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Kinking of the internal carotid artery
Kinking of the Internal Carotid Artery Clinical Significance and Surgical Management Robert S. Vannix, MD, Los Angeles, California E. J. Joergenson, MD, Los Angeles, California Richard Carter, MD, Los Angeles, California
Dramatic advances in diagnosis and surgical treatment of extracranial occlusive disease have developed since 1954 when Eastcott, Pickering, and Rob [I] reported the first successful carotid reconstruction. The cerebrovascular insufficiency in most cases is due to an underlying atheroma at the carotid bifurcation, which is usually segmental, well localized, and accessible to surgical correction. Although kinking of the internal carotid artery has been recognized for many years, the clinical importance of this phenomenon still remains controversial. The purpose of this report is to emphasize that this lesion is not an anatomic curiosity but a potentially disabling, even fatal condition which represents challenging clinical and technical problems. History
As early as 1898 tortuosity or kinking of the internal carotid artery was noted in four cases by Brown Kelly [2] in the Glasgow Medical Journal. He emphasized the potential danger in these cases of hemorrhage during tonsillectomy or drainage of a peritonsillar abscess. Recognizing the neurologic importance of the kinked internal carotid artery, Riser et al [3] in 1951 advocated arteriopexy by suturing the tortuous artery to the medial margin of the sternocleidomastoid muscle. The first direct surgical resection of a kinked internal carotid artery was reported by Hsu and Kistin [4] in 1956 and was unsuccessful. In 1959 Quattlebaum, Upson, and Neville [5] successfully resected the common carotid artery with end-to-end anastomosis in three patients with kinked internal carotid arteries. In the same year Freeman and Lippitt [6] reported ten additional cases. In 1962 Derrick and Smith [7] suggested that carotid kinking was a more common cause of strokes than previously recognized and recommended transplantation of the internal carotid artery beneath the sternocleidomastoid muscle. (Figure 1.) From the Departments of Surgery, University of Southern California, Los Angeles, and University of California, Irvine, Irvine, California. Reprint requests should be addressed to Robert S. Vannix, MD, Department of Surgery, University of Southern California, Los Angeles, California 90033. Presented at the Forty-EighthAnnual Meeting of the Pacific Coast Surgical Association, Palm Springs, California, February 20-23, 1977.
a2
Incidence and Etiology
By definition, coiling is elongation and redundancy of an internal carotid artery resulting in an exaggerated S-shape curvature or a circular configuration, whereas kinking is angulation of one or more segments of the artery, often associated with stenosis. Coiling is usually ascribed to embryologic causes and is generally asymptomatic, whereas kinking or buckling is predominantly associated with atherosclerosis and may be accompanied with recurrent transient ischemic attacks. Patients with cerebrovascular symptoms who have significant kinking of the internal carotid artery without plaques may require surgical correction, especially if aggravated by head rotation. Precise angiographic definition of coils and kinks is fundamental to determine if surgical correction is indicated. The incidence of coiling or kinking in the general population has been estimated as high as 16 per cent by Metz et al [8] based on a series of 1,000 angiograms. Cioffi et al [9] found this lesion in 10.1 per cent of 1,010 unselected angiograms, while Najafi et al [IO] reported a 5 per cent incidence of kinking in a series of 308 patients undergoing carotid procedures. There were 15 instances of kinking in our series of 312 carotid reconstructions (4.8 per cent). Cerebrovascular insufficiency associated with coils and kinks has been attributed to atherosclerosis and failure of embryologic development of the carotid arterial system. Coiling or looping has been observed in infants and fetuses. Embryologically the internal carotid artery is derived from the third aortic arch and the dorsal aortic root. In the embryo the internal carotid artery is normally kinked, and straightening occurs when the fetal heart and great vessels descend into the mediastinum. Inordinate differential growth of the internal carotid artery and the descending heart may lead to persistence of coiling and kinking which, when present, is bilateral in approximately 50 per cent of cases. Kinking of the internal carotid artery is almost always accompanied by atherosclerosis with subintimal deposits, loss of elasticity, elongation, and even formation of aneurysms. As the vessel elongates, it bows on fixed points at the base of the The American Journal of Surgery
Kinking of Internal Carotid Artery
J
1
Figure 1. A, tortuous Internal cafotld aftery ( tCA ) sutured to stemoc~ekiomastold muscle as advocated by Riser et al [ 31; 8, redundant /CA resected and reanastomosed [41; C, klnked ICA straightened by resecting common cafut/d artery segment [5]; D, relmplantatlon of ICA without resection (Lorkner); and E, segmental resection and reimplantation of /CA.
