Hazards and Safeguards during Carotid Endarterectomy Technical Considerations
G. H. Matsumoto, MD, Boston, Massachusetts D. Cossman, MD, Boston, Massachusetts A. D. Cillow, MD, Boston, Massachusetts
Since 1954, when Eastcott, Pickering, and Rob [I] reported on the reconstruction of the internal carotid artery in a patient with intermittent attacks of hemiplegia, carotid endarterectomy has undergone an evolution in management and technic. Regional anesthesia, intraluminal shunts, continuous electroencephalogram (EEG) monitoring, measurements of internal carotid back pressure, and monitoring of jugular oxygen tension have all been employed in various combinations to detect and correct cerebral hypoxia during cross clamping [2--61 to minimize postoperative neurologic complications. Much attention has also been devoted to careful dissection of the carotid and its branches and it is now common knowledge that embolization and stroke can occur even before the carotid itself is opened. Reports of postoperative strokes after placement of carotid sinus pacemakers illustrate the danger of embolization [ 71 even with closed manipulation of a fragile arteriosclerotic plaque. The operative field also includes several peripheral nerves that, if injured, lead to functional and cosmetic difficulties. Surprisingly little has been written about this, perhaps because the surgeon is more preoccupied with avoiding the more catastrophic central neurologic complications. The complication rate in 130 consecutive carotid endarterectomies is reported herein. Complications are divided into transient central nervous system deficits, permanent strokes, peripheral nerve injuries, and major medical complications. Technical factors crucial to safe surgery are reiterated. An anatomic review of peripheral nerves in the operative field and the consequences of injuring them are included. From the Deparbwnt of Surgery, Tufts New England Medical Center, Boston, Massachusetts. This work was supported in part by the Earl Tupper Foundation, the Eunice V. Rand and Morris Rand Charitable Foundation, and General Research Support Grant #27418. Reprint requests should be addressed to G. H. Matsumoto, MD, Box 18. Department of Surgery, Universityof South Florida, 12901 North 30th Street, Tampa, Florida 33612. Presented at the Fifty-Seventh Annual Meeting of the New England Surgical Society, Whitefield. New Hampshire, September 23-26, 1976.
458
Material and Results During the period from January 1974 through February 1976,130 consecutive carotid endarterectomies were performed. The immediate postoperative complications include six cases (4.6 per cent) of transient neurologic deficits, all completely resolving within 24 hours (expressive aphasia and disorientation; contralateral central facial weakness; bilateral hand numbness; contralateral hemiparesis; amaurosis fugax; and slurred speech), and two cases (1.5 per cent) of permanent central nervous system deficits. One patient had a mild hand weakness that completely cleared within one month. The other patient is listed under permanent neurologic deficit because his hand is clumsy eight months postoperatively. This patient had a normal neurdogic examination in the immediate postoperative period. However, 12 hours postoperatively, he developed renal failure, pulmonary edema, hypoxia, and finally cardiac arrest. After resuscitation, he was noted to have a hemiparesis contralateral to the side of surgery. He eventually recovered with a residual hand weakness. The incidence of peripheral nerve paresis was 12.3 per cent (16 cases): hypoglossal nerve (11 cases, 8.5 per cent); vocal cord (3 cases, 2.3 per cent); and cervical branch of the facial nerve (2 cases, 1.5 per cent). Although some required two to three months to clear, all resolved. There were eight major medical complications(6.9 per cent), with twodeaths (Id per cent), all due to myocardial infarction: myocardial infarction (3 cases, 2.3 per cent); pulmonary edema (5 cases, 3.8 per cent); and pulmonary embolus (1 case, 0.8 per cent). Minor myocardial abnormalities, ischemia, and arrhythmias are not listed. There were no stroke-related deaths. One patient (0.8 per cent) was reexplored for bleeding.
