Selective Management of Extracranial Carotid Arterial Aneurysms
Ronald W. Busuttll, MD, PhD, Los Angeles, California Robin K. Davldson, MS, Los Angeles, California Kevin T. Foley, MD, Los Angeles, California James 1. Llvesay, MD, Los Angeles, California Wiley F. Barker, MD, Los Angeles, California
While surgical repair of extracranial carotid occlusive disease involves standardized indications and techniques, the operative approach to extracranial carotid arterial aneurysms is more difficult to define because of its relative rarity. Rupture and hemorrhage are distinctly unusual complications of these aneurysms, yet central neurologic symptoms secondary to embolism or thrombosis are relatively common [1,2]. On the other hand, despite the neurologic sequelae of these aneurysms, surgical resection can be difficult or even impossible because they extend into the high cervical carotid artery, which precludes distal control. Thus, from the standpoint of surgical decisionmaking and operative strategy, extracranial carotid arterial aneurysms represent a major challenge to the vascular surgeon. To determine an appropriate method for selective management, a 24 year experience with these rare and difficult vascular lesions at UCLA Hospital and Sepulveda Veterans Hospital was reviewed. The findings, treatment and results are presented herein in the interest of formulating guidelines for surgical management. Patients and Methods
During the 24 year period from July 1954July 1978, more than 500 patients with occlusive disease of the extracranial carotid artery were surgically treated at the UCLA Hospital and the Sepulveda Veterans Hospital. Only 19 patients were treated for extracranial carotid arterial aneurysm during the same period, and their records From tfm Department of Surgery, Section of Vascular Svgery. UCLA Medical School, Los Angeles: and the Department of Surgery, Sepulveda Veterans Administration Hospital, Sepulveda, California. Requests for reprints should be addressed to Ronald W. Susuttil. MD. PhD, c/o Ediior’s Office, Department of Surgery, UCLA Medical School, Los Angeles, California 90024. Presented at the 51st Annual Meeting of the Pacific Coast Surgical Association, Kauai, Hawaii, February 17-20, 1980.
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form the basis of this report. Their mean age was 57 years (range 22 to 80), and the male to female ratio was 14 to 5. The average length of follow-up is 4.5 years (range 6 months to 15 years), but four patients were lost to followup. The causes of the aneurysms were almost equally divided among trauma, degenerative arteriosclerosis and previous carotid surgery (Table I). Of the aneurysms that developed after carotid surgery, all were false. Of the five pseudoaneurysms, three occurred after carotid endarterectomy with Dacron@ patch, one after Dacron aortocarotid bypass for Takayasu’s aortitis and one after ligation of the external carotid artery for bleeding after tonsillectomy. In the latter patient, the stump of the external carotid artery became infected with Staphylococcus aureus and this process extended into the distal common and proximal internal carotid arteries (Figure 1). The majority (59 percent) of the aneurysms were localized to the carotid bifurcation; however, 26 percent involved the high cervical internal carotid artery up to and beyond the foramen lacerum and 16 percent were diffuse in nature, encompassing the entire common carotid and internal carotid arteries. The propensity for the development of associated aneurysms in this patient population was high; 26 percent had other aneurysms. Abdominal aortic aneurysms were predominant, occurring in three patients; others were vertebral, femoral, popliteal and visceral. One patient had femoral, superior mesenteric and isolated hypogastric artery aneurysms in addition to extracranial carotid arterial aneurysm. Only two patients (11 percent) in this series were totally asymptomatic at the time extracranial carotid arterial aneurysm was diagnosed. The remainder presented with a neck lump (five patients), a transient ischemic attack (five patients) or stroke (seven patients). Results
Surgical treatment varied and was largely determined by several factors that included anatomic extent of the aneurysm, etiology, adequacy of con-
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Figvre 1. Left, preoperative arteriogram of a leakiinfected pseudoaneurysm. Right, postoperative anglogram taken 1 year after aneurysmectomy with vein patch.
