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Carotid endarterectomy in a neurosurgical unit: a retrospective review
Journal of Clinical Neuroscience (1999) 6(2), 138-142 © 1999 Harcourt Brace & Co. Ltd
Clinical studies
Carotid e n d a r t e r e c t o m y in a neurosurgical unit: a retrospective review M. B e s s e r ~ MB BS FRCSC FRACS, R. P a r k i n s o n 2 MB BS BSC MED, R. Traill 3 MB BS FANZCA
1Clinical Associate Professor and Head, Department of Neurosurgery, Royal Prince Alfred Hospital, Sydney, Australia 2Departmentof Neurosurgery, Royal Prince Alfred Hospital, Sydney, Australia 3Departmentof Anaesthetics, Royal Prince Alfred Hospital, Sydney, Australia
Summary A retrospective survey of 262 carotid endarterectomies performed in the Neurosurgical Unit at Royal Prince Alfred Hospital over a 15 year period was conducted. A total of 141 patients were operated on for transient ischaemic attacks referable to stenosis of the ipsilateral internal carotid artery. Eighty-eight percent of patients had angiographic evidence of greater than 80% stenosis of the affected internal carotid artery. A postoperative new permanent neurological deficit of 1.9% and death rate of 0.6% was achieved. No deaths and two postoperative strokes were recorded after 1987. These resuffs are comparable with published series. The use of barbiturate therapy with electroencephalography changes on cross clamping of the internal carotid artery is described. Keyworde: carotid endarterectomy, barbiturates, electroencephalography
INTRODUCTION
Stroke is the commonest neurological disease affecting man? It is a major cause of prolonged disability and the third leading cause of death in the community. Strokes are often preceded by transient ischaemic attacks (TIA) with the majority of patients suffering from intracranial embolic or occlusive arterial disease. Data suggests that at least 60% are attributable to carotid disease and patients with high grade stenosis make up about 50% of stroke victims. 2 Recent multicentre randomized prospective trials have demonstrated a clear benefit of surgery over medical therapy for patients with greater than 70% stenosis of the internal carotid artery. 1,2,7 However, carotid endarterectomy (CEA) needs to be performed by surgeons and anaesthetists in a unit with low perioperative mortality and morbidity. This prompted review of our experience with this procedure. MATERIALS
AND METHODS
The hospital records of 246 patients who had carotid endarterectomy (CEA) and the 6 week follow-up records of one surgeon (MB), who performed the endarterectomies in the years between 1980 and 1995, were examined. Data obtained included age, sex, preoperative medical conditions, medical risk factors (Fig. I), indication for operation, angiographic findings, the use of intraoperative shunt, the results of electroencephalograph (EEG) monitoring and barbiturate use. Data on postoperative outcome after completion of surgery, status on discharge from hospital and on 6 week follow-up were also obtained from the medical records. The indications for operation were classified according to the North American symptomatic carotid endarterectomy trial's (NASCET) five groups. 4 All patients had formal angiography performed and the severity of stenosis was also categorized using the NASCET criteria, with the percentage reduction in diameter being based on the outflow vessel (i.e. the maximal diameter of the distal ICA). A narrowing of less than 20% was considered normal. Stenosis
Received 22 October 1996 Accepted 8 May 1997 Correspondence to; M. Besser Tel: +61 2 9519 9669; Fax: +61 2 9517 2503
138
of between 20 and 59% was considered mild, 60-79% was considered moderate and 80%-99% was considered severe. The angiograms were reviewed by both the records of the surgeon and by formal reports from the Department of Neuroradiology at Royal Prince Alfred Hospital. Patients were also classified according to the grading system proposed by Sundt in 19755 (Table 1). Most patients were reviewed by a cerebrovascular neurologist prior to operation. A total of 262 carotid endarterectomies were performed on 246 patients, with 16 patients having bilateral procedures at the time of a separate admission. Two patients had repeat CEA on the same side (8 years and 11 years later). Two patients had attempted CEAs but subsequent ligation of the ICA was required; they are not included in this study. All procedures were performed in the Neurosurgical Unit at the Royal Prince Alfred Hospital by one surgeon (MB). For simplicity, each endarterectomy was treated as a separate patient. Seventy-one percent (n=184) of the study reviewed were male, and 29.0% (n=76) female. The mean age of the series was 63.1 years. Clinical c h a r a c t e r i s t i c s
Fifty-four percent (n=141) of the endarterectomies were performed for ipsilateral hemispheric transient ischaemic attacks (TIA) (including ipsilateral amaurosis fugax). Five percent (n= 12) of patients were operated on for asymptomatic severe stenoses discovered incidentally, and the rest for either submaximal strokes in the affected area, or severe global cerebral ischaemia (i.e. nonspecific cerebral symptoms such as multi-infarct dementia, and multiple areas of infarction seen on computed tomography [CT] scanning). D e g r e e of s t e n o s i s on a n g i o g r a p h i c criteria
Eight-eight percent (n=231) of endarterectomies were performed on ICA lesions of over 80% stenosis on the side to which symptoms were referable. Nine percent (n--24) were for 60-80% ulcerated symptomatic stenoses. Three percent (n=8) were for stenoses less than 60%, but with ulceration and appropriate symptoms. Fifty-two percent (n=137) of patients had a contralateral carotid stenosis of over 60%; of these, 59% (n=81) had a contralateral
Carotid endarterectomy 139
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o k.\\'~
N-35
N=20I
N-98
Do,.,o,o, m..o
N=53
N=23
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N-~3
~=166
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Fig. 1 Risk factors. IHD - ischaemic heart disease, PVD - peripheral vascular disease.