Comments
Operating technic bears little upon medical complications but obviously influences the incidence and severity of central and peripheral neurologic damage. A rational, consistent approach, based upon sound anatomic and physiologic principles coupled with sensitive monitoring systems can minimize the hazards of carotid endarterectomy. It should be emphasized that strict adherence to the operative rou-
The American Journal of Surges
Carotid Endarterectomy
tine is necessary to avoid the potential trouble at virtually every step of the operation. Central nervous system deficits can occur as a result of cerebral ischemia leading to irreversible neuronal damage. This may occur during carotid cross clamping or following internal carotid thrombosis. Embolic accidents, either platelet-fibrin aggregates or air, can also result in central nervous system deficits. General anesthesia with continuous 10 lead EEG monitoring was used on all patients in this series. Intraluminal shunts were inserted in patients whose EEG tracings showed an ischemic pattern. We believe the shunt should be employed selectively and not in all patients because of the potential hazards involved and its interference with a complete endarterectomy of the internal carotid. Gentle and systematic dissection of the common carotid and its branches is required to avoid embolization of platelet-fibrin debris loosely adherent to ulcerated plaques. The internal carotid artery should be the first branch dissected and encircled with a tape passed above the diseased segment. The common and external carotid branches can then be dissected safely. Tractioncan be placed on the internal carotid, temporarily occluding the vessel for a few seconds while dissection is carried out around the bifurcation. If intraluminal fragments are dislodged, they are more apt to wash into the external carotid system. If an intraluminal shunt becomes necessary (in this series determined by the EEG), it is recommended that the distal margin of the internal carotid endarterectomy be completed before shunt insertion to avoid intimal damage as illustrated in Figure 1. Whether or not a shunt is used, the remaining intima must remain securely attached to the arterial wall to avoid intimal elevation which may result in subintima1 dissection or thrombosis. Heparinized saline should he streamed into the arteriotomy to visualize any fragment of arteriosclerotic plaque left behind. These fragments may embolize upon removal of the occluding clamps. Air embolus may also occur upon releasing clamps. To avoid this, the internal carotid is backbled and then reclamped. This allows air in the lumen to be expressed through the suture line. Next, the external and common carotid clamps are removed. Any remaining air, debris, or clot wili enter the external carotid system. Finally, the internal carotid clamp is removed. (Figure 2.) Most surgeons do not use a patch graft. It may give one a false sense of security due to the appearance of a wide lumen at the center of the graft. In fact, the stenosis occurs at the most distal margin of the patch.
VohmN 193, April 1977
Figure 1. lntimai damage cawed by inserfion of an intfaiuminai shunt.
If the arteriotomy is directly closed using 1 mm bites 1 mm apart, stenosis will not occur. Postoperative arteriograms show distension of the endarterectomized segment closed without a patch. Additional sutures necessary for hemostasis should be carefully placed to prevent constriction and tied with the common carotid temporarily occluded in order to avoid tearing the thin endarterectomized wall. Avoiding Peripheral
Nerve Paresis
There are a number of nerves which lie in the vicinity of the carotid artery and its branches. (Figure 3.) The normal position of the vagus nerve is between the carotid artery and the internal jugular vein. The vagus nerve usually lies posterolateral to the internal and common carotid but occasionally lies antero-
459
Matsumoto, Cossman, and Callow
STEP 1.
_
RELEASE and RECLAYP
STEP STEP 2. RELEASE
4. RELEASE ASAIN
STEP 3. RELEASE
2
Figure 2. Recommended order of releasing occluding clamps to prevent cerebral embolization.
medial. During the course of dissection of the carotid artery, the plane of dissection must be kept close to the wall of the artery to prevent injury to the nerve. Injury to the vagus is manifested as vocal cord paresis. Vocal cord paresis may also occur if the recurrent laryngeal nerve is traumatized. This is most apt to happen if the nerve takes an anomalous nonrecurrent course, traversing behind the common carotid. (Figure 3.1 To avoid injury, the dissection must be kept on the wall of the artery. The inferior ganglion of the vagus, the nodose ganglion, is not usually seen during dissection. A branch of this ganglion, the superior laryngeal nerve, courses behind the internal carotid and then bifurcates into the external branch, which innervates the inferior constrictor and the cricothyroid muscles, and the internal branch, which has sensory fibers to the orifice of the larynx. Dissection around the carotid bifurcation and the superior thyroid artery must be kept close to the arterial wall, fortrauma to the superior laryngeal nerve will result in unilateral numbness of the orifice of the larynx, mild difficulty in swallowing, and change in the quality of voice due to cricothyroid muscle dysfunction. Injury to these nerves is also likely to occur during unclamping and reclamping of the vessels during backbleeding. The hypoglossal nerve descends along the course of the internal carotid, then passes medially over the external carotid in a more superficial position. During carotid dissection this nerve is usually encountered. It can be mobilized medially to expose the most distal
YUGEAL U. 11 1 LAR78f%hL
N.