tralateral cerebral blood flow and the presence or absence of infection (Figure 2). The selection of various operative methods was influenced by the anatomic location of the aneurysm (Table II). Extracranial carotid arterial aneurysm secondary to arteriosclerosis or previous carotid surgery tended to occur at or slightly above the carotid bifurcation, which made resection technically feasible. Traumatic aneurysms were usually located at the base of the skull (Figure 3). Noninvasive studies of cerebral
blood flow and operative carotid arterial stump pressures were not performed with sufficient frequency during this series to allow conclusions to be drawn. However, in all cases but one, an intraluminal shunt was employed during repair of the aneurysm. When infection was present, as it was in two of the patients, autogenous tissue rather than synthetic material was used in reconstruction. With respect to the six patients who were treated without definitive repair, the principal reason for this
Figure 2. Diagrammatic’ illustration of tectm@res used to repair extracranial carotkt arteklal aneury&m. A, occlusion with a Seiverstone clamp: 6, aneurysmectomy with graft; C, aneurysmectomy utllklng an&tomoskz between the exteinal and the distal internal carotid artery; 0, aneurysmectomy with a vein patch.
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Extracranial
TABLE I
Carotid Arterial
Aneurysms
Cause and Location ot Carotid Aneurysms
Location High internal Bifurcation Diffuse
ASCVD
Trauma
1 4
3 1 2
... 5 26
Total no. Percent of total
Carotid Suraerv
Mvcotic
...
...
1
5
1
...
...
...
6 32
5 26
Unknown
1
1 5
2 11
ASCVD = arteriosclerotic cardiovascular disease.
Figure 3. A high traumatic cervical aneurysm at fhe base of the skull extending to the foramen iacerum.
decision was an inability to obtain distal control. Among these patients, one was lost to follow-up, one had amaurosis fugax in the early follow-up period but has remained asymptomatic during the past 6 years, and the other four patients have been neurologically stable. Three patients were treated with proximal occlusion of the extracranial carotid arterial aneurysm. In two patients previously reported on [3], Selverstone clamps were applied. One patient had a small stroke with deviation of the tongue and loss of rapid fine motor movement of the right arm, which have resolved; the other patient is neurologically stable. A third patient became hemiparetic after emergency ligation of the common carotid artery owing to massive intraoperative hemorrhage secondary to rupture of aneurysm. Aneurysmorrhaphy with or without patch was performed in three patients. Aneurysmectomy with vein interposition or anastomosis between proximal external and distal internal carotid artery was performed in seven patients. In the 10 patients who underwent definitive surgical repair, 9 have been followed up for a mean of 2.3 years, and all are neurologically stable. One
TABLE Ill
TABLE II
Methods of Treatment for Carotid Aneurysms
Type of Treatment
Location of Aneurvsm
No.
Expectant Exploration without repair Occlusion
5 1
High cervical Diffuse
3
Aneurysmectomy with patch Aneutysmectomy with graft
3
Diffuse (2); bifurcation (1) Bifurcation
7
Bifurcation
patient who was lost to follow-up 6 years after aneurysmorrhaphy with a Dacron patch was doing well at her last visit (Table III). Excluding the 4 patients who have been lost to follow-up, 3 patients died, for a mortality rate of 20 percent (3 of 15). The causes of death included myocardial infarction, liver failure and ruptured aneurysm of the hypogastric artery. There were no operative deaths. Comments In 1808, Sir Astley Cooper [4] was the first to successfully ligate an internal carotid artery aneurysm, and the patient lived without neurologic deficit for
Results According to Type of Treatment for Carotid Aneurysms
Treatment
No. of Patients
Expectant Occlusion Aneurysmectomy with patch Aneurysmectomy with graft
6” 3 3’ 7
TIA 1
Complications Related to Aneurysm Treatment Rupture Stroke
‘it ... .
‘,‘t’ ... ...
Neuroiogically Stable
Follow-up (yr)
4 1 2 7
4.6 11.5 2.0 2.5
+ Patients lost to follow-up excluded from results. 7 Rupture and stroke occurred in the same patient. TIA = transient ischemic attack.
