World J. Surg. 3, 155-165, 1979

WoddJournal

of Stirgery

Complications of Carotid Endarterectomy and Their Prevention Jesse E. T h o m p s o n , M.D. Department of General Surgery, Baylor University Medical Center, Dallas, Texas, U.S.A. Mortality and morbidity associated with carotid endarterectomy may be minimized by proper selection of patients and proper operative and postoperative management. Complications include cardiac and airway problems related to anesthesia, infection, hematoma, nerve pareses, parotitis, arterial disruption, false aneurysms, and carotid-cavernous fistula. The most serious complication is the occurrence of neurologic deficits as a result of cerebral emboli or ischemia. Emboli are due to excessive manipulation of the artery, while ischemia results from hypotension, intracerebral thrombosis, or inadequate cerebral protection. Adequacy of collateral blood flow during carotid clamping is determined by temporary occlusion under local anesthesia, measurement of internal carotid artery stump pressure, or EEG monitoring. The most reliable method of cerebral protection is a temporary inlying shunt. Selective shunting is used if the patient is intolerant of temporary clamping, if stump pressure is below 55 mm Hg, or if EEG changes occur. For maximum safety, the author suggests routine shunting and general anesthesia. Operative mortality for patients experiencing transient ischemic attacks should be less than 1% and operation-related neurologic deficits no more than 2%. Meticulous attention to technical details is obligatory. Hypotension should be avoided during and after operation to avert thrombosis, and excessive hypertension postoperatively must be treated promptly to avoid cerebral hemorrhage and edema. Operation is contraindicated on patients with acute profound and progressing strokes.

e m p l o y e d operations in vascular surgery [1]. K n o w l e d g e of the complications related to this procedure and methods by which they m a y be prevented is m a n d a t o r y if acceptable clinical results are to be obtained. Complications peculiar to this field m a y be disastrous, particularly when the operations are being p e r f o r m e d on patients with transient ischemic attacks (TIA) or a s y m p t o m a t i c carotid bruits who, prior to the procedure, have no dem o n s t r a b l e neurologic deficit, but m a y incur a paralytic stroke as a result of the operation. Although carotid e n d a r t e r e c t o m y is therapeutic in its relief o f s y m p t o m s , its m o s t important role is prevention of strokes. In its broadest sense, prevention implies not only p r o p e r selection of patients for operation, but also p r o p e r operative and postoperative m a n a g e m e n t , so that strokes related to the operative p r o c e d u r e are reduced to an absolute minimum. Complications associated with carotid endartere c t o m y are listed in Table 1. Although the list is imposing, if the surgeon is meticulous with details o f m a n a g e m e n t , the actual incidence of any complication is quite low. Operative Mortality

Carotid e n d a r t e r e c t o m y for c e r e b r o v a s c u l a r insufficiency has b e c o m e one of the most c o m m o n l y

O f p r i m a r y concern is operative mortality. The average age o f patients undergoing operation is a b o u t 65 years. There is a high incidence of h y p e r t e n s i o n and diabetes, and atherosclerotic lesions are fre-

Reprint requests: Jesse E. Thompson, M.D., 3600 Gaston Avenue, Suite 505, Dallas, Texas 75246, U.S.A.

0364-2313/79/0003-0155 $02.20 9 1979 Soci6t6 Internationale de Chirurgie 155

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Table 1. Complications of carotid endarterectomy. Related to anesthesia, general or local Cardiac problems Airway problems Hypotension Related to cervical wound Infection Hematoma Nerve paresis Vagus Hypoglossal Marginal branch of facial Parotitis Tracheal obstruction Related to carotid artery Disruption False aneurysms Carotid-cavernous A-V fistula Infection of Dacron graft Production or aggravation Of neurological deficits Operative causes Embolism Cerebral ischemia Postoperative causes Thrombosis of endarterectomized segment Hypotension Intracerebral hemorrhage or edema Hypertension Miscellaneous Postoperative headache Cerebral edema

quent in other areas of the peripheral vasculature, especially in the coronary arteries. At the outset, therefore, these patients constitute a high-risk group. Table 2 shows operative mortality rates over a 20year period for patients operated on by the author and his associates [2, 3]. Mortality varies directly with the severity of the clinical category. Among the 27 deaths, 19 were from cerebral causes, 7 from cardiac causes, and 1 from pulmonary embolism. In the past 14 years, with routine use of general anesthesia together with a temporary inlying shunt and avoidance of operation on patients with acute and progressing strokes, the mortality rate in the frank stroke group has been reduced to 3.9%, while that in the TIA group has been 0.8%, with an overall mortality rate of carotid surgery for all indications of 1.4%. At the present time, the operative mortality rate for patients with TIA, as reported by most authors, is in the vicinity of 1%, which is acceptable for this elderly group with atherosclerosis. That such an acceptable rate may not be universally achieved in community hospitals in the United States is pointed up in a recent report listing the operative mortality rate for TIA as 7% and that for frank strokes as 10.8% [4].