L^Rlxtl N.
?---#7Pcw.@ssAL MT
H In
LARYNGEAL N.
f&XT. LARYNMAL
N.
-*us* -REC%RRIENT LARYIYOEAL N.
Figure 3. Abnormal relationship of the “recurrent” laryngeal nerve.
460
Figure 4. Location of the cervical branch of the facial nerve.
The American Journal of Surgery
CarotidEndarterectomy
reaches of the internal carotid. Mobilization is recommended because traction on the nerve usually causes tongue deviation to the side of the endarterectomy. A branch of the hypoglossal nerve, the ansa hypoglossus, originates in various positions and may lie in the field. It innervates the strap muscles and usually can be mobilized medially. If, however, it fixes the hypoglossal nerve in the operative field, it may be sacrificed. The carotid sinus nerve, the nerve of Hering, originates from the glossopharyngeal nerve. It is a tiny nerve lying in the areolar tissue between the carotid bifurcation. Stimulation of the carotid sinus can cause hypotension and bradycardia, the reflex arc mediated by the vagus nerve. Infiltration of the areolar tissue with xylocaine will eliminate this reflex. Division of some end plates of this nerve is unavoidable because they are located in the wall of the common, internal, and external arteries. This may account for the severe hypertension encountered in the immediate postoperative period in a few patients. The glossopharyngeal nerve is usually not visualized during this dissection. The cervical branch of the facial nerve (VII) lies beneath the platysma inferior to the angle of the jaw. (Figure 4.) In some patients it may send twigs to the mandibular branch of the facial nerve [s]. If this anomaly exists and the cervical branch is divided, ipsilateral lower lip paresis will result. This can be avoided by curving the upper end of the skin incision posteriorly toward the mastoid process. The marginal mandibular nerve itself may be injured if the incision is carried too high. Clauss et al [9] and Sensenig [IO] have reported simultaneous bilateral carotid endarterectomies for bilateral carotid disease. This policy exposes the patient to an unnecessarily increased hazard. Both vocal cords may be paretic from operative trauma to both recurrent laryngeal nerves, superior laryngeal nerves, or vagus nerves. Edema of the false cords may result from local trauma. These patients may suffer severe upper respiratory obstruction necessitating prolonged intubation or tracheostomy. For this reason we advocate bilateral carotid endarterectomies in two stages, to permit evaluating laryngeal function between operations. Summary
The hazards and safeguards of carotid endarterectomy are presented in a consecutive series of 130 patients over a fourteen month period. The mortality rate of 1.5 per cent was due to myocardial infarction. Two patients (1.5 per cent) suffered minor but permanent neurologic deficit. There was an incidence of 4.6 per cent transient neurologic deficits, all of
voklme 133; April 1977
which cleared within 24 hours. Special emphasis is placed on peripheral nerve injuries (12.3 per cent). Local neurologic anatomy is reviewed to facilitate safe dissection and an avoidance of nerve injury. References 1. Eastcott HHG, Pickering GW, Rob CG: Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 2: 994, 1954. 2. Hobson RW. Wright CB, Sublett JW, Fedde CW, Rich NM: Carotid artery back pressure and endarterectomy under regional anesthesia. Arch Surg 109: 662, 1974. 3. Thompson JE, Austin DJ, Patman RD: Carotid endarterectomy for cerebrovascular insufficiency: long term results in 592 patients followed up to thirteen years. Ann Surg 172: 663, 1970. 4. Baker JD, Gluecklich B, Watson CW, Marcus E, Kamat V, Callow AD: An evaluation of electroencephalographic monitoring for carotid surgery. Surgery 78: 787, 1975. 5. Moore WS, Yee JM, Hall AD: Collateral cerebral blood pressure: an index of tolerance to temporary carotid occlusions. Arch Surg 106: 520, 1973. 6. Larson CP Jr, Ehrenfeld WK, Wads JG, Wylie EJ: Jugular venous oxygen saturation as an index of adequacy of cerebral oxygenation. Surgery 62: 31, 1967. 7. Scott SM. Sethi GK, Takaro T: Perioperative cerebral embolism in association with carotid arterial surgery: a significant hazard. Stroke 7: 13, 1976. 8. Paff GH: Anatomy of the Head and Neck. Philadelphia, WB Saunders, 1973. p 28. 9. Clauss RH, Bole, Prafull V, Paredes M, Doscher W, Kreminitzer MW: Simultaneous bilateral carotid endarterectomies. ICVS scientific program, 1976. 10. Sensenig D: Bilateral carotid artery endarterectomy at one operation. J Me A&d Assoc 65: 304, 1974.