stenosis greater than 80%, and 16% (n=22) had contralateral occlusion (1 acute occlusion). Eight percent of all patients (n=22) had angiographic evidence of severe diffuse cerebral disease, defined as evidence of irregular atheromatous narrowing in the carotid siphon and/or the middle cerebral vessels. Treatment
General anaesthesia was used for all cases. Continuous electroencephalography (EEG) monitoring was always used, and six patients had ipsilateral middle cerebral artery flow measured concurrently with transcranial Doppler (TED). Direct arterial pressure monitoring was always performed, and continued in the immediate postoperative period for at least 12 h. The BP was kept at preoperative levels and normocarbia was maintained. Surgery
Endarterectomy always proceeded in a standard manner with a sharp dissection to the carotid sheath and mobilization of the hypoglossal nerve. All patients were heparinized and the carotid vessels cross clamped sequentially beginning with the ICA. If there was any EEG change not responsive to increasing the BP 10% above baseline, the clamps were removed and a barbiturate infusion was commenced to EEG burst suppression. An internal shunt was not routinely used. BP manipulation was also undertaken if required. Cross clamping was then resumed and arteriotomy was proceeded with. The endarterectomy was carried out
meticulously under magnification, and closure was always with an uninten-upted running, non-interlocking 6/0 (monofilament nylon) suture. No venous patch was routinely used; one patient required a Dacron graft. Heparinization was not reversed. Stump pressure was measured in all patients (where it was technically feasible) up to 1987 and the carotid sinus was infiltrated with 1% lignocaine in all patients up to 1988. All patients were admitted to the Neurosurgical Intensive Care Unit for BP and neurological status observation postoperatively, for a minimal period of 12 h. All patients were commenced on aspirin in the immediate postopera, tive period. One patient was noted to have an acutely occluded ICA postoperatively, but was neurologically unchanged and was treated conservatively. One patient was returned to theatre for operation on an acutely occluded left ICA and suffered a submaximal stroke which later necessitated an external carotid to middle cerebral artery (ECA-MCA) bypass. Cross clamp time was recorded in a total of 149 patients, giving an average of 43 min. There was no relationship seen between the cross clamp time and the development of subsequent complications. Anaesthesia/monitoring
All patients had intra-arterial BP and ECG monitoring prior to induction. End tidal CO 2 (ETCO2) was measured in all patients. After 1987 all patients had oxygen saturation (SO2) monitoring. EEG monitoring was always used; prior to 1987 this consisted of a single channel Cerebral Function Monitor (a single channel EEG) which was placed in a fronto-mastoid montage on the side
Table 1 Risk factors for carotid endarteretomy, Sundt (1975) (A) Medical risk factors Angina/MI last 6/12 CCF HT-severe > 180/100 CAL Age >70 Obesity
Neurological risk factors Progressive deficit <24h Recent TIA Multiple strokes
Angiographic risk factors Contralateral occlusion Plaque extension >3cm proximally Bifurcation at C2 with thick neck Soft thrombus extending from ulcerative lesion
(B) Group 1
Group 3
No medical risk factors No angiographic risk factors Neurologically stable
Medical risk factors +/- angiographic risk factors Neurologically stable
Group 2
Group 4
Angiographic risk factors
Neurologically unstable
© 1999 Harcourt Brace & Co. Ltd
Journal of Clinical Neuroscience (1999) 6(2), 138-142
140
Besser et aL
t
.....
30
.\~~L-
20
~\\~ \\\x~ ,.\\-..\
N=103 Stroke
N-141 [ ] TIA-referable
/
N-37 l TIA-other
N=65
[]Amaurosis
N=I2 ~]Asymptomatic
Fig.2 Preoperativesymptoms. being operated on. After 1987 a 2 channel Biological Navigator was used with raw EEG and Compressed Spectral Array processing. Electrodes were placed at Fpl, Fp2, C31 and C41. Any unilateral reduction of high frequency or increase in low frequency activity (or both) was treated as a change. The EEG was recorded continuously from before induction until after emergence. BP was maintained within 20% of the average of the preoperative BPs; reductions lower than this were treated sequentially with a reduction in the concentration of inhalational anaesthetic, fluid loading and a vasopressor (usually a phenylephrine infusion). Reductions less than 20% that were not associated with EEG changes were not treated. Increases in BP were treated with increases in the inhalational agent or (at the end of the case) with diazoxide and/or metoprolol. All patients had general anaesthesia with a thiopentone induction, fentanyl, maintenance with N20 and 02, halothane (before 1987) or isoflurane (after 1987). All were paralysed and ventilation adjusted to maintain the ETCO 2 at approximately 35 torr. At cross clamping, if the EEG changed on the side clamped and the BP was below the baseline pressure, then the BP was increased to approximately 10% above baseline (this often happened spontaneously); if this did not resolve the EEG changes then the clamp was removed. A methohexitone infusion was started and run until the EEG showed marked burst suppression or iso-electricity and the carotid was re-clamped. The patient was maintained on 100% 02 and no other anaesthetic agents were used during this time. BP was maintained approximately 10% above baseline. The methohexitone infusion was adjusted to maintain the burst suppression until the carotid was unclamped. In one patient methohexitone was used in addition to a shunt; he had marked changes on the EEG at cross clamping and a partial endarterectomy had to be done prior to the shunt being inserted; it was felt that the time to do this would be too long without cerebral protection. The methohexitone was ceased once the shunt was opened (approximately 15 min of ischaemia); however, as soon as EEG activity returned, a loss of high frequency activity was apparent on the operative side. Methohexitone was again used with shunt removal, but the asymmetry persisted until the end of the case and the patient awoke with a deficit. Ahnost always the patients who had methohexitone were able to be extubated within 60 rain of the infusion being ceased and were then able to be assessed neurologically. Extubation almost always occurred in the recovery ward.