World J. Surg. Voi. 3, No. 2, 1979 Complications Related to Anesthesia, General or Local

Cardiac arrhythmias of various sorts occur frequently during operation, even when local anesthesia is used, but they are more common when general anesthesia is employed. Such arrhythmias may lead to impaired cardiac function, hypotension, or cardiac arrest. Their presence must be recognized and prompt treatment instituted. Continuous operative ECG monitoring permits immediate detection of cardiac arrhythmias and the use of appropriate drugs for their control. Airway obstruction or aspiration of secretions may occur during or following carotid endarterectomy, and may, in turn, lead to hypoxia, aspiration pneumonitis, or cardiac arrest. Airways, endotracheal tubes, suction apparatus, oxygen, and other respiratory equipment must be available in the recovery areas for prevention and treatment of airway problems.

Complications Related to the Cervical Wound

Hematomas may occur from improper hemostasis, leakage from the arterial suture line, postoperative hypertension, or excessive anticoagulation. If massive, they may cause tracheal obstruction, require tracheostomy, and predispose to wound infection. They may necessitate reoperation to control the source of hemorrhage. Meticulous hemostasis during operation, careful closure of the arteriotomy, and avoidance of excess anticoagulation will prevent this complication. Several major cervical nerves are encountered during the performance of carotid endarterectomy and may be affected, temporarily or permanently, by the procedure. They include the superficial sensory nerves, marginal branch of the facial, ansa hypoglossi, hypoglossal, vagus, recurrent laryngeal, superior laryngeal, and cervical sympathetic trunk [5]. The superficial segmental sensory nerves frequently are divided for proper operative exposure, which only causes minor discomfort from postoperative paresthesia. It is important to avoid injury to the marginal branch of the facial nerve since drooping of the corner of the mouth results if this nerve is cut or traumatized. Such injury may be avoided by curving the upper end of the skin incision posteriorly behind the lobe of the ear. The ansa hypoglossi may be divided with impunity, if necessary, for proper arterial exposure and suture. The hypoglossal nerve, on the other hand, should be carefully preserved. It frequently overlies the area of endarterectomy and must be gently re-

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Table 2. Operative mortality rates following carotid endarterectomy, performed over a period of 20 years.

Clinical category

Number of patients

Number of operations

Number of deaths

Patient mortality rate

Procedure mortality rate

Frank stroke Transient ischemia Chronic ischemia Asymptomatic bruit Total

296 575 19 132 1,022

358 737 24 167 1,286

20 7 0 0 27

6.8% 1.2% 0 0 2.6%

5.6% 0.~ 0 0 2.1%

tracted with a tape. Its upward retraction is facilitated by ligation and division of a small branch of the external carotid artery passing to the sternomastoid muscle, which normally holds the nerve downward in a sling. Some weakness of tongue muscles occasionally occurs from traction on the nerve, but function returns to normal within a week or so. The vagus nerve is frequently found intimately applied to the carotid artery, especially to the internal carotid artery from the bifurcation to the base of the skull, and occasionally lies on the anterior surface of the common carotid artery. Care should be exercised not to clamp or divide the vagus inadvertently, since at this level, it is above the origin of the recurrent laryngeal nerve and injury results in ipsilateral vocal cord paralysis. The recurrent nerve itself, or the superior laryngeal nerve, may be injured if the dissection is extended medially as the carotid artery and its branches are being isolated. The cervical sympathetic trunk lies under a thin layer of fascia in a plane deep to the vagus nerve and is not ordinarily visualized during carotid endarterectomy. The carotid sinus nerve may be sectioned to facilitate exposure with no deleterious effect. The surgeon undertaking operations on the carotid artery should have a clear knowledge of the anatomical locations of these nerves and the physiological consequences resulting from their injury. Damage to them is easily avoided by careful operative dissection. In some patients, the parotid gland lies more inferiorly than usual and may present in the upper end of the incision, especially if the bifurcation of the common carotid artery is high. Under these circumstances, the inferior portion of the gland may be manipulated or even incised; a mild parotitis may develop postoperatively. The author has not observed any major episodes of parotitis, nor any leak of saliva, although a few patients have had marked swelling with discomfort lasting 1-2 weeks postoperatively. Tracheal obstruction is a serious complication following carotid endarterectomy. It may result from multiple or prolonged endotracheal intubations, performance of arteriography and endarterectomy on the same day, one-stage bilateral ca-

rotid endarterectomies, vagus or recurrent laryngeal nerve damage, hematomas in the operative site, or from operation on patients with acute profound strokes. Tracheostomy should be performed promptly when indicated. It must be used judiciously, however, since it presents the potential hazard of infection near an arterial suture line, a complication which in itself may be catastrophic.