Discussion Nathan P. Couch (Boston, MA): I congratulate the authors on a very fine series. They have brought their morbidity and mortality almost to an irreducible minimum. This is where careful technic really shows. There is no operation in vascular surgery that is more unforgiving of carelessness than the carotid endarterectomy. I agree that the handling of distal intima when positioning the shunt is crucial, although one does not always have to perform a distal endarterectomy before insertion. (Slide) The Javid shunt, in our opinion, is to be preferred. In addition, the arteriotomy should be generous. Care in the manipulation of the artery with very early distal control is all-important in preventing distal passage of atheromatous debris. After the shunt is removed, it is simpler if one completes most of the arteriotomy closure with a running stitch and places two or three interrupted sutures before removing the shunt,. Jeffrey K. Raines (Boston, MA): Our diagnostic evaluation in the Vascular Laboratory at the Massachusetts General Hospital includes a combination of three technics: ocular plethysmography; carotid audiofrequency analysis; and cerebral Doppler evaluation. We have investigated the use of ocular plethysmography during carotid endarterectomy. In this technic 14 mm eyecups are placed on the
461
Matsumoto, Cossman, and Callow
sclera of the patient’s eyes. Since this is an air-filled system, it can be used in surgery when the patient is placed on his or her side. In addition to producing a vacuum at the surface of the sclera these eyecups are also plethysmographic sensors. This allows the recording of ocular arterial pulsations as intraocular pressure is increased by the surface vacuum. When intraocular pressure is above systolic ophthalmic artery pressure, pulsations cease. In this way systolic ophthalmic artery pressure can be measured accurately during the recqnstruction. This procedure may prove to be of significant value in identifying problems when performing carotid endarterectomy. There are two questions I would like to ask. What criteria do the authors recommend for the use of a shunt? Do they recommend the use of EEG monitoring during carotid reconstruction? A. D. Callow (closing): We wish to thank the discussants. I should like to show some slides. The comments and recommendations that Doctor Matsumoto made are based upon our experience dating back to 1957. (Slide) Our 1957-1968 experience consisting of 266 endarterectomies illustrates the fallacy of attempting to operate on patients with completed strokes or acute strokes. The incidence of improvement was minimal and insofar as acute strokes are concerned, operative
462
mortality was considerable. (Slide) Shown here are the results of 292 endarterectomies in our 1968-1973 series. These patients were all operated with continuous ten lead electroencephalographic monitoring. For patients with recurrent transient ischemic attacks the incidence of improvement consisting of complete cessation of transient ischemic attack was 88 per cent for a minimum period of two years with many patients going well beyond this time. In this series as in the previous one, the three deaths were all from myocardial infarction. None of these patients underwent operation with completed strokes or with acute strokes. (Slide) This slide has reference to Doctor Raines’ comment. Although the technic he proposes is most useful, we have come to be very cautious in the interpretation of the so-called distal stump pressure. Several of our patients had stump pressures from 50 to 90 mm Hg in whom under continuous EEG monitoring, ischemic changes occurred and an intraluminal shunt was required. We rely very heavily, therefore, upon the EEG. Possibly the somewhat high incidence of peripheral nerve injuries, transient as they are, is due to the extensive, lengthy, and very meticulous endarterectomy we usually perform. Finally, our indication for the need for an intraluminal shunt is the appearance of ischemic changes in the EEG. In our last series of 186 consecutive endarterectomies, this has occurred in only 7 per cent of our patients.
