighton JD, Stoneham MD. Carotid endarterectomy. A survey of UK anaesthetic practice. Anaesthesia 2000; 55: 481–5[ISI][Medline]

18 Davies MJ, Silbert BS, Scott DA, Cook RJ, Mooney PH. Superficial and deep cervical plexus block for carotid artery surgery: a prospective study of 1000 blocks. Reg Anesth 1997; 22: 442–6[ISI][Medline]

19 Bowyer MW, Zierold D, Loftus JP, et al. Carotid endarter ectomy: a comparison of regional versus general anesthesia in 500 operations. Ann Vasc Surg 2000; 14: 145–51[ISI][Medline]