Complications Related to Carotid Artery Surgery

Following endarterectomy in the proper plane of cleavage, the internal carotid artery wall, although thin, is quite strong, holds sutures well, and usually causes no postoperative problems. Disruption of the artery and aneurysm formation in the endarterectomized segment have been reported, however [6, 7]. If it is obvious at the time of operation that the artery wall has been fragmented by dissection in the wrong plane, or if it is totally degenerated, appropriate repair should be done at that time by patch-graft reconstruction or segmental replacement with Dacron| or autologous vein. Except in rare instances, this complication is a technical one and should be recognized and repaired at the primary operation, rather than secondarily following postoperative disruption. False aneurysms may occur in the endarterectomized segment of the carotid artery, most commonly where Dacron| patch grafts have been employed for arterial reconstruction, sewn in place with silk sutures. The silk deteriorates with time, the suture line disrupts in varying degrees, and false aneurysms form. Arterial silk was routinely employed before satisfactory polyester sutures, which do not deteriorate, were developed. The author has experience with 7 instances of this complication in patients operated on early in his series. All were successfully repaired. It is now clear that patch-graft reconstruction is only rarely necessary in carotid endarterectomy. If the artery is very small, a patch of vein or Dacron| may be used and sewn in place with polyester sutures. Procedures for repair of these false aneurysms vary with the individual circumstances [8]. If the

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Table 3. Complications occurring in 1,140 carotid endarterectomy operations on 903 patients.

Number Percentage Hematoma requiring reoperation False aneurysm in Dacron* patch graft, silk sutures Tracheostomy Thrombosis requiring reoperation Wound infection Graft or artery infection Arterial disruption

8

0.7

7 4 3 1 0 0

0.6 0.35 0.26 0.09 0 0

disruption is localized, the sac and old Dacron| patch may be trimmed away and the defect reconstructed using a patch graft of vein or Dacron| and polyester sutures. If the disruption is extensive, segmental replacement may be required. A tubular prosthesis of either saphenous vein or 8-mm Dacron| is satisfactory. Since repair of false aneurysms may require clamping of the carotid artery for considerable periods of time, adequate cerebral protection must be employed to avoid neurologic complications. The simplest and most effective means is a temporary inlying shunt. Carotid-cavernous sinus fistula has been reported as a complication of too-vigorous instrumentation in attempts to open totally occluded internal carotid arteries [9]. This lesion may be treated by trapping or by guided embolism and proximal carotid ligation. Wound infection is a serious complication of endarterectomy. If the arterial suture line is involved, disruption almost invariably occurs, particularly if a Dacron| patch has been used. The resulting incidence of serious neurologic complications is quite high. Improper skin preparation, breaks in sterile technique, wound hematomas, and secondary operations increase the incidence of infections. It is not necessary to use prophylactic antibiotic therapy in patients undergoing carotid endarterectomy unless a Dacron| prosthesis is employed. Should infection occur in a carotid wound, it should be adequately drained and treated with the appropriate antibiotics, given both parenterally and by topical irrigation. If a Dacron| patch graft is present, it will in all likelihood have to be removed and replaced with a vein graft, employing monofilament arterial sutures to avoid foci of infection that may be harbored in braided suture material. Table 3 lists complications encountered by the author and his associates.

Production or Aggravation of Neurologic Deficits

The most serious complication of carotid endarterectomy is the occurrence or aggravation of a neuro-

logic deficit. Many of these are episodes of transient weakness lasting only a few hours or a few days with complete clearing, while others remain as permanent deficits, either mild or severe. If surgery for neurologically intact patients with transient cerebral ischemia or asymptomatic carotid bruits is advocated, it is imperative that every effort be made to avoid such neurologic complications.

Operative Causes A common cause of neurologic deficits related to the operative procedure itself is cerebral embolization of platelet aggregations or debris from necrotic atherosclerotic plaques. Excessive manipulation or rough handling of the carotid artery is responsible for such emboli. Embolization is avoided by gentleness in dissection of the artery and by delaying the placing of a tape around the area of the plaque until the final step. Improper flushing of the vessels following closure of the arteriotomy may also result in cerebral embolization of debris. The second cause of operatively induced deficits is cerebral ischemia. Although many patients can tolerate temporary carotid clamping without deleterious effects, some require cerebral protection if neurologic deficits are to be avoided. Patients with severe vascular disease and multiple large-vessel occlusions are least tolerant of carotid clamping. Cerebral ischemia may result from hypotension, arterial thrombosis of intracerebral vessels, or inadequate cerebral protection. Hypotension may be caused by manipulation of the carotid sinus area or inappropriate anesthesia. Infiltration of the carotid bifurcation region with 1% lidocaine helps prevent the reflex effects of carotid sinus stimulation. Blood pressure should be maintained near or slightly above normal for the individual patient by intravenous administration of 5001,000 ml of lactated Ringer's solution or small amounts of vasopressors. The critical threshold value for regional cerebral blood flow (rCBF) under halothane anesthesia and with a PaCO2 of 30-40 mm Hg is 18-23 ml/100 g per minute. When rCBF falls below this level, cerebral circulation becomes insufficient to support cerebral metabolic activity, physiologic paralysis ensues, and changes occur in the EEG. Clamping of the internal carotid artery results in reduction of rCBF, which can be restored to preocclusive levels by insertion of a shunt [10, 11]. Internal carotid artery stump pressure correlates closely with rCBF and the EEG. The critical stump pressure was found by Boysen [10] and Engell [12] to be 50-55 mm Hg, below which EEG changes occurred and rCBF dropped below the threshold value of 18-23 ml/100 g per minute.