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13 years. Since then numerous techniques have been employed in the management of this unusual condition, including proximal ligation of the common carotid artery; distal ligation of the common, external and internal carotid arteries; excision after proximal and distal ligation; and gradual obliteration by wrapPing with fascia or cellophane [5]. However, because of the high incidence of neurologic sequelae subsequent to these techniques, they have been largely abandoned in favor of direct resection of the aneurysm with reestablishment of arterial continuity. Several recent reports in the literature have attested to the feasibility of and success achieved by direct arterial reconstruction [6,7]. These reports are substantiated by the present series, which has shown that the best results of a surgically accessible aneurysm are accomplished by direct reconstruction. It is now recognized that there are many causes of extracranial carotid arterial aneurysm, although they have changed over the years. While syphilis and local infection were the most common etiologic factors 40 years ago, they are rarely seen today. Instead, arteriosclerosis, trauma and previous carotid surgery now account for the majority of extracranial carotid arterial aneurysm, and they prevailed in our series also, led by trauma [1,7]. After penetrating or blunt cervical trauma, aneurysms of the carotid artery are rare; the most common complications of these injuries are arteriovenous fistula [s] and thrombosis, respectively [9]. However, after blunt trauma, an injury of lesser magnitude can disrupt the intima and media, with the subsequent development of an aneurysm rather than early thrombosis. The precise mechanism by which blunt arterial injury produces an aneurysm is not clear, but it is likely that acute hyperextension and rotation of the neck compresses the internal carotid artery at the level of the first and second cervical vertebrae. The stretching and torsion of this site are capable of producing an intimal tear and medial disruption which, if extensive, would lead to carotid thrombosis; if less severe it would predispose to formation of an aneurysm. Another factor implicated in this condition is the association of mandibular fractures and extracranial carotid arterial aneurysm [JO]. Forces applied to the angle of the mandible, which may or may not fracture the mandible itself, can be transmitted to the internal carotid artery, thus compressing the artery against the transverse process of the atlas. Batzdorf et al [II] have suggested that injury of the carotid artery may produce a spectrum of clinical and radiologic abnormalities ranging from spasm to intimal tear to medial tear, to aneurysmal formation or to complete severance of the vessel followed by thrombosis. 00
Whatever the mechanism of injury, the majority of extracranial carotid arterial aneurysms secondary to trauma are located in the high cervical carotid artery, making them difficult to approach surgically. There are three options from which to choose: ligation of the carotid artery proximal to the aneurysm, an attempt at surgical repair, and no action. As mentioned previously, proximal ligation should be used only under the most select circumstances. Specifically, if a patient has a large, high extracranial carotid arterial aneurysm that is embolizing to the brain or eyes and is destined to produce a serious neurologic event, then no other course may be available but ligation. After ligation, some type of extracranial-intracranial bypass should be considered if cerebral complications occur, The incidence of complications varies; in one series Watson and Selverstone 1121reported a mortality of 55 percent within 5 days of operation in a group of patients who had ligation of the common carotid artery. They emphasize that the variation from case to case depended on the completeness of the circle of Willis and the collateral circulation. Several other investigators [13] estimate the incidence of cerebral complications at 20 to 30 percent. On the other hand, Rogers [14] reported that among 19 patients who had had carotid artery ligation, there was one case of transient neurologic deficit and one death unrelated to the ligation. In the present series, three patients underwent carotid arterial ligation, two of whom had a neurologic defect. Although an accurate preoperative assessment of the status of collateral flow is essential before ligation is performed, methods of testing collateral circulation have been notoriously inaccurate. Doppler flow studies [15] may be valuable in detecting increased collateral blood flow through the supraorbital branch of the external carotid artery when the internal carotid artery is occluded, but the degree of increased flow that will protect from a stroke is yet to be determined. More recently, oculopneumoplethysmography has been accurate in evaluating high grade carotid stenosis, exceeding the accuracy achieved with Doppler studies [15]. The second option, resection of high aneurysms, presents a difficult challenge because distal control is often impossible. In a technique proposed by Hershey [16], a tapered shunt is placed within the aneurysm after proximal control of the aneurysm has been obtained, and the shunt is wedged up into the internal carotid at the foramen lacerum. Once flow to the brain is established, a aneurysmorrhaphy is performed. Experience with this technique has been limited primarily to saccular aneurysms, which lend themselves to aneurysmorrhaphy. The American Journal of Surgery
Extracranial Carotid Arterial Aneurysms
The third option, expectant treatment for high extracranial carotid arterial aneurysms, is one that arouses antipathy in the vascular surgeon. Winslow [17] found that 71 percent of untreated patients ultimately died from aneurysm of the internal carotid artery. However, in his collective series all aneurysms were considered, and doubtless the natural history of arteriosclerotic and mycotic aneurysm is probably far different from that of traumatic aneurysm, owing to the ongoing degeneration in the former two. Thus, expectant treatment of the small, high cervical traumatic aneurysm may not have such a bleak outlook. In our series of five such aneurysms, only one patient had a transient ischemic attack, which occurred early in the follow-up period. Based on our favorable experience and the fact that some aneurysms have become smaller spontaneously [II], we feel that small, asymptomatic, high cervical aneurysms should be treated conservatively. Pseudoaneurysm after carotid surgery is an unusual complication that frequently results in embolization. In a recent report by McCollum et al [7] on 21 pseudoaneurysms, 16 followed carotid endarterectomy with Dacron patching. A collective review of 44 pseudoaneurysms reported in the literature and including the present series (Table IV) indicates that pseudoaneurysm formation is more than four times as common after endarterectomy with patching than after endarterectomy alone. Although the overall incidence is low, significant morbidity (12 percent) is associated with these pseudoaneurysms. We believe that all pseudoaneurysms should be repaired because of their propensity to embolize. In the vast majority of cases, such aneurysms occur in a surgically accessible location and can be treated with resection and patch angioplasty or tube replacement. We agree with Ehrenfeld and Hays [6], who recommend the use of autogenous tissue in reconstruction because some of the pseudoaneurysms will be infected. In two of the four cases they reported, the pseudoaneurysm was infected with Staphylococcus aureus, as in two of our five cases.