Intensive care unit management Strict BP monitoring and correction was carried out in the immediate postoperative period for 12-24h. Labile BP was not uncommon and undoubtedly related to carotid sinus dissection
Journal of Clinical Neuroscience (1999) 6(2), 138-142
(intraoperative local anaesthetic infiltration of the sinus did not correlate with postoperative changes). The BP seemed to 'reset' at a satisfactory level within 24 h of surgery, but during this period extremes of hyper-or hypotension could occur.
RESULTS Mortality There were two postoperative deaths in this series, giving an overall mortality rate of 0.6%. 1. A 62-year-old male arteriopath undergoing a right CEA for ulcerative stenotic TIA. The contralateral ICA was occluded. An intimal tear was sustained during the surgery. He awoke in the recovery room with a left hemiplegia and a non-dominant hemisphere syndrome. Angiography showed an occluded right ICA. He did not improve, and suffered a fatal pulmonary embolus 6 days postoperatively. 2. A 57-year-old male with diabetes mellitus and hypertension (Sundt Grade 4) had surgery 4 weeks after a submaximal stroke. He had a large fatal intracerebral haemorrhage on day five postoperatively into the area of infarction. Following 1987 there were no deaths in this series and two post operative referable submaximal ischaemic events.
Major morbidity The major postoperative complications in the 261 carotid endarterectomies performed are shown in Table 2. Minor morbidity
These are detailed in Table 3. One TIA occurred during cerebral angiography and is not included in this postoperative report.
Eeg abnormalities Twenty-six patients were noted to have EEG changes on carotid artery cross clamping. Of these, two patients' EEG resolved followed BP elevation, and 24 required a barbiturate infusion to burst suppression on the EEG. Two patients suffered neurological events despite these measures; one patient, as previously described, was also shunted due to severe diffuse carotid disease (bilateral, multiple lesions) and suffered a referable TIA; the other patient suffered postoperative seizures. The two patients who did not receive barbiturates were either well or unchanged, and overall 24 (84.6%) of patients were either neurologically normal or unchanged.
© 1999 Harcourt Brace & Co. Ltd
Carotid endarterectomy 141 Table 4 Sundt series (1975) - 331 endarterectomies
Table 2 Morbidity-major Neurological
Grade
Referable ischaemic strokes-5 Non-referable ischaemic strokes-4
Other
1 2 3 4
MI postop-1 DVT/PE-2
No. operations
Mortality
129 56 76 70
0 0 2 0
MI - myocardial infarct; DVT - deep venous thrombosis; PE - pulmonary embolism.
MI - myocardial infarct.
Table 3 Morbidity-minor
Table 5 RPAH series - 262 endarterectomies
Neurological
Other
Referable TIAs-3 Non-referable TIAs-7
Cardiovascular Bradycardic episodes-22 Hypertension- >180mm Hg-14 Labile BP-9 Arrhythmias-2 (1 x VEBs, 1 x RAF)
XII paresis-1 Orbicularis oris palsy-1 Neck haematomas-6 (4 re-explored) Wound infections-4 (2 re-explored) all healed well
Grade
Morbidity MI Stroke
%
0 0 3 3
1 2 7 10
1 1 1 1
Morbidity MI Stroke
No. operations
Mortality
1
118
0
0
1
2 3 4
19 51 74
0 1 1
0 1 0
1 2 5
% 0.8 5.3 7.8 8.1
MI - myocardial infarct.
VEB - ventricular ectopic beat; RAF - rapid atrial fibrillation.