J.E. Thompson: Complications of Carotid Endarterectomy

Fig. 1. L,Jawing illustrating the technique of carotid endarterectomy employing a temporary inlying shunt. A No. l0 Fr. plastic catheter 9 cm in length is first inserted into the distal internal carotid artery and blood is allowed to backflow. The proximal end of the shunt is then placed into the common carotid lumen, and the umbilical tapes with rubber tourniquets are made snug. Cerebral blood flow is thus restored through the shunt, a step requiring approximately 60 seconds. The appropriate plane is entered with a fine pointed clamp and endarterectomy of the common carotid bifurcation, origin of the external carotid artery, and internal carotid artery is accomplished under full visualization. The distal end of the plaque in the internal carotid artery usually feathers off quite smoothly. If not, the distal intima may be secured with a few interrupted sutures of 6-0 polyester to prevent dissection. (From J.E. Thompson and C.M. Talkington, Carotid endarterectomy, Ann. Surg. 184:1, 1976. Used by permission.) Methods presently available to determine the adequacy o f collateral blood flow during carotid clamping include temporary occlusion under local anesthesia while the neurologic status is being checked [13]; determination of stump pressure in the occluded distal internal carotid artery [14]; and E E G monitoring [10, 11, 15]. Although actual determination of r C B F by the 'aaxenon method would be ideal, the technique is rarely available. Clinical investigations indicate that carotid stump pressures of 50-55 mm Hg or higher reflect adequate cerebral collateral [10, 12, 16-18]. Techniques designed to enhance cerebral protection during carotid surgery include general anesthesia, induced hypertension, hypercapnia, hypocapnia, temporary intraluminal bypass shunts, and combinations of these. General anesthesia is indeed helpful by increasing the tolerance of the brain to ischemia and reducing cerebral metabolic demands for oxygen [19]. Induced hypertension is o f only moderate benefit in patients with poor collaterals and should not be relied on [10, 12]; blood pressure should be maintained at or slightly above levels that are normal for the individual patient. Many studies have now been published on hypercapnia and hypocapnia as methods of cerebral protection [10, 12, 19, 20]. Hypercapnia, instead o f improving regional perfusion, may result in an "intracerebral steal." Likewise, hypocapnia may be detrimental in areas of focal cerebral ischemia. In

159

all likelihood, neither hypocapnia nor hypercapnia can be relied on to increase regional perfusion. PaC02 should be maintained at as near a normal level as possible during carotid endarterectomy [211. The use of a temporary inlying bypass shunt remains the most reliable m e t h o d for cerebral support (Fig. 1). Recent discussion has centered on the necessity for its routine use. Some surgeons employ it routinely in all partially occlusive lesions [2, 22], some use it selectively based on an assessment o f cerebral collateral circulation [12-14, 16, 18], while a few state they rarely or n e v e r use it [23-26]. That an inlying shunt is a satisfactory method o f cerebral protection is based on both clinical and laboratory data. Its insertion promptly restores depressed r C B F to preocclusive values and reverses changes in the E E G [10]. Internal carotid artery flow studies with a shunt in place are within the normal range. Those who advocate selective shunting base its use on the inadequacy o f cerebral collateral circulation. Some test the patient under local anesthesia and use a shunt if temporary clamping cannot be tolerated. Others, using general anesthesia, insert a shunt if internal carotid artery stump pressure is below 5055 mm Hg or if E E G changes o c c u r when the carotid artery is clamped [15, 21]. From data in the literature on operative mortality and morbidity associated with carotid endarterectomy, it is clear that an assessment of collateral circulation is necessary in all patients, and that provision for cerebral protection must be made for those with inadequate flow (Table 4). Internal carotid artery stump pressure and E E G appear to be fairly reliable indicators for the use o f a shunt, although not infallible. When stump pressure is used, the duration o f carotid clamping must also be considered. A stump pressure that may be safe for a short period of occlusion may not be safe for unexpected long periods of occlusion [10, 16, 21, 27]. This is not the case when a shunt is in place. Operation-related strokes can occur, even with a shunt, from emboli or intracranial thrombosis. Those who advocate selective shunting cite the disadvantages of having a shunt in the operative field. This is not a hindrance once the surgeon becomes accustomed to its use [3]. In addition to providing constant internal carotid artery flow during operation, the shunt is simple, reliable, allows for unhurried surgery in cases o f complicated lesions, and is useful as a stent for closure of the arterio t o m y without a patch graft (Fig. 1). It is particularly advantageous in teaching institutions where residents and fellows are being trained in vascular surgery. Patients with more severe forms o f cerebrovascular disease require cerebral protection more often.