TABLE IV
Several reports [1,7,18], including the present one, recommend aneurysmectomy with arterial reconstruction as the treatment of choice. The means to achieve this will vary according to the cause of the aneurysm, its location and the surgeon’s experience. Direct end-to-end anastomosis can usually be performed if the aneurysm is small and the vessel elongated and tortuous, However, when end-to-end anastomosis is impossible owing to inadequate vessel length, then an alternative technique of anastomosing the proximal external to the distal internal carotid artery can be performed, either end-to-end or end-to-side, although the former is preferable. Aneurysmectomy with patch is particularly useful in managing small, saccular aneurysms or pseudoaneurysms after endarterectomy. In such cases it is unlikely that total excision of the parent vessel would be required; in fact it would be meddlesome to do so. The majority of extracranial carotid arterial aneurysms, particularly those secondary to arteriosclerosis, are best managed by resection and replacement with autogenous saphenous vein or Dacron graft. Good results have been reported with either method [1,7]. As reported by Rhodes et al [I], complete dissection and excision of very large aneurysms should be approached cautiously because of the close attachment of the vagus, the laryngeal nerves and the sympathetic chain. Whatever technique is used in aneurysmectomy, it is imperative to prevent cerebral ischemia. The easiest and most reliable method is an intraluminal shunt, which we used in all but one of our cases. Although carotid endarterectomy can be performed successfully without shunting, the duration of cerebral ischemia is usually brief. On the other hand, because aneurysm resection and reconstruction are much lengthier procedures, the standard guidelines of carotid back-bleeding and stump pressure used for endarterectomy cannot be relied on. In a collective series [18] of 24 extracranial carotid arterial aneurysms treated by excision and restoration of arterial
Collective Review of Pseudoaneurysms After Carotid Surgery Procedure
Series
Total
Carotid Endarterectomy
Carotid Endarterectomy Patch
Other Carotid Procedure
Outcome* Successful
Stroke+ or Deaths
Ehrenfeld and Hays
20
7
11
2
15
3t.55
(collective 1972 series) McCollum et al, 1978 UCLA, 1980
19 5
. ...
16 3
3 2
16 4
1t 17
7 16
30 68
7 16
35 88
Total no. Percent of total l
44 100
5 12
Outcome unknown in four patients.
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continuity, there were eight postoperative deficits, three of which were permanent.
neurologic
In 75 percent of the patients who developed a neurologic deficit and in all of those who developed permanent deficits, no shunt was used. We believe that shunting is an important part of the technique of resection of extracranial carotid arterial aneurysms, facilitating the reconstruction by serving as a stent when autogenous vein interposition is used. Whatever modality is used in the treatment of these aneurysms, we agree with Beall et al [19] that “the incidence of cerebral damage from a specific procedure varies considerably from individual to individual and no one technique is applicable to every case of extra-cranial carotid aneurysm.”