The Amarhxn Journal ul Surgery
G. H. Matsumoto, MD, Boston, Massachusetts D. Cossman, MD, Boston, Massachusetts A. D. Cillow, MD, Boston, Massachusetts
Since 1954, when Eastcott, Pickering, and Rob [I] reported on the reconstruction of the internal carotid artery in a patient with intermittent attacks of hemiplegia, carotid endarterectomy has undergone an evolution in management and technic. Regional anesthesia, intraluminal shunts, continuous electroencephalogram (EEG) monitoring, measurements of internal carotid back pressure, and monitoring of jugular oxygen tension have all been employed in various combinations to detect and correct cerebral hypoxia during cross clamping [2--61 to minimize postoperative neurologic complications. Much attention has also been devoted to careful dissection of the carotid and its branches and it is now common knowledge that embolization and stroke can occur even before the carotid itself is opened. Reports of postoperative strokes after placement of carotid sinus pacemakers illustrate the danger of embolization [ 71 even with closed manipulation of a fragile arteriosclerotic plaque. The operative field also includes several peripheral nerves that, if injured, lead to functional and cosmetic difficulties. Surprisingly little has been written about this, perhaps because the surgeon is more preoccupied with avoiding the more catastrophic central neurologic complications. The complication rate in 130 consecutive carotid endarterectomies is reported herein. Complications are divided into transient central nervous system deficits, permanent strokes, peripheral nerve injuries, and major medical complications. Technical factors crucial to safe surgery are reiterated. An anatomic review of peripheral nerves in the operative field and the consequences of injuring them are included. From the Deparbwnt of Surgery, Tufts New England Medical Center, Boston, Massachusetts. This work was supported in part by the Earl Tupper Foundation, the Eunice V. Rand and Morris Rand Charitable Foundation, and General Research Support Grant #27418. Reprint requests should be addressed to G. H. Matsumoto, MD, Box 18. Department of Surgery, Universityof South Florida, 12901 North 30th Street, Tampa, Florida 33612. Presented at the Fifty-Seventh Annual Meeting of the New England Surgical Society, Whitefield. New Hampshire, September 23-26, 1976.
458
Material and Results During the period from January 1974 through February 1976,130 consecutive carotid endarterectomies were performed. The immediate postoperative complications include six cases (4.6 per cent) of transient neurologic deficits, all completely resolving within 24 hours (expressive aphasia and disorientation; contralateral central facial weakness; bilateral hand numbness; contralateral hemiparesis; amaurosis fugax; and slurred speech), and two cases (1.5 per cent) of permanent central nervous system deficits. One patient had a mild hand weakness that completely cleared within one month. The other patient is listed under permanent neurologic deficit because his hand is clumsy eight months postoperatively. This patient had a normal neurdogic examination in the immediate postoperative period. However, 12 hours postoperatively, he developed renal failure, pulmonary edema, hypoxia, and finally cardiac arrest. After resuscitation, he was noted to have a hemiparesis contralateral to the side of surgery. He eventually recovered with a residual hand weakness. The incidence of peripheral nerve paresis was 12.3 per cent (16 cases): hypoglossal nerve (11 cases, 8.5 per cent); vocal cord (3 cases, 2.3 per cent); and cervical branch of the facial nerve (2 cases, 1.5 per cent). Although some required two to three months to clear, all resolved. There were eight major medical complications(6.9 per cent), with twodeaths (Id per cent), all due to myocardial infarction: myocardial infarction (3 cases, 2.3 per cent); pulmonary edema (5 cases, 3.8 per cent); and pulmonary embolus (1 case, 0.8 per cent). Minor myocardial abnormalities, ischemia, and arrhythmias are not listed. There were no stroke-related deaths. One patient (0.8 per cent) was reexplored for bleeding.