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Table 4. Mortality and morbidity rates in carotid endarterectomy for transient ischemic attacks associated with different methods of management. Author

Method of management

DeWeese et al., 1973 [25]

General anesthesia, no stump pressure, no shunt Joint study, various General anesthesia, EEG, no shunt Regional anesthesia, no shunt Regional anesthesia, stump pressures, no shunt General anesthesia, stump pressures, no shunt General anesthesia, stump pressures, no shunt General anesthesia, stump pressures, no shunt General anesthesia, hypercapnia, shunt Local anesthesia, stump pressures, selective shunt General anesthesia, routine shunt

Fields et al., 1970 [32] Baker et al., 1975 [15] Rich et al., 1975 [33] Hobson et al., 1974 [17] Smith, 1974 [17] Moore et al., 1973 [14] Hays et al., 1972 [16] Connolly et al., 1977 [13]

Thompson, 1978

Mortality rate

Transient deficits

Permanent deficits

1%

15%

6%

3.5% 1.4%

1.8% 1.4%

7.7% 0.5%

2.6% *

3.0% 6%

2.2% 4%

*

2.7%

2.7%

*

3.1%

1%

*

2.5%

1%

1.6%

1.1%

1.6%

1%

0

0

0.5%

0.95%

1.42%

*Data not available Since present methods o f assessing the adequacy of collateral circulation are not infallible, we recommend the use of a shunt routinely in all partially occlusive lesions, particularly for patients with TIA and asymptomatic stenoses, who have no demonstrable neurologic deficit prior to operation and who should, therefore, have none postoperatively. Our results and those of others bear out the efficacy o f the shunt [22]. In the hands o f experienced surgeons, comparable results may be obtained using selective shunting. An additional strenuous test for any method o f cerebral protection is its efficacy in the patient undergoing operation for ipsilateral carotid stenosis in the presence o f contralateral total carotid occlusion. In a series of 92 patients, Bloodwell et al. [24], using only general anesthesia and hypercapnia, reported an operative mortality rate due to stroke of 7.6% and a neurologic worsening rate of 5.4%. In the author's series of 136 carotid operations on patients with unilateral stenosis and contralateral occlusion, in which a shunt was used routinely, there was no operative death and only one instance o f neurologic deficit.

Postoperative Causes Occasionally patients incur neurologic deficits following a successful operative procedure. The causes o f such comPlications include thrombosis of the endarterectomized arterial segment, hypoten-

sion, hypertension, and intracerebral hemorrhage or edema. Thrombosis o f the operative site occurs from technical error. If the distal intima has not been tailored properly, either by feathering or suturing, it may dissect cephalad and cause thrombosis o f the internal carotid artery. Improper suturing o f the arteriotomy with compromise of the arterial lumen may also result in occlusion. When these problems occur, the patient should be reoperated on immediately, the clots removed, and an appropriate surgical repair o f the offending lesion carried out. If there is concern about completeness o f endart e r e c t o m y or the status of the distal intima or internal carotid artery lumen at the time o f the original operation, arteriograms may be performed on the operating table. Some surgeons perform this step in all cases, and if problems are encountered, corrective repair is carried out. With our technique of complete visualization of the endarterectomized area (Fig. 1), the author has not found the routine use of operative arteriography necessary. Postoperative hypotension may lead to arterial thrombosis at the operative site, or intracranially if there are distal stenoses. Such hypotension may result from blood loss, inadequate fluid administration, over-medication, myocardial infarction, congestive heart failure, and tachycardia or other cardiac arrhythmias. These patients must be monitored carefully in the intensive care unit for the first 24 hours postoperatively so that hypotension, if it occurs, does not persist but is treated promptly by the

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Table 5. Operation-related neurological deficits in patients with transient cerebral ischemia and asymptomatic bruits after operations using a temporary inlying shunt.

Indications for surgery

Number ofpatients

Transient cerebralischemia 323 Asymptomatic bruits 72 Total 395

Operative mortality Number of Patient Procedure Death operamortality mortality from tions Deaths rate--% rate--% strokes

Transient Mild

422

2

0.6

0.47

1

4 (0.95%) 2 (0.47%)

4 (0.95%) 10 (2.37%)

94 516

0 2

0 0.5

0 0.39

0 0 1 (1.06%) 1 (0.19%) 4 (0.78%) 3 (0.58%)