Summary Aneurysms of the extracranial carotid arteries are rare vascular lesions that produce a high incidence of unfavorable neurologic sequelae. In the past 24 years, 19 patients at UCLA Hospital were treated for angiographically demonstrable extracranial carotid arterial aneurysms. These cases were reviewed to determine the natural history of these lesions as influenced by various modes of therapy in order to develop a logical treatment plan for these difficult patients. Because of the varied location of these lesions, proper treatment requires a diversity of techniques. Gratifying results can be achieved when a carefully selected operative approach is undertaken. References 1. Rhodes EL, Stanley JC, Hoffman GL, Cronenwett JL, Fry WJ. Aneurysm of extracranial carotid arteries. Arch Surg 1976;111:339. 2. McEntyre JM, Keates EU. Whiteley WH. Retinal embolus from extracranial carotid artery aneurysm. Arch Ophthal Mol 1967;77:317. 3. Webb RC, Barker WF. Aneurysms of the extracranial internal carotid artery. Arch Surg 1969;99:501. 4. Cooper A. Account of the first successful operation performed on the common carotid artery for aneurysm in the year of 1808 with post mortem examination in the year 1821. Guys Hosp Rep 1836; 1:53. 5. Thompson JE, Austin DJ. Surgical management of cervical carotid aneurysms. Arch Surg 1957;74:80. 6. Ehrenfeld WK, Hays RJ. False aneurysm after carotid endarterectomy. Arch Surg 1972;104:288. 7. McCollum CH, Wheeler WG, Noon GP, DeBakey ME. Aneurysms of the extracranial carotid artery. Twenty-one years’ experience. Am J Surg 1979;137:196. 8. Elkin DC, Shumacker HB. Arterial aneurysms and arteriovenous fistulas. General considerations. In: Elkin DC, DeBakey ME, eds. Vascular Surgery in World War II. Washington DC: Department of the Army, 1955: 149-80. 9. Salmon JH, Blatt ES. Aneurysm of the internal carotid artery due to closed trauma. J Thorac Cardiovasc Surg 1968;56: 28.
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10. Boldrey E, Maass L. Miller E. The role of atlantoid compression in the etiology of internal carotid thrombosis. J Neurosurg 1956;13:127. 11. f3atzdorf U, Bentson JR, Machleder HI. Blunt trauma to the high cervical carotid artery. Neurosurgery 1979; 5:19. 12. Watson WL, Selverstone SM. Ligature of the common carotid artery with cancer of the head and neck. Ann Surg 1939; 109:l. 13. Pilcher C, Thuss C. Cerebral blood. Ill. Cerebral effects of occlusion of the common or internal carotid arteries. Arch Surg 1934;29:1024. 14. Rogers L. Ligation of the common carotid artery: report of 19 personal cases. Lancet 1949; 1:949. 15. Machleder HI, Barker WF. Non-invasive methods for evaluation of extracranial cerebrovascular disease: a comparison. Arch Surg 1977;112:944. 16. Hershey FB. Operation for aneurysm of the internal carotid artery high in the neck: a new and an old technique. Angiology 1974;25:24. 17. Winslow N. Extracranial aneurysm of the internal carotti artery: history and analyses of the cases registered up to August 1, 1925. Arch Surg 1926; 13:689. 18. Raphael HA, Bernatz PE, Spittell JA, Ellis FH. Cervical carotid aneurysms: treatment by excision and restoration of arterial continuity. Am J Surg 1963;105:771. 19. Beall AC, Crawford ES, Cooley DA, DeBakey ME. Extracranial aneurysms of the carotid artery: report of seven cases. Postgrad Med 1962;323:93.