Comments
Operating technic bears little upon medical complications but obviously influences the incidence and severity of central and peripheral neurologic damage. A rational, consistent approach, based upon sound anatomic and physiologic principles coupled with sensitive monitoring systems can minimize the hazards of carotid endarterectomy. It should be emphasized that strict adherence to the operative rou-
The American Journal of Surges
Carotid Endarterectomy
tine is necessary to avoid the potential trouble at virtually every step of the operation. Central nervous system deficits can occur as a result of cerebral ischemia leading to irreversible neuronal damage. This may occur during carotid cross clamping or following internal carotid thrombosis. Embolic accidents, either platelet-fibrin aggregates or air, can also result in central nervous system deficits. General anesthesia with continuous 10 lead EEG monitoring was used on all patients in this series. Intraluminal shunts were inserted in patients whose EEG tracings showed an ischemic pattern. We believe the shunt should be employed selectively and not in all patients because of the potential hazards involved and its interference with a complete endarterectomy of the internal carotid. Gentle and systematic dissection of the common carotid and its branches is required to avoid embolization of platelet-fibrin debris loosely adherent to ulcerated plaques. The internal carotid artery should be the first branch dissected and encircled with a tape passed above the diseased segment. The common and external carotid branches can then be dissected safely. Tractioncan be placed on the internal carotid, temporarily occluding the vessel for a few seconds while dissection is carried out around the bifurcation. If intraluminal fragments are dislodged, they are more apt to wash into the external carotid system. If an intraluminal shunt becomes necessary (in this series determined by the EEG), it is recommended that the distal margin of the internal carotid endarterectomy be completed before shunt insertion to avoid intimal damage as illustrated in Figure 1. Whether or not a shunt is used, the remaining intima must remain securely attached to the arterial wall to avoid intimal elevation which may result in subintima1 dissection or thrombosis. Heparinized saline should he streamed into the arteriotomy to visualize any fragment of arteriosclerotic plaque left behind. These fragments may embolize upon removal of the occluding clamps. Air embolus may also occur upon releasing clamps. To avoid this, the internal carotid is backbled and then reclamped. This allows air in the lumen to be expressed through the suture line. Next, the external and common carotid clamps are removed. Any remaining air, debris, or clot wili enter the external carotid system. Finally, the internal carotid clamp is removed. (Figure 2.) Most surgeons do not use a patch graft. It may give one a false sense of security due to the appearance of a wide lumen at the center of the graft. In fact, the stenosis occurs at the most distal margin of the patch.
VohmN 193, April 1977
Figure 1. lntimai damage cawed by inserfion of an intfaiuminai shunt.
If the arteriotomy is directly closed using 1 mm bites 1 mm apart, stenosis will not occur. Postoperative arteriograms show distension of the endarterectomized segment closed without a patch. Additional sutures necessary for hemostasis should be carefully placed to prevent constriction and tied with the common carotid temporarily occluded in order to avoid tearing the thin endarterectomized wall. Avoiding Peripheral
Nerve Paresis
There are a number of nerves which lie in the vicinity of the carotid artery and its branches. (Figure 3.) The normal position of the vagus nerve is between the carotid artery and the internal jugular vein. The vagus nerve usually lies posterolateral to the internal and common carotid but occasionally lies antero-
459
Matsumoto, Cossman, and Callow
STEP 1.
_
RELEASE and RECLAYP
STEP STEP 2. RELEASE
4. RELEASE ASAIN
STEP 3. RELEASE
2
Figure 2. Recommended order of releasing occluding clamps to prevent cerebral embolization.
medial. During the course of dissection of the carotid artery, the plane of dissection must be kept close to the wall of the artery to prevent injury to the nerve. Injury to the vagus is manifested as vocal cord paresis. Vocal cord paresis may also occur if the recurrent laryngeal nerve is traumatized. This is most apt to happen if the nerve takes an anomalous nonrecurrent course, traversing behind the common carotid. (Figure 3.1 To avoid injury, the dissection must be kept on the wall of the artery. The inferior ganglion of the vagus, the nodose ganglion, is not usually seen during dissection. A branch of this ganglion, the superior laryngeal nerve, courses behind the internal carotid and then bifurcates into the external branch, which innervates the inferior constrictor and the cricothyroid muscles, and the internal branch, which has sensory fibers to the orifice of the larynx. Dissection around the carotid bifurcation and the superior thyroid artery must be kept close to the arterial wall, fortrauma to the superior laryngeal nerve will result in unilateral numbness of the orifice of the larynx, mild difficulty in swallowing, and change in the quality of voice due to cricothyroid muscle dysfunction. Injury to these nerves is also likely to occur during unclamping and reclamping of the vessels during backbleeding. The hypoglossal nerve descends along the course of the internal carotid, then passes medially over the external carotid in a more superficial position. During carotid dissection this nerve is usually encountered. It can be mobilized medially to expose the most distal
YUGEAL U. 11 1 LAR78f%hL
N.