0 1 (1.06%) 4 (0.78%) 11 (2.13%)

appropriate means, namely, blood, fluids, vasopressors, or cardiac therapy. Hypertension following carotid endarterectomy, which is not uncommon, may also be deleterious and must be treated aggressively [8]. Hypertension may occur from excessive administration of salt solutions during operation in a patient with previous hypertension, and following the use of hypercarbic general anesthesia. The most important complications of hypertension are hemorrhage in the operative wound, disruption of the arterial reconstruction, and cerebral hemorrhage and edema. The blood pressure should be kept below 200 mm Hg, if necessary with an intravenous drip of 500 mg of trimethaphan (Arfonad| in 500 ml of 5% dextrose in water, which lowers blood pressure within minutes. Intermittent injections or a properly titrated constant drip of this solution will keep the blood pressure at proper levels until either spontaneous resolution occurs or other longer acting hypotensive agents take effect. Sodium nitroprusside (Nipride| solution, 50 mg in 500-1,000 ml of 5% dextrose in water, by intravenous drip may also be employed as a rapidly acting antihypertensive agent. Intracerebral hemorrhage may occur from postoperative hypertension or following operation on patients with acute strokes and cerebral infarction. A number of reports now attest to the inadvisability of early operations on patients with acute profound strokes [2, 28, 29]. Many such strokes are associated with total carotid occlusions. When cerebral blood flow is restored, a so-called white infarct may become a hemorrhagic infarct. This complication is a serious one with an operative mortality rate of 2060%. The morbidity rate in survivors is correspondingly high. Arteriography and operation should be delayed in patients with acute strokes, allowing such patients to stabilize for 2-6 weeks, at which time angiographic studies and possible operation can be considered. Cerebral edema may result from hypertension, sodium overload, operation on patients experiencing acute strokes, and prolonged anesthesia with bilateral carotid blood flow interruption with-

Operative and postoperative deficits Permanent Severe

Total deficits

out use of a temporary shunt. One-stage bilateral carotid endarterectomy is inadvisable because of the complications that may ensue, including respiratory difficulties, postoperative hypertension, and aggravation of neurologic deficits. When bilateral operations are required, the procedures should be staged at least ! week apart, and preferably at longer intervals. Cerebral edema, if severe, should be treated with hypertonic parenteral solutions, diuretics, or steroids. Table 5 details the incidence of operation-related deficits in the personal series of the author, all operations having been performed by the same surgeon. Two recent reports on results of carotid endarterectomy are at variance with those shown in Tables 4 and 5. In one [30], 34 strokes occurred in 317 operations, an incidence of 10.7%, while in the second [4], 10 strokes occurred in 68 operations for TIA and asymptomatic bruits, an incidence of 14.7%. The incidence of operation-related deficits should be no more than 2-4%. This is of the utmost importance since, as Toole et al. [31] point out, if mortality and morbidity rates incident to surgical repair are high, overall mortality and stroke incidence become comparable in surgically and nonsurgically treated patients.

Miscellaneous Complications Ipsilateral headache occurs occasionally following endarterectomy of a tightly stenotic lesion. Its course is self-limited and may be treated by analgesic medications. Inappropriate antidiuretic hormone secretion occurs rarely after endarterectomy in patients with severe degrees of cerebrovascular insufficiency. The basic problem is water retention due to sustained release of the hormone, leading to conservation of water despite serum hypotonicity. The hypotonicity suppresses aldosterone secretion and, therefore, sodium loss is increased despite the already hypotonic state of body fluids. Hyponatremia and hypernatruria are associated with the clinical picture of

162

water intoxication, which is accompanied by cerebral edema, increased intracranial pressure, and aggravation of neurologic signs. Treatment consists of restricting fluid intake to approximately 1,000 ml daily until the edema has disappeared, sodium excretion has been reduced, and sodium resorption has returned to normal. H y p e r t o n i c saline infusions may be required. In summary, carotid e n d a r t e r e c t o m y is a safe and effective method of treatment of cerebrovascular insufficiency. With p r o p e r selection of patients, care in the choice and administration of anesthesia, meticulous attention to technical details of operation, including the use of an effective method of cerebral protection during carotid clamping, and special attention to the prevention of hypotension and excessive hypertension postoperatively, most of the complications can be avoided, and the operation can be performed with acceptable mortality and morbidity rates.

REsumE Une selection adequate des malades fi opErer, une operation bien faite, une surveillance et une thErapeutique post-opEratoires de qualitE rEduisent la mortalitE et la morbiditE de l'endartEriectomie carotidienne. Les complications peuvent 6tre des accidents cardiaques ou respiratoires en rapport avec l'anesthEsie, des infections, des hEmatomes, des parEsies par atteinte nerveuse, des parotidites, des ruptures artErielles, des faux anEvrismes, des fistules carotido-caverneuses. L a complication la plus grave est l'accident vasculaire cErEbral par embolie ou ischEmie cErEbrale. Les embolies sont dues des manipulations traumatisantes de l'artEre; les ischEmies rEsultent d'Episodes d'hypotension, de thromboses intracErEbrales, d'insuffisance de protection du cerveau. Pour Etre certain que la circulation collatErale sera adequate pendant la pEriode de clampage carotidien, il faut clamper temporairement la carotide sous anesthEsie locale, mesurer la pression intracarotidienne et surveiller I ' E E G . L a meilleure technique de protection cErEbrale est le shunt temporaire intracarotidien. Ce shunt interne dolt ~tre utilisE si l'opEr6 prEsente des symptomes de souffrance cErEbrale pendant le clampage temporaire, se la pression intracarotidienne s'abaisse en-dessous de 55 mm Hg, si I ' E E G s'altEre. Nous estimons cependant que, pour Eviter tout accident, l'opEration dolt ~tre faite dans tous les cas sous anesthEsie gEnErale avec shunt interne. L a mortalitE opEratoire, pour les malades qui avaient eu avant l'opEration des Episodes ischEmiques transitoires, dolt 6tre infErieure ~ 1% et les sEquelles neurologiques post-opEratoires infErieures /t 2%.