Contralateral carotid artery occlusion
Twenty patients (7%) were noted to have an occluded contralateral ICA on preoperative angiography. Following endarterectomy, two patients had acute postoperative occlusions which were managed conservatively as they were neurologically unchanged. Seventeen patients were either normal or unchanged, two patients required ECA-MCA bypass (as above), one patient suffered a referable stroke, and there was one death (Case I, see above). Six w e e k f o l l o w - u p
Twelve patients were lost to follow-up. Four required subsequent ECA-MCA bypass procedures for intracranial carotid disease. One patient suffered postoperative epilepsy, one suffered worsening multi-infarct dementia, and one suffered a vertebrobasilar stroke 3 weeks postoperatively. All other patients were either neurologically normal, unchanged or improved at follow-up. DISCUSSION
Few operations have been subject to more intense scrutiny than CEA. Performed initially in 1953, 6,12it has changed from an emergency operation to a routinely performed elective procedure which offers real reduction in stroke risk for patients with TIAs. Patients who have suffered submaximal strokes and asymptomatic patients with surgically correctable significant (i.e. >70%) stenoses have also been shown to benefit from CEA. 1,2,3,7 Prospective randomized multicentre trials of the benefits of CEA vs maximal medical therapy have demonstrated a clear reduction of risk (both major morbidity and mortality) for the patient undergoing surgery in a unit demonstrating a low risk from the surgery itself. 7 In a review of the literature, Smith and Capel 2 describe the current state of the trials of symptomatic carotid stenosis. The three randomized multicentre trials in progress are the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the VA Symptomatic Stenosis Trial, and the European Carotid Stenosis Trial (ECST). NASCET demonstrated a clear benefit for symptomatic patients with greater than 70% stenosis, which was confirmed by the other trials. NASCET quotes an overall morbidity and mortality rate of 2.1% with a major stroke/death rate of 0.6%. Mild stenosis © 1999 Harcourt Brace & Co. Ltd
(0-29%) was associated with no benefit for surgery versus medical therapy for symptomatic lesions. The combined morbidity and mortality for this study of 1.9% compares favourably with NASCET figures. Sundt s divided his patients into 'at risk' groups, according to perceived angiographic, neurological and medical risks. In a progressive follow-up of 342 carotid endarterectomies over a 4 year period, Sundt found that most patients were referred for surgery with amaurosis fugax, TIA or submaximal stroke, or a combination of these. His postoperative combined morbidity (stroke) and mortality (from any cause) are comparable to the Royal Prince Alfred Hospital data (Tables 4 and 5). Other investigators have used EEG monitoring; 5,8,9,~°,~1,14most used EEG monitoring as a guide to shunting. Barbiturates given to burst suppression were used in two studies from the same group of investigators, 11,14in which they were used for all patients. Sundt 5,~° found a direct correlation between cerebral blood flow measurements with Xe ~33 clearance and changes in the EEG. In a retrospective study of 1935 patients, he also found a persistent change in the EEG was always associated with a new deficit. This statement correlates with our results - all four patients noted to have deficits in the recovery room had persistent EEG asymmetry noted. Whittlemore 8 found no clear correlation between EEG changes and new deficits, possibly a function of the anaesthetic agent used. In conclusion, in experienced hands CEA is a safe and effective operation in stroke prevention. The figures from the Royal Prince Alfred Neurosurgical Unit are comparable with quoted series worldwide. The use of barbiturates for EEG change remains controversial in CEA. However, EEG monitoring gives a very sensitive appraisal of cerebral function during carotid clamping. Direct arterial monitoring of the BP in the postoperative period is, in our view, essential for prevention of complications relating to postoperative hypotension (thrombosis of endarterectomy site) or hypertension (intracerebral haemorrhage or arteriotomy repair disruption). ACKNOWLEDGMENTS
The authors would like to thank Dr J. Leicester, Neurologist, and Dr J Hallinan, Neuroradiologist, for their help in the management of these patients. The assistance of Sandra Profilio, Secretary to the Department of Neurosurgery, in the preparation of this paper is also gratefully acknowledged. Journal of Clinical Neuroscience (1999) 8(2), 138-142
142
Besser et aL
REFERENCES 1. Lord, RSA. Carotid Endarterectomy: Options and Outcomes. Aust NZ J Surg 1995; 65:151-159 2. Smith RR, Capel WT. The State of Carotid Endarterectomy. Neurosurgery Quarterly 6 1996; 1: 21-30. 3. Appleberg M, Cottier D et al. Carotid endarterectnmy for asymptomatic carotid artery stenosis: patients with severe bilateral disease, a high risk subgroup. Aust NZ J Surg 1995; 65: 160-165. 4. Gasecki AP et al. Long-term prognosis and effect of endarterectomy in patients with symptomatic severe carotid stenosis and contralateral carotid stenosis or occlusion Results From NASCET. J Neurosnrgery 1995; 1h 778-782. 5. Sundt TM Jr., Sandok BA, Whisnant JR Mayo Clin Proc 1975; 50:301-306. 6. Eastcott HHG, Picketing GW, Rob CG. Reconstruction of internal carotid arteryin a patient with intermittent attacks of hemiplegia. Lancet 1954; 2: 994-996. 7. Moore WS et al. Guidelines for carotid endarterectomy: a multidisciplinary consensus. Statement from the Ad Hoc Committee, American Heart Association. Circulation 1995; 91: 566-579.