skull and thoracic inlet, and rotational ischemia is most likely to occur when the head is turned toward the side of the kink. Signs and Symptoms
Roberts et al [II] demonstrated that in man the internal carotid arteries carry about 90 per cent of cerebral blood flow. They further showed that as the head is moved through a normal range of movements, blood flow through the carotid or vertebral arteries may be obstructed. The neutral position of the head is the one most favorable for maximal cerebral flow. However, the presence of atherosclerosis, vertebral artery compression, anomalies of the circle of Willis, and blood pressure variations such as hypovolemia and antihypertensive drugs may make angulation more critical and produce transient ischemic attacks. In view of these facts, clinical and angiographic evaluation of these patients must be a dynamic one. Experimental studies have shown that graded occlusion of the carotid artery does not reduce cerebral blood flow until more than 90 per cent of the lumen has been obstructed [12]. The clinical symptoms associated with atheromatous ulceration, stenosis, or occlusion of the internal carotid artery are well described in the literature. Transient ischemic attack is a focal neurologic deficit due to a temporarily occluded blood supply to a portion of the brain. Although complete and spontaneous recovery usually occurs, a transient ischemic attack frequently precedes frank cerebral infarction. The patient with a kinked internal carotid artery may also present with a transient ischemic attack. Prophylactic surgery directed toward the clinically significant kinked internal carotid artery may prevent a completed stroke. Volume 134, July 1977
Surgical treatment is advisable when atheromatous ulceration, critical stenosis, and/or significant kinking with occlusion is present in the internal carotid artery when associated with appropriate cerebral vascular symptoms. Desai and Toole [13] observed that indisputable evidence for an exact causal connection between kinking of the internal carotid artery and cerebrovascular symptoms is difficult to establish. However, surgical correction should be carefully considered in patients with recurrent cerebrovascular episodes with internal carotid kinking in which other causes have been excluded, particularly in those exhibiting cervical rotational ischemia. Material and Methods This study is based on fifteen patients (12 male, 3 female) with kinking of the internal carotid artery, fourteen of whom were successfully treated within the past twenty-four months. The age range was thirty-one to seventy-five years (mean, 64 years). Preoperative evaluation of all patients included a complete neurologic evaluation, electroencephalogram, skull x-ray fiis, static and dynamic brain scan, cardiac evaluation, and complete extracranial and intracerebral angiography. Computerized axial tomography was obtained in the last seven patients treated. (Table I.) Case Reports
Salient clinical features of the kinked internal carotid artery are illustrated by the following case reports: Case I. A seventy-four year old normotensive diabetic woman without neck bruits had five transient syncopal episodes with visual changes during a six month period. Dynamic brain scan showed a marked decrease flow in the left carotid distribution. Arteriogram showed 70 per cent occlusive plaquing of the origin of the left internal carotid artery, with a tortuous coil above the plaque and retarda83
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Clinical
71/F
75/F
63/F
58/F
62/F
57/F
74/F
65/F
AT
HL
El3
JB
EB
oc
BK
Note:
FS
CS
LR
CVA
71/F
69/F
60/M
fugax.
Amaurosir
31/M
WW
MM
fugar.
Amaurosis
71/F
hemlpareslr.
Mental
hemiparesis.
left
Translent
heml-
hemI.
Left
arm
= cerebravascular
rotation.
Syncope
accident;
on head
Right hemlparesls. Apharla.
monopares1r.
Syncope.
syncope. Poor coord#nation.
paresIs.
rtght
Transient pare*,*.
fugax.
Gait mstablllty. Syn. cope. Amaurow
Aphasia.
Right
deterloratlo”.
Syncope.
Gart tnstablllty.
Right
fugax.
hemipareris.
Amaurosls
Left
fugax.
Tranrtent
amaurosir
Residual
hemi-
paresis.
rrght
aprax\a.
Transient
loratlo”.
Men-
Poor
left arm.
DB
tal detc
cow&nation.
Amaurosls.
Monoplegla
car&d.
left
carotid.
No
No
= electrocardlogmm:
bruits.
No
No
Bruit
murmur.
Notmotensive.
heart
No bruits.
brult5.
No
Bruit
murmur.
carotid.
Normotensive.
heart
left
BP 180/84.
murmur.
Basal heart
left
BP 150/80.
bruits. No “l”r”l”rs.
Normotensive.
carotid.
Bruit
rys-
murmur.
Aortlc
right
Normotenswe.
tolic
t,d.
Bruit
caro-
No heart
left caro-
Bruit
neck
murmur. Normotenslve.
tld.
Bruit
BP 176/300.
left
BP 150/80.
brwts.