World J. Surg. Vol. 3, No. 2, 1979

L'opEration doit 6tre parfaitement menEe, avec une attention minutieuse ~ t o u s l e s details. Pour prEvenir les thromboses, il faut Eviter toute hypotension per- et post-opEratoire. Pour prEvenir l'hEmorragie et l'oedEme cErEbral, tout Episode d'hypertension doit Etre rapidement corrig6. L'opEration est contre-indiquEe en cas d'accident vasculaire cErEbral aigu, grave et d'allure progressive.

References 1. Wylie, E.J., Ehrenfeld, W.K.: Extracranial Occlusive Cerebrovascular Disease. Philadelphia, W.B. Saunders Co., 1970 2. Thompson, J.E., Austin, D.J., Patman, R.D.: Carotid endarterectomy for cerebrovascular insufficiency: Long-term results in 592 patients followed up to thirteen years. Ann. Surg. 172:663, 1970 3. Thompson, J.E., Talkington, C.M.: Carotid endarterectomy: surgical progress. Ann. Surg. 184:1, 1976 4. Easton, J.D., Sherman, D.G.: Stroke and mortality rate in carotid endarterectomy: 228 consecutive operations. Stroke 8:565, 1977 5. Verta, M.J., Applebaum, E.L., McClusky, D.A., Yao, J.S.T., Bergan, J.J.: Cranial nerve injury during carotid endarterectomy. Ann. Surg. 185:192, 1977 6. Ehrenfeld, W.K., Hays, R.J.: False aneurysm after carotid endarterectomy. Arch. Surg. 104:288, 1972 7. Smith, R.B., III, Perdue, G.D., Jr., Collier, R.H., Stone, H.H.: Postoperative false aneurysm of the carotid artery. Am. Surg. 36:335, 1970 8. Thompson, J.E.: Prevention of complications of cerebral arteriography and surgery. In Management of Arterial Occlusive Disease, Dale, W.A., editor. Chicago, Year Book Medical Publishers, Inc., 1971, pp. 353-374 9. Barker, W.F., Stern, W.E., Krayenbuhl, H., Senning, A.: Carotid endarterectomy complicated by carotid cavernous sinus fistula. Ann. Surg. 167:568, 1968 10. Boysen, G.: Cerebral hemodynamics in carotid surgery. Acta Neurol. Scand. 49[Suppl. 52]:1, 1973 11. Sundt, T.M., Jr., Sharbrough, F.W., Anderson, R.E., Michenfelder, J.D.: Cerebral blood flow measurements and electroencephalograms during carotid endarterectomy. J. Neurosurg. 41:310, 1974 12. Engell, H.C.: Studies in cerebral circulation. Bull. Am. Coll. Surg. 58:7, 1973 13. Connolly, J.E., Kwaan, J.H.M., Stemmer, E.A.: Improved results with carotid endarterectomy. Ann. Surg. 186:334, 1977 14. Moore, W.S., Yee, J.M., Hall, A.D.: Collateral cerebral blood pressure: an index of tolerance to temporary carotid occlusion. Arch. Surg. 106:520, 1973 15. Baker, J.D., Gluecklich, B., Watson, C.W., Marcus, E., Kamat, V., Callow, A.D.: An evaluation of electroencephalographic monitoring for carotid study. Surgery 78:787, 1975 16. Hays, R.J., Levinson, S.A., Wylie, E.J.: Intraoperative measurement of carotid back pressure as a guide to operative management for carotid endarterectomy. Surgery 72:953, 1972 17. Hobson, R.W., Wright, C.B., Sublett, J.W., Fedde,

J.E. Thompson: Complications of Carotid Endarterectomy

18. 19. 20.

21. 22. 23. 24. 25.

26.