L^Rlxtl N.
?---#7Pcw.@ssAL MT
H In
LARYNGEAL N.
f&XT. LARYNMAL
N.
-*us* -REC%RRIENT LARYIYOEAL N.
Figure 3. Abnormal relationship of the “recurrent” laryngeal nerve.
460
Figure 4. Location of the cervical branch of the facial nerve.
The American Journal of Surgery
CarotidEndarterectomy
reaches of the internal carotid. Mobilization is recommended because traction on the nerve usually causes tongue deviation to the side of the endarterectomy. A branch of the hypoglossal nerve, the ansa hypoglossus, originates in various positions and may lie in the field. It innervates the strap muscles and usually can be mobilized medially. If, however, it fixes the hypoglossal nerve in the operative field, it may be sacrificed. The carotid sinus nerve, the nerve of Hering, originates from the glossopharyngeal nerve. It is a tiny nerve lying in the areolar tissue between the carotid bifurcation. Stimulation of the carotid sinus can cause hypotension and bradycardia, the reflex arc mediated by the vagus nerve. Infiltration of the areolar tissue with xylocaine will eliminate this reflex. Division of some end plates of this nerve is unavoidable because they are located in the wall of the common, internal, and external arteries. This may account for the severe hypertension encountered in the immediate postoperative period in a few patients. The glossopharyngeal nerve is usually not visualized during this dissection. The cervical branch of the facial nerve (VII) lies beneath the platysma inferior to the angle of the jaw. (Figure 4.) In some patients it may send twigs to the mandibular branch of the facial nerve [s]. If this anomaly exists and the cervical branch is divided, ipsilateral lower lip paresis will result. This can be avoided by curving the upper end of the skin incision posteriorly toward the mastoid process. The marginal mandibular nerve itself may be injured if the incision is carried too high. Clauss et al [9] and Sensenig [IO] have reported simultaneous bilateral carotid endarterectomies for bilateral carotid disease. This policy exposes the patient to an unnecessarily increased hazard. Both vocal cords may be paretic from operative trauma to both recurrent laryngeal nerves, superior laryngeal nerves, or vagus nerves. Edema of the false cords may result from local trauma. These patients may suffer severe upper respiratory obstruction necessitating prolonged intubation or tracheostomy. For this reason we advocate bilateral carotid endarterectomies in two stages, to permit evaluating laryngeal function between operations. Summary
The hazards and safeguards of carotid endarterectomy are presented in a consecutive series of 130 patients over a fourteen month period. The mortality rate of 1.5 per cent was due to myocardial infarction. Two patients (1.5 per cent) suffered minor but permanent neurologic deficit. There was an incidence of 4.6 per cent transient neurologic deficits, all of
voklme 133; April 1977
which cleared within 24 hours. Special emphasis is placed on peripheral nerve injuries (12.3 per cent). Local neurologic anatomy is reviewed to facilitate safe dissection and an avoidance of nerve injury. References 1. Eastcott HHG, Pickering GW, Rob CG: Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 2: 994, 1954. 2. Hobson RW. Wright CB, Sublett JW, Fedde CW, Rich NM: Carotid artery back pressure and endarterectomy under regional anesthesia. Arch Surg 109: 662, 1974. 3. Thompson JE, Austin DJ, Patman RD: Carotid endarterectomy for cerebrovascular insufficiency: long term results in 592 patients followed up to thirteen years. Ann Surg 172: 663, 1970. 4. Baker JD, Gluecklich B, Watson CW, Marcus E, Kamat V, Callow AD: An evaluation of electroencephalographic monitoring for carotid surgery. Surgery 78: 787, 1975. 5. Moore WS, Yee JM, Hall AD: Collateral cerebral blood pressure: an index of tolerance to temporary carotid occlusions. Arch Surg 106: 520, 1973. 6. Larson CP Jr, Ehrenfeld WK, Wads JG, Wylie EJ: Jugular venous oxygen saturation as an index of adequacy of cerebral oxygenation. Surgery 62: 31, 1967. 7. Scott SM. Sethi GK, Takaro T: Perioperative cerebral embolism in association with carotid arterial surgery: a significant hazard. Stroke 7: 13, 1976. 8. Paff GH: Anatomy of the Head and Neck. Philadelphia, WB Saunders, 1973. p 28. 9. Clauss RH, Bole, Prafull V, Paredes M, Doscher W, Kreminitzer MW: Simultaneous bilateral carotid endarterectomies. ICVS scientific program, 1976. 10. Sensenig D: Bilateral carotid artery endarterectomy at one operation. J Me A&d Assoc 65: 304, 1974.