No
Bruit
hyperten-
510”. No
Lablle
bruits
Normotenwe.
carotid.
BP 156/90.
left
No
murmurs.
bruits.
heart
No
bruits.
No
Internal
Signs
of the
Normotenslve.
Kinking
EKG
with
episodes.
Symptoms
in 15 Patients
5 syncopal
Data
60/M
Sex
Age(w)/
I
RH
EL
Care
TABLE
ICA
Artery
Enlarged “onrpeclf-
ventricle.
scar.
normal.
ventricular
normal
normal.
EKG
carotrd
normal.
= Internal
EKG
old posscar.
EKG: terior
Hypertensmn.
EKG
normal.
olemia.
Hypercholester-
EKG
Ischemla.
EKG:
normal.
Drabetes.
EKG
hne abnormal.
enlargement. EKG: border-
Left
History of hypertension. AngIna.
Left calf claudication. EKG: LVH
EKG
largement.
scar. Cardiac
old posterior
EKG: en-
old myo-
normal.
Diabetes.
EKG
cardlal
EKG:
of anemia.
normal.
History
EKG
ic abnormalltles.
EKG:
left
Diabetes.
Associated Findings
Carotid
artery;
Flow
done
left
BP = blood
Normal
“orm21.
rschemia.
Preop
Normal
Portop
pressure;
Postop
cerebral
hemlspheilc
Ischemla.
Left
Normal.
Normal.
Normal
Normal
Not
left
cerebrum.
normal.
normal.
Preoo
Flow
decreased
oosterlor
Flow
Normal.
normal.
clearing
infarct.
nghtpost-
parletal 1975:
of defect.
Oct.
error
1975:
tld dlstributlo”.
Sept.
de.
I” left caro-
normal.
creased
Scan
Flow Study
Brain Scan and
LVH
atherosclerotic
ICA. angle
kinks
ICA.
= left
angled ICA. ventricular
right
2 acute
both orrg,”
plaque
80%
left
ICA.
carotlds.
Co11
occfus~ve
ICA.
hypertrophy.
kinks
orlgl”
C2 level. Internal Left ICA.
ICAs.
of both
right
ICA
atherosclerotic ICA.
Plaqu-
with right
klnkrng narrowing
kink
left
with
C2
or-
Two
ICA.
proximal
ICAs.
left
& clot
right
plaque Tight
Kinking
Tortuoslty
W-shaped
plaques
Kinking
significant
right
loop
of
1976:
left ICA with plaque origr”
plaqulng
ICA.
stenosis
and
plaque
& mlnimal
kinks both left ICA.
Co11 left
wth
Atheromatous
ICA.
Kink
Redundant Ing orjgi”
atherosclerotic
2 rrght
right
95% origin occlusion kinkrng. Ulcerative
ICA.
ICA.
2 sites.
lgin right ICA wrth 360” level. Kink of left ICA.
Ulcerated
ICA.
to right. left
June unchanged.
C2 level+tlght-
of left
atherosclerorls.
kInking
Mammal
Sharp
ICA
klnkr
hyperextension
right
head rot&o”
ened wtth
36O”co1l
angle
C2
1975:
3 cm an-
left
Left
orlgln
normal.
% occlusion
r,ght
80+
ICA
clot.
poststenotx
right
contalmng
level with eurysm
stenosrs
ICA
Sept.
& kInkIng
C3 level & re-
right
plaque.
elongation
wlthout
1974:
carotid
h,gh grade
ICAs
April
flow.
loop
orlgl”s--left
Complete
carotid
0ccIus1~e.
Internal
Internal
tarded
left
60-70%
Plaquing
Angiogram car&d
segmental
segmental
ICA.
rioht
segmental
plantation
cc/mi”. Segmental
left
ICA.
resectlo”
200 and ream
Flow
resectjon ICA.
and
and ream-
[CA. right ICA. endarterectomy
resection
lmplantatlo”
wth
plantation Left carotid
Segmental
resectton
and
and relm-
Flow
endarterectomy segmental
carotid
120
and
110
and
100
and
150
and
ream-
Flow wth ICA.
left ICA. cc/ml”.
reimplantation
wth
Left
Flow
resectto” ICA. resection
plantation Flow 250+
Flow
resectlo”
i20 ccfmi”. _ Segmental resection
olantatio”
cc/min. Segmental
ICA.
resectlo”
endarterectomv segmental
carotid
reimplqntation
wth
Left
cc/mm.
Flow
endarterectomy reimplantatlo”
wth
cc/min. Left carotid
ICA.
resection
125
reimFlow
with
re-
reimplanpatch
endarterectomy relmplantatron
with
carotid
ccjrmn. Left
with Vein cc/mm.