Journal of Clinical Neuroscience (1999) 6(2), 138-142
8. Whittlemore AD et al. Routine encephalographic (EEG) monitoring during carotid endarterectomy, Ann Surg 1983; 197; 707-713. 9. Fletcher JP, Morris JGL, Little JM, Kershaw LZ. EEG monitoring during carotid endarterectomy. Aust NZ J Surg 1988; 58: 285-288. 10. Sundt TM Jr., Sharbrough FW, Piepgras DG, et al. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy. Mayo Clin Proc 1981; 56: 533-543. 11. Hicks RG, Kerr DR, Horton DA. Thiopentone cerebral protection under EEG control during carotid endartereetomy. Anaes Intens Care 1986; 14: 22-28. 12. Molins M, Surgical treatment of the internal carotid artery in the neck: carotid-carotidal anastomosis. ACTU Neurologica Latino America 1955; 1: 171-178. 13. Haynes RB et al. Prevention of functional impairment by endarterectomy for symptomatic high-grade carotid stenosis. JAMA 1994; 271: 1256-1259. 14. Frawley JE, Hicks RG, Horton DA, Niesche JW, Matheson JM. Thiopental sodium protection during carotid endarterectomy: perioperative disease and death. J Vasc Surg 1994; 19: 732-738.
© 1999 Harcourt Brace & Co. Ltd
Clinical studies
Carotid e n d a r t e r e c t o m y in a neurosurgical unit: a retrospective review M. B e s s e r ~ MB BS FRCSC FRACS, R. P a r k i n s o n 2 MB BS BSC MED, R. Traill 3 MB BS FANZCA
1Clinical Associate Professor and Head, Department of Neurosurgery, Royal Prince Alfred Hospital, Sydney, Australia 2Departmentof Neurosurgery, Royal Prince Alfred Hospital, Sydney, Australia 3Departmentof Anaesthetics, Royal Prince Alfred Hospital, Sydney, Australia
Summary A retrospective survey of 262 carotid endarterectomies performed in the Neurosurgical Unit at Royal Prince Alfred Hospital over a 15 year period was conducted. A total of 141 patients were operated on for transient ischaemic attacks referable to stenosis of the ipsilateral internal carotid artery. Eighty-eight percent of patients had angiographic evidence of greater than 80% stenosis of the affected internal carotid artery. A postoperative new permanent neurological deficit of 1.9% and death rate of 0.6% was achieved. No deaths and two postoperative strokes were recorded after 1987. These resuffs are comparable with published series. The use of barbiturate therapy with electroencephalography changes on cross clamping of the internal carotid artery is described. Keyworde: carotid endarterectomy, barbiturates, electroencephalography
INTRODUCTION
Stroke is the commonest neurological disease affecting man? It is a major cause of prolonged disability and the third leading cause of death in the community. Strokes are often preceded by transient ischaemic attacks (TIA) with the majority of patients suffering from intracranial embolic or occlusive arterial disease. Data suggests that at least 60% are attributable to carotid disease and patients with high grade stenosis make up about 50% of stroke victims. 2 Recent multicentre randomized prospective trials have demonstrated a clear benefit of surgery over medical therapy for patients with greater than 70% stenosis of the internal carotid artery. 1,2,7 However, carotid endarterectomy (CEA) needs to be performed by surgeons and anaesthetists in a unit with low perioperative mortality and morbidity. This prompted review of our experience with this procedure. MATERIALS
AND METHODS
The hospital records of 246 patients who had carotid endarterectomy (CEA) and the 6 week follow-up records of one surgeon (MB), who performed the endarterectomies in the years between 1980 and 1995, were examined. Data obtained included age, sex, preoperative medical conditions, medical risk factors (Fig. I), indication for operation, angiographic findings, the use of intraoperative shunt, the results of electroencephalograph (EEG) monitoring and barbiturate use. Data on postoperative outcome after completion of surgery, status on discharge from hospital and on 6 week follow-up were also obtained from the medical records. The indications for operation were classified according to the North American symptomatic carotid endarterectomy trial's (NASCET) five groups. 4 All patients had formal angiography performed and the severity of stenosis was also categorized using the NASCET criteria, with the percentage reduction in diameter being based on the outflow vessel (i.e. the maximal diameter of the distal ICA). A narrowing of less than 20% was considered normal. Stenosis
Received 22 October 1996 Accepted 8 May 1997 Correspondence to; M. Besser Tel: +61 2 9519 9669; Fax: +61 2 9517 2503
138
of between 20 and 59% was considered mild, 60-79% was considered moderate and 80%-99% was considered severe. The angiograms were reviewed by both the records of the surgeon and by formal reports from the Department of Neuroradiology at Royal Prince Alfred Hospital. Patients were also classified according to the grading system proposed by Sundt in 19755 (Table 1). Most patients were reviewed by a cerebrovascular neurologist prior to operation. A total of 262 carotid endarterectomies were performed on 246 patients, with 16 patients having bilateral procedures at the time of a separate admission. Two patients had repeat CEA on the same side (8 years and 11 years later). Two patients had attempted CEAs but subsequent ligation of the ICA was required; they are not included in this study. All procedures were performed in the Neurosurgical Unit at the Royal Prince Alfred Hospital by one surgeon (MB). For simplicity, each endarterectomy was treated as a separate patient. Seventy-one percent (n=184) of the study reviewed were male, and 29.0% (n=76) female. The mean age of the series was 63.1 years. Clinical c h a r a c t e r i s t i c s
Fifty-four percent (n=141) of the endarterectomies were performed for ipsilateral hemispheric transient ischaemic attacks (TIA) (including ipsilateral amaurosis fugax). Five percent (n= 12) of patients were operated on for asymptomatic severe stenoses discovered incidentally, and the rest for either submaximal strokes in the affected area, or severe global cerebral ischaemia (i.e. nonspecific cerebral symptoms such as multi-infarct dementia, and multiple areas of infarction seen on computed tomography [CT] scanning). D e g r e e of s t e n o s i s on a n g i o g r a p h i c criteria
Eight-eight percent (n=231) of endarterectomies were performed on ICA lesions of over 80% stenosis on the side to which symptoms were referable. Nine percent (n--24) were for 60-80% ulcerated symptomatic stenoses. Three percent (n=8) were for stenoses less than 60%, but with ulceration and appropriate symptoms. Fifty-two percent (n=137) of patients had a contralateral carotid stenosis of over 60%; of these, 59% (n=81) had a contralateral
Carotid endarterectomy 139
80~ 7060- g 504030. 20_ 1O.