W., Rich, N.M.: Carotid artery back pressure and endarterectomy under regional anesthesia. Arch. Surg. 109:682, 1974 Hughes, R.K., Bustos, M., Byrne, J.P., Jr.: Internal carotid artery pressures. A guide for use of shunt during carotid repair. Arch. Surg. 109:494, 1974 Alexander, S.C., Lassen, N.A.: Cerebral circulatory response to acute brain disease: implications for anesthetic practice. Anesthesiology 32:60, 1970 Ehrenfeld, W.K., Hamilton, F.N., Larson, C.P., Jr., Hickey, R.F., Severinghaus, J.W.: Effect of CO2 and systemic hypertension on downstream cerebral arterial pressure during carotid endarterectomy. Surgery 67:87, 1970 Sundt, T.M.: Surgical therapy of occlusive vascular diseases of the brain. Surg. Annu. 6:393, 1974 Javid, H., Dye, W.S., Hunter, J.A., Najafi, H., Goldin, M.D., Serry, C.: Surgical treatment of cerebral ischemia. Surg. Clin. North Am. 54:239, 1974 Baker, W.H., Dorner, D.B.: Carotid endarterectomy: is an indwelling shunt necessary? Surgery 82:321, 1977 Bloodwell, R.D., Hallman, G.L., Keats, A.S., Cooley, D.A.: Carotid endarterectomy without a shunt. Arch. Surg. 96:644, 1968 Deweese, J.A., Rob, C.G., Satran, R., Marsh, D.O., Joynt, R.J., Summers, D., Nichols, C.: Results of carotid endarterectomies for transient ischemic attacks--five years later. Ann. Surg. 178:258, 1973 Young, J.R., Humphries, A.W., Beven, E.G., deWolfe, V.G.: Carotid endarterectomy without a shunt. Arch. Surg. 99:293, 1969

Invited Commentary Anthony M. Imparato, M.D. New York University Medical School, New York, New York, U.S.A. T h o m p s o n has properly emphasized factors that are critical for the performance of safe carotid arterial surgery. The proper selection of patients and the e m p l o y m e n t of impeccably correct surgical technique are the keystones upon which safe carotid surgery can be performed. We are in complete agreement that acute strokes and strokes in evolution introduce prohibitively high operative risks, while asymptomatic patients and those with transient neurologic symptoms can undergo surgical procedures with operative risks of 1-2% neurologic worsening and 1-2% mortality. Safe surgical technique depends on adequate exposure o f the internal carotid artery, made possible by adequate mobilization o f the hypoglossal nerve and, if necessary, by transection o f the digastric

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27. Ranson, J.H.C., Imparato, A.M., Clauss, R.H., Reed, G.E., Hass, W.K.: Factors in the mortality and morbidity associated with surgical treatment of cerebrovascular insufficiency. Circulation 39[Suppl. I]:269, 1969 28. Blaisdell, F.W., Clauss, R.H., Galbraith, J.G., Imparato, A.M., Wylie, E.J.: Joint Study of Extracranial Arterial Occlusion. IV. A review of surgical considerations. J.A.M.A. 209:1889, 1969 29. Wylie, E.J., Hein, M.F., Adams, J.E.: Intracranial hemorrhage following surgical revascularization for treatment of acute strokes. J. Neurosurg. 21:212, 1964 30. Prioleau, W.H., Jr., Aiken, A.F., Hairston, P.: Carotid endarterectomy: neurologic complications as related to surgical techniques. Ann. Surg. 185:678, 1977 31. Toole, J.F., Janeway, R., Choi, K., Cordell, R., Davis, C., Johnston, F., Miller, H.S.: Transient ischemic attacks due to atherosclerosis. A prospective study of 160 patients. Arch. Neurol. 32:5, 1975 32. Fields, W.S., Maslenikov, V., Meyer, J.S., Hass, W.K., Remington, R.D., MacDonald, M.: Joint Study of Extracranial Arterial Occlusion: V. Progress report of prognosis following surgery or nonsurgical treatment for transient cerebral ischemic attacks and cervical carotid artery lesions. J.A.M.A. 211:1993, 1970 33. Rich, N.M., Hobson, R.W., II: Carotid endarterectomy under regional anesthesia. Am. Surg. 41:253, 1975

muscle. In our technique, no tapes are placed around that nerve and, consequently, hypoglossal palsy is no longer seen [1]. It is absolutely essential to visualize the site of the distal transection o f the intima, whether it feathers to a fine, thin intima or not. E v e n where apparent feathering occurs, direct inspection may reveal heaped up intima that can be the site o f platelet adherence and subsequent thrombosis. Our arteriotomy in the internal carotid artery, therefore, always extends to b e y o n d the site of intimal transection. We have found that in order to extend the arteriotomy into the internal carotid artery, closure with a patch o f autologous saphenous vein has avoided the very minor stenosis that can o c c u r at the uppermost angle of the suture line. This slight narrowing may result in sufficient hemodynamic disturbance to promote the d e v e l o p m e n t o f intimal hyperplasia and late stenosis. This has not occurred when vein patch closure has been performed. Closure with plastic materials is avoided, since the late appearance o f these plastic patches in the carotid location has revealed marked distortion and fibrosis. The o c c u r r e n c e of any neurologic deft-