Discussion Nathan P. Couch (Boston, MA): I congratulate the authors on a very fine series. They have brought their morbidity and mortality almost to an irreducible minimum. This is where careful technic really shows. There is no operation in vascular surgery that is more unforgiving of carelessness than the carotid endarterectomy. I agree that the handling of distal intima when positioning the shunt is crucial, although one does not always have to perform a distal endarterectomy before insertion. (Slide) The Javid shunt, in our opinion, is to be preferred. In addition, the arteriotomy should be generous. Care in the manipulation of the artery with very early distal control is all-important in preventing distal passage of atheromatous debris. After the shunt is removed, it is simpler if one completes most of the arteriotomy closure with a running stitch and places two or three interrupted sutures before removing the shunt,. Jeffrey K. Raines (Boston, MA): Our diagnostic evaluation in the Vascular Laboratory at the Massachusetts General Hospital includes a combination of three technics: ocular plethysmography; carotid audiofrequency analysis; and cerebral Doppler evaluation. We have investigated the use of ocular plethysmography during carotid endarterectomy. In this technic 14 mm eyecups are placed on the
461
Matsumoto, Cossman, and Callow
sclera of the patient’s eyes. Since this is an air-filled system, it can be used in surgery when the patient is placed on his or her side. In addition to producing a vacuum at the surface of the sclera these eyecups are also plethysmographic sensors. This allows the recording of ocular arterial pulsations as intraocular pressure is increased by the surface vacuum. When intraocular pressure is above systolic ophthalmic artery pressure, pulsations cease. In this way systolic ophthalmic artery pressure can be measured accurately during the recqnstruction. This procedure may prove to be of significant value in identifying problems when performing carotid endarterectomy. There are two questions I would like to ask. What criteria do the authors recommend for the use of a shunt? Do they recommend the use of EEG monitoring during carotid reconstruction? A. D. Callow (closing): We wish to thank the discussants. I should like to show some slides. The comments and recommendations that Doctor Matsumoto made are based upon our experience dating back to 1957. (Slide) Our 1957-1968 experience consisting of 266 endarterectomies illustrates the fallacy of attempting to operate on patients with completed strokes or acute strokes. The incidence of improvement was minimal and insofar as acute strokes are concerned, operative
462
mortality was considerable. (Slide) Shown here are the results of 292 endarterectomies in our 1968-1973 series. These patients were all operated with continuous ten lead electroencephalographic monitoring. For patients with recurrent transient ischemic attacks the incidence of improvement consisting of complete cessation of transient ischemic attack was 88 per cent for a minimum period of two years with many patients going well beyond this time. In this series as in the previous one, the three deaths were all from myocardial infarction. None of these patients underwent operation with completed strokes or with acute strokes. (Slide) This slide has reference to Doctor Raines’ comment. Although the technic he proposes is most useful, we have come to be very cautious in the interpretation of the so-called distal stump pressure. Several of our patients had stump pressures from 50 to 90 mm Hg in whom under continuous EEG monitoring, ischemic changes occurred and an intraluminal shunt was required. We rely very heavily, therefore, upon the EEG. Possibly the somewhat high incidence of peripheral nerve injuries, transient as they are, is due to the extensive, lengthy, and very meticulous endarterectomy we usually perform. Finally, our indication for the need for an intraluminal shunt is the appearance of ischemic changes in the EEG. In our last series of 186 consecutive endarterectomies, this has occurred in only 7 per cent of our patients.
The Amarhxn Journal ul Surgery