o k.\\'~
N-35
N=20I
N-98
Do,.,o,o, m..o
N=53
N=23
[],,o
No,,
N-~3
~=166
[]Ch°le ter°l NSm°ker
Fig. 1 Risk factors. IHD - ischaemic heart disease, PVD - peripheral vascular disease.
stenosis greater than 80%, and 16% (n=22) had contralateral occlusion (1 acute occlusion). Eight percent of all patients (n=22) had angiographic evidence of severe diffuse cerebral disease, defined as evidence of irregular atheromatous narrowing in the carotid siphon and/or the middle cerebral vessels. Treatment
General anaesthesia was used for all cases. Continuous electroencephalography (EEG) monitoring was always used, and six patients had ipsilateral middle cerebral artery flow measured concurrently with transcranial Doppler (TED). Direct arterial pressure monitoring was always performed, and continued in the immediate postoperative period for at least 12 h. The BP was kept at preoperative levels and normocarbia was maintained. Surgery
Endarterectomy always proceeded in a standard manner with a sharp dissection to the carotid sheath and mobilization of the hypoglossal nerve. All patients were heparinized and the carotid vessels cross clamped sequentially beginning with the ICA. If there was any EEG change not responsive to increasing the BP 10% above baseline, the clamps were removed and a barbiturate infusion was commenced to EEG burst suppression. An internal shunt was not routinely used. BP manipulation was also undertaken if required. Cross clamping was then resumed and arteriotomy was proceeded with. The endarterectomy was carried out
meticulously under magnification, and closure was always with an uninten-upted running, non-interlocking 6/0 (monofilament nylon) suture. No venous patch was routinely used; one patient required a Dacron graft. Heparinization was not reversed. Stump pressure was measured in all patients (where it was technically feasible) up to 1987 and the carotid sinus was infiltrated with 1% lignocaine in all patients up to 1988. All patients were admitted to the Neurosurgical Intensive Care Unit for BP and neurological status observation postoperatively, for a minimal period of 12 h. All patients were commenced on aspirin in the immediate postopera, tive period. One patient was noted to have an acutely occluded ICA postoperatively, but was neurologically unchanged and was treated conservatively. One patient was returned to theatre for operation on an acutely occluded left ICA and suffered a submaximal stroke which later necessitated an external carotid to middle cerebral artery (ECA-MCA) bypass. Cross clamp time was recorded in a total of 149 patients, giving an average of 43 min. There was no relationship seen between the cross clamp time and the development of subsequent complications. Anaesthesia/monitoring
All patients had intra-arterial BP and ECG monitoring prior to induction. End tidal CO 2 (ETCO2) was measured in all patients. After 1987 all patients had oxygen saturation (SO2) monitoring. EEG monitoring was always used; prior to 1987 this consisted of a single channel Cerebral Function Monitor (a single channel EEG) which was placed in a fronto-mastoid montage on the side
Table 1 Risk factors for carotid endarteretomy, Sundt (1975) (A) Medical risk factors Angina/MI last 6/12 CCF HT-severe > 180/100 CAL Age >70 Obesity
Neurological risk factors Progressive deficit <24h Recent TIA Multiple strokes
Angiographic risk factors Contralateral occlusion Plaque extension >3cm proximally Bifurcation at C2 with thick neck Soft thrombus extending from ulcerative lesion
(B) Group 1
Group 3
No medical risk factors No angiographic risk factors Neurologically stable
Medical risk factors +/- angiographic risk factors Neurologically stable
Group 2
Group 4
Angiographic risk factors
Neurologically unstable
© 1999 Harcourt Brace & Co. Ltd
Journal of Clinical Neuroscience (1999) 6(2), 138-142
140
Besser et aL
t
.....