ICA.
with
120
end-
no
de-
No
and reim-
endarterectomy
left
segmental
carotid
relmplantatro”
wth
Right
cc/ml”.
pfantatlo”
ICA. 200
resection
graft. Segmental
right Flow
tatron
resection
ICA.
Segmental
resection
plantation
ICA
Flow
with
endarterectomy
anastomosis.
carot,d
with
angiogram:
reoperatlo” lntraop
aneurysm
Stat
postop
endarterectomy. Immediate
segmental
Left
cc/nun.
to-end
Resected
flap.
clotting.
CVA.
resectlo”.
Left
Treatment
7th.
CVA.
improvement
recovery
Complete
Complete
Complete
Complete
Complete
Complete
Complete
Complete
recovery.
recovery.
recovery.
recovery
recovery.
recovery.
recovery
recovery
Continued imorovement presurglcal CVA.
Unchanged.
10th.
nerve
from
from
12th.
dysfunc-
and aphasia.
recovery.
9th,
recovery
presurglcat
Continued
Complete
Comolete
Complete
tion:
craneal
hemiparesis
Transient
Right
Results
$
L
_z
2
d
Kinking of Internal Carotid Artery
tion of blood flow. (Figure 2.) Left carotid endarterectomy without carotid resection was performed. In the immediate postoperative period the patient had transient recovery and then developed right hemiparesis. Angiogram indicated no evidence of an intimal flap, and at reoperation thrombectomy of the clotted coiled artery was performed. Comment. This patient illustrates the necessity of simultaneously correcting both the occluding intimal plaque and the coiled carotid artery. The decrease in left hemispheric perfusion was due to the coil and not the occlusive plaque. Case II. A sixty year old normotensive man without neck bruits had sudden left arm monoparesis with transient amaurosis. Retrograde arch study showed elongation and kinking of both internal carotid arteries with no evidence of plaque or clot formation. (Figure 3, left.) Seventeen months later the symptoms recurred with persistent weakness in the left arm. Brain scan suggested an infarct in the right posterior parietal region. Repeat scan one month later indicated almost complete clearing. Angiography showed high grade stenosis of the right internal carotid artery with poststenotic aneurysm formation and intraluminal clot. (Figure 3, right.) At surgery, a 3 X 2 cm aneurysm was resected and the internal carotid artery was reconstructed by end-to-end anastomosis, establishing a flow of 150 ml per minute. The patient recovered satisfactorily. Repeat angiography nine months later showed the right internal carotid artery to be normal with the left internal carotid still kinked and elongated. Comment. This patient illustrates that kinking can cause cerebral symptoms of the carotid type that may lead to a completed stroke. Furthermore, kinking may also produce poststenotic aneurysm and clot formation. An important technical consideration is the ease of resecting and reimplanting a kinked internal carotid artery compared with resecting an aneurysm with reanastomosis at the base of the skull. Case III. A seventy-one
year old normotensive woman with a left carotid bruit had a right transient hemiparesis with partial aphasia and amaurosis. Brain scan was normal Retrograde arch study showed 80 per cent occlusion of the left internal carotid origin with two acutely angled kinks above the plaque. (Figure 4.) At surgery, a carotid endarterectomy and segmental resection with reimplantation of the left internal carotid artery was performed without sequelae. Comment. This amplifies the importance of recognizing the coexistence of atherosclerotic changes with marked kinking. Endarterectomy weakens the wall further at the site of the kink and tends to accentuate the angulation. It is manditory to treat both problems at the time of surgical correction. Case IV. A thirty-one year old normotensive man without cervical bruits was chasing a fly ball and suddenly fell with a left hemiparesis and visual aberrations. Brain scan was normal. Retrograde arch study showed the right internal carotid artery had a 360’ coil which tightened with
Volume 134, July 1977
Figure 2. Case 1.Illustration of plague in /CA with a complete loop and confirmatory arteriogram.