Discussion William K. Ehrenfeld (San Francisco, CA): Dr. Busuttil’s group has carefully reviewed a large and varied experience with extracranial carotid arterial aneurysm at the UCLA Hospital. They have defined the necessary therapeutic considerations in selectively managing this often-challenging clinical disorder. I think it is quite significant that 12 of the 19 patients presented with territorial neurologic dysfunction including transient ischemic attacks and stroke. We are in complete agreement with the UCLA group that the definitive surgical management in these patients with accessible aneurysms, whatever the cause, is resection and interposition grafting. We also recommend autogenous tissue grafts whenever possible, particularly with postoperative false aneurysms because infection may have played a role in the pathogenesis of the aneurysm. We use internal shunts when they are indicated by a low stump pressure. This judgment is based on information gained from about 2,000 carotid endarterectomies. We use 50 mm Hg as the lowest level allowable without a shunt. As indicated by Dr. Busuttil, the shunt is also useful during anastomosis as a stent. Thus there seems to be little difference in indication and technique regarding applicability to the symptomatic accessible carotid aneurysm. The biggest problems lie in the management of the inaccessible aneurysm. One of our patients had a large aneurysm that could be easily exposed at the inferior margin but would be exceedingly difficult or impossible to adequately and safely expose superiorly because it lay close to the carotid foramen. For these inaccessible aneurysms the available options are expectant therapy or cervical carotid ligation. In this regard I would like to add some experience that may
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allow ligation to be applied more safely. Two of three ligated patients in the series presented herein had strokes; do the authors have any information regarding stump pressure in these patients? Dr. Jack Wylie and I have ligated the carotid arteries for varied indications in 17 patients, 7 of whom had symptomatic extracranial carotid aneurysms that were inaccessible. Again we are guided by the retrograde stump pressure. Ligation effectively removes the aneurysmal source of retinal or cerebral emboli. We have found ligation safe if the stump pressure exceeds 70 mm Hg. Most patients will tolerate ligation safely with a marginal stump pressure of 55 to 70 mm Hg. These patients are given systemic heparin during operation and for 2 to 7 days postoperatively. The heparin is given to prevent extension of the thrombus beyond the ipsilateral ophthalmic artery. Ligation is highly likely to cause stroke when the stump pressure falls below 50 to 55 mm Hg. This study helps define the clinical problems of extracranial carotid aneurysmal disease. F. William Heer (San Francisco, CA): I compliment the authors on their remarkable series and for their succinct presentation of the alternative means of treatment. I would like to remind you of a historically defined entity of internal carotid aneurysm first described by Hunter and subsequently about 180 times in the literature, I have a brief anecdotal case to present representing this entity. An 11 year old boy who was chronically demented had a 5 day history of fever and an inflamed mass in the right side of the neck. His ear, nose and throat physician had made a diagnosis of peritonsillar abscess. Fortunately, before he used the knife, he introduced a needle and obtained spurting bleeding. After this a deep hemiparesis occurred and the patient was referred to a neurosurgeon. An arteriogram was taken, concentrating on the intracranial portion of the distribution. A large tortuous vessel was demonstrated in the cervical region. Another film revealed that a similar defect existed on the other side. It was not inflamed clinically. The child had a temperature of 107’F, which was treated. He was obtunded. The next day we explored the mass after his temperature decreased and he was well hydrated. The results of cultures of the throat and blood and the operative specimen were negative. Despite its serpentine form angiographically and pathologically, the aneurysm appeared, grossly, as a globular mass. Histologically, this appeared to be a dilated vessel with no specific identifiable defect and with considerable surrounding chronic and acute inflammation. A vein interposition graft was
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Carotid Arterial Aneurysms
utilized. This is a deadly disease when it is not identified, and it is characteristically described as such throughout the literature. Since I have also had a second case similar to those described by Dr. Ehrenfeld requiring Selverstone clamp application, I would like to ask whether temporal arterial bypass for cortical protection preceding such ligation or application of the clamp should be considered. Wiley F. Barker (closing): Dr. Ehrenfeld, you asked about stump pressure in the patients with untreatable lesions; they were operated on before the concept of stump pressure was understood and therefore we cannot answer this. Dr. Heer, we had no primary inflammatory aneurysms. My concluding comments should focus on the question of what to do with a very high aneurysm that one cannot reach for satisfactory and safe repair. These are lesions that you cannot attack without risk of either an inadequate anastomosis or such a hemorrhagic catastrophe that you have to carry out immediate ligation. We would today precede any such operation with careful evaluation by the Gee-oculopneumoplethysmograph of the back pressure, using carotid compression. One simple way to measure the stump pressure in the internal carotid artery involves occlusion of the internal carotid and placement of the needle distally without any other clamping, maintaining flow into the external carotid system. Subtraction of this pressure from the reading obtained by concomitant occlusion of the external carotid artery gives the component of the central internal carotid pressure provided by external carotid flow, which may vary from 0 to 55 mm Hg. If there is a generous contribution by the external carotid flow, we place a shunt into the external carotid. I recommend this procedure if protracted occlusion of the internal carotid artery is needed. One last comment about the Selverstone clamp. If we thought we were going to have to use it, we would perform an external bypass first. There are some tricks to using the Selventone clamp. I believe it is critical to place the clamp, leave it open and then allow the patient to recover his full level of consciousness. Gradual closure of the clamp over several days can be accomplished while monitoring neurologic signs carefully. During the time of gradual occlusion, the patient should receive heparin to protect against clotting, embolization from the stenotic artery under the clamp, and the propagation of further clot into the intracranial system.
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