30
.\~~L-
20
~\\~ \\\x~ ,.\\-..\
N=103 Stroke
N-141 [ ] TIA-referable
/
N-37 l TIA-other
N=65
[]Amaurosis
N=I2 ~]Asymptomatic
Fig.2 Preoperativesymptoms. being operated on. After 1987 a 2 channel Biological Navigator was used with raw EEG and Compressed Spectral Array processing. Electrodes were placed at Fpl, Fp2, C31 and C41. Any unilateral reduction of high frequency or increase in low frequency activity (or both) was treated as a change. The EEG was recorded continuously from before induction until after emergence. BP was maintained within 20% of the average of the preoperative BPs; reductions lower than this were treated sequentially with a reduction in the concentration of inhalational anaesthetic, fluid loading and a vasopressor (usually a phenylephrine infusion). Reductions less than 20% that were not associated with EEG changes were not treated. Increases in BP were treated with increases in the inhalational agent or (at the end of the case) with diazoxide and/or metoprolol. All patients had general anaesthesia with a thiopentone induction, fentanyl, maintenance with N20 and 02, halothane (before 1987) or isoflurane (after 1987). All were paralysed and ventilation adjusted to maintain the ETCO 2 at approximately 35 torr. At cross clamping, if the EEG changed on the side clamped and the BP was below the baseline pressure, then the BP was increased to approximately 10% above baseline (this often happened spontaneously); if this did not resolve the EEG changes then the clamp was removed. A methohexitone infusion was started and run until the EEG showed marked burst suppression or iso-electricity and the carotid was re-clamped. The patient was maintained on 100% 02 and no other anaesthetic agents were used during this time. BP was maintained approximately 10% above baseline. The methohexitone infusion was adjusted to maintain the burst suppression until the carotid was unclamped. In one patient methohexitone was used in addition to a shunt; he had marked changes on the EEG at cross clamping and a partial endarterectomy had to be done prior to the shunt being inserted; it was felt that the time to do this would be too long without cerebral protection. The methohexitone was ceased once the shunt was opened (approximately 15 min of ischaemia); however, as soon as EEG activity returned, a loss of high frequency activity was apparent on the operative side. Methohexitone was again used with shunt removal, but the asymmetry persisted until the end of the case and the patient awoke with a deficit. Ahnost always the patients who had methohexitone were able to be extubated within 60 rain of the infusion being ceased and were then able to be assessed neurologically. Extubation almost always occurred in the recovery ward.
Intensive care unit management Strict BP monitoring and correction was carried out in the immediate postoperative period for 12-24h. Labile BP was not uncommon and undoubtedly related to carotid sinus dissection
Journal of Clinical Neuroscience (1999) 6(2), 138-142
(intraoperative local anaesthetic infiltration of the sinus did not correlate with postoperative changes). The BP seemed to 'reset' at a satisfactory level within 24 h of surgery, but during this period extremes of hyper-or hypotension could occur.
RESULTS Mortality There were two postoperative deaths in this series, giving an overall mortality rate of 0.6%. 1. A 62-year-old male arteriopath undergoing a right CEA for ulcerative stenotic TIA. The contralateral ICA was occluded. An intimal tear was sustained during the surgery. He awoke in the recovery room with a left hemiplegia and a non-dominant hemisphere syndrome. Angiography showed an occluded right ICA. He did not improve, and suffered a fatal pulmonary embolus 6 days postoperatively. 2. A 57-year-old male with diabetes mellitus and hypertension (Sundt Grade 4) had surgery 4 weeks after a submaximal stroke. He had a large fatal intracerebral haemorrhage on day five postoperatively into the area of infarction. Following 1987 there were no deaths in this series and two post operative referable submaximal ischaemic events.
Major morbidity The major postoperative complications in the 261 carotid endarterectomies performed are shown in Table 2. Minor morbidity
These are detailed in Table 3. One TIA occurred during cerebral angiography and is not included in this postoperative report.
Eeg abnormalities Twenty-six patients were noted to have EEG changes on carotid artery cross clamping. Of these, two patients' EEG resolved followed BP elevation, and 24 required a barbiturate infusion to burst suppression on the EEG. Two patients suffered neurological events despite these measures; one patient, as previously described, was also shunted due to severe diffuse carotid disease (bilateral, multiple lesions) and suffered a referable TIA; the other patient suffered postoperative seizures. The two patients who did not receive barbiturates were either well or unchanged, and overall 24 (84.6%) of patients were either neurologically normal or unchanged.
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Carotid endarterectomy 141 Table 4 Sundt series (1975) - 331 endarterectomies
Table 2 Morbidity-major Neurological
Grade
Referable ischaemic strokes-5 Non-referable ischaemic strokes-4
Other
1 2 3 4
MI postop-1 DVT/PE-2
No. operations
Mortality
129 56 76 70
0 0 2 0
MI - myocardial infarct; DVT - deep venous thrombosis; PE - pulmonary embolism.
MI - myocardial infarct.
Table 3 Morbidity-minor
Table 5 RPAH series - 262 endarterectomies
Neurological
Other
Referable TIAs-3 Non-referable TIAs-7
Cardiovascular Bradycardic episodes-22 Hypertension- >180mm Hg-14 Labile BP-9 Arrhythmias-2 (1 x VEBs, 1 x RAF)
XII paresis-1 Orbicularis oris palsy-1 Neck haematomas-6 (4 re-explored) Wound infections-4 (2 re-explored) all healed well
Grade
Morbidity MI Stroke
%
0 0 3 3
1 2 7 10
1 1 1 1
Morbidity MI Stroke
No. operations
Mortality
1
118
0
0
1
2 3 4
19 51 74
0 1 1
0 1 0
1 2 5
% 0.8 5.3 7.8 8.1
MI - myocardial infarct.
VEB - ventricular ectopic beat; RAF - rapid atrial fibrillation.
Contralateral carotid artery occlusion
Twenty patients (7%) were noted to have an occluded contralateral ICA on preoperative angiography. Following endarterectomy, two patients had acute postoperative occlusions which were managed conservatively as they were neurologically unchanged. Seventeen patients were either normal or unchanged, two patients required ECA-MCA bypass (as above), one patient suffered a referable stroke, and there was one death (Case I, see above). Six w e e k f o l l o w - u p
Twelve patients were lost to follow-up. Four required subsequent ECA-MCA bypass procedures for intracranial carotid disease. One patient suffered postoperative epilepsy, one suffered worsening multi-infarct dementia, and one suffered a vertebrobasilar stroke 3 weeks postoperatively. All other patients were either neurologically normal, unchanged or improved at follow-up. DISCUSSION
Few operations have been subject to more intense scrutiny than CEA. Performed initially in 1953, 6,12it has changed from an emergency operation to a routinely performed elective procedure which offers real reduction in stroke risk for patients with TIAs. Patients who have suffered submaximal strokes and asymptomatic patients with surgically correctable significant (i.e. >70%) stenoses have also been shown to benefit from CEA. 1,2,3,7 Prospective randomized multicentre trials of the benefits of CEA vs maximal medical therapy have demonstrated a clear reduction of risk (both major morbidity and mortality) for the patient undergoing surgery in a unit demonstrating a low risk from the surgery itself. 7 In a review of the literature, Smith and Capel 2 describe the current state of the trials of symptomatic carotid stenosis. The three randomized multicentre trials in progress are the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the VA Symptomatic Stenosis Trial, and the European Carotid Stenosis Trial (ECST). NASCET demonstrated a clear benefit for symptomatic patients with greater than 70% stenosis, which was confirmed by the other trials. NASCET quotes an overall morbidity and mortality rate of 2.1% with a major stroke/death rate of 0.6%. Mild stenosis © 1999 Harcourt Brace & Co. Ltd
(0-29%) was associated with no benefit for surgery versus medical therapy for symptomatic lesions. The combined morbidity and mortality for this study of 1.9% compares favourably with NASCET figures. Sundt s divided his patients into 'at risk' groups, according to perceived angiographic, neurological and medical risks. In a progressive follow-up of 342 carotid endarterectomies over a 4 year period, Sundt found that most patients were referred for surgery with amaurosis fugax, TIA or submaximal stroke, or a combination of these. His postoperative combined morbidity (stroke) and mortality (from any cause) are comparable to the Royal Prince Alfred Hospital data (Tables 4 and 5). Other investigators have used EEG monitoring; 5,8,9,~°,~1,14most used EEG monitoring as a guide to shunting. Barbiturates given to burst suppression were used in two studies from the same group of investigators, 11,14in which they were used for all patients. Sundt 5,~° found a direct correlation between cerebral blood flow measurements with Xe ~33 clearance and changes in the EEG. In a retrospective study of 1935 patients, he also found a persistent change in the EEG was always associated with a new deficit. This statement correlates with our results - all four patients noted to have deficits in the recovery room had persistent EEG asymmetry noted. Whittlemore 8 found no clear correlation between EEG changes and new deficits, possibly a function of the anaesthetic agent used. In conclusion, in experienced hands CEA is a safe and effective operation in stroke prevention. The figures from the Royal Prince Alfred Neurosurgical Unit are comparable with quoted series worldwide. The use of barbiturates for EEG change remains controversial in CEA. However, EEG monitoring gives a very sensitive appraisal of cerebral function during carotid clamping. Direct arterial monitoring of the BP in the postoperative period is, in our view, essential for prevention of complications relating to postoperative hypotension (thrombosis of endarterectomy site) or hypertension (intracerebral haemorrhage or arteriotomy repair disruption). ACKNOWLEDGMENTS
The authors would like to thank Dr J. Leicester, Neurologist, and Dr J Hallinan, Neuroradiologist, for their help in the management of these patients. The assistance of Sandra Profilio, Secretary to the Department of Neurosurgery, in the preparation of this paper is also gratefully acknowledged. Journal of Clinical Neuroscience (1999) 8(2), 138-142
142
Besser et aL
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8. Whittlemore AD et al. Routine encephalographic (EEG) monitoring during carotid endarterectomy, Ann Surg 1983; 197; 707-713. 9. Fletcher JP, Morris JGL, Little JM, Kershaw LZ. EEG monitoring during carotid endarterectomy. Aust NZ J Surg 1988; 58: 285-288. 10. Sundt TM Jr., Sharbrough FW, Piepgras DG, et al. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy. Mayo Clin Proc 1981; 56: 533-543. 11. Hicks RG, Kerr DR, Horton DA. Thiopentone cerebral protection under EEG control during carotid endartereetomy. Anaes Intens Care 1986; 14: 22-28. 12. Molins M, Surgical treatment of the internal carotid artery in the neck: carotid-carotidal anastomosis. ACTU Neurologica Latino America 1955; 1: 171-178. 13. Haynes RB et al. Prevention of functional impairment by endarterectomy for symptomatic high-grade carotid stenosis. JAMA 1994; 271: 1256-1259. 14. Frawley JE, Hicks RG, Horton DA, Niesche JW, Matheson JM. Thiopental sodium protection during carotid endarterectomy: perioperative disease and death. J Vasc Surg 1994; 19: 732-738.
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