head rotation to the right and with hyperextension. (Figure 5.) CAT scan showed nothing abnormal. Resection of a segment of the right internal carotid artery with reimplantation and a vein patch graft at the site of maximum coiling was performed. Postoperative flow was 250 ml per minute and recovery was uneventful. Comment. This case is unique because it demonstrates that a coil may cause major cerebral vascular symptoms even in a young person. It also shows that the angiogram can be used dynamically to demonstrate positional narrowing of the coiled or kinked artery. Coiling or kinking may be present without any associated atherosclerosis. Case V. A seventy-one year old normotensive woman without carotid bruits was admitted with a persistent right hemiplegia. Brain scan showed a reduction of flow to the left cerebral hemisphere. Retrograde arch study showed tortuosity, elongation, and an acutely angulated left internal carotid artery at two sites without atherosclerotic ulceration or occlusion. (Figure 6.) Segmental resection and reimplantation of the left internal carotid artery was done five weeks later. There was no associated atherosclerosis although a recent clot was present. Postoperative flow was 125 ml per minute and she made continued improvement from the antecedent cerebrovascular accident. Comment. This case illustrates that a cerebral infarction can occur from a kinked carotid artery in the absence of atherosclerosis. SurgicalTreatment
Meticulous anesthetic and surgical technics are mandatory for the successful treatment of cerebrovascular disease. The coiled or kinked internal carotid artery presents special technical problems. The artery wall in the
85
Vannix, Joergenson, and Carter
Figure 3. Drawings and angiograms showing: Left, elongation and kinking of right /CA without plaque. Right, stenosis with poststenotic aneurysm and intraluminal clot.
Figure 4. Retrograde arch study showing two critical kinks above plaque formation.
66
coiled or kinked segment is very thin and can be disrupted with minimal dissection. Furthermore, the artery must be mobilized from its bifurcation to the base of the skull and. all fibrous bands completely severed. If adequate mobilization is not completed, accentuation of the kink may result after resection of proximal internal carotid artery and reanastomosis. A tension-free anastomosis is axiomatic. Straightening of a coil after arterectomy may leave a residual twist requiring patch graft angioplasty. After mobilization of the artery and heparinization are completed, an arteriotomy is done on the distal common carotid and for a short distance onto the origin of the internal carotid. (Figure 7.) A shunt is passed distally into the internal carotid artery and then proximally into the common carotid and flow is reestablished. An obliquely resected segment of the internal carotid artery of appropriate length is excised so that the anastomotic lumen will be maximal. The sectioned internal carotid artery is sutured end-to-end to the common carotid artery. The internal shunt is important not only because of poor collateral circulation, which is frequently found in this lesion, but also because the splint facilitates ease of anastomosis. The internal shunt is removed through the arteriotomy in the common carotid artery. End-to-end internal carotid anastomosis is technically difficult because of its thin wall and narrow lumen. Completion arteriography is helpful in the problem case.
The American Journal of Surgery
Kinking of Internal Carotid Artery
Figure 6. Atthogram showing critical kinking of fhe left /CA withouf plaque resulfing in cerebra/ infarction.
Figure 5. Arteriogram illustrating a 360 ’ coil of the right /CA without plaquing which led to a stroke.
artery and cerebrovascular symptoms is sometimes difficult to establish, it is our belief that a more aggressive surgical approach may be warranted in this potentially disabling and even fatal condition.
Summary
Observations of a series of fifteen surgically treated coiled and kinked internal carotid arteries are reported. The kinked internal carotid artery may be clinically significant and can cause cerebral infarction, even in the absence of atherosclerosis. Each patient must be thoroughly investigated and evaluated individually. One must distinguish simple tortuosity without blood flow obstruction from critical kinking of the internal carotid artery. If a patient with angiographic confirmation is symptomatic and other causes are eliminated, surgical correction should be carefully considered, especially if rotational cerebral ischemia is present. The surgical treatment of choice is resection of the redundant internal carotid artery with reimplantation and thromboendarterectomy of any associated plaque. Kinking of the internal carotid artery may lead to aneurysm formation requiring a difficult surgical resection. Although the evidence for a precise causal relationship between kinking of the internal carotid Volume 134, July 1977
References 1. Eastcott HHG, Pickering FW, Rob CG: Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancef 2: 994, 1954. 2. Edington GH: Tortuositv of both internal carotid arteries. 6r A& J-2: 1526, 1901. 3. Riser MM, Geraud J, Ducoudray J, Ribaut L: Dolicho-internal carotid with vertiainous svndrome. Rev Neural 85: 10, 1951. 4. Hsu I, Kistin AD:‘Buckling of the great vessels. Arch Intern A&d 98: 712. 1956. 5. Quattlebaum JK Jr, Upson ET, Neville RL: Stroke associated with elongation and kinking of the internal carotid artery. Ann Surg 150: 824, 1959. 6. Freeman TR, Lippitt WH: Carotid artery syndrome due to kinking: Surgical treatment in forty-four cases. J A-ledAssoc Georgia 48: 573. 1959. 7. Derrick JR. Smith T: Carotid kinkina as a cause of cerebral insufficiency. Circulation 25: 849: 1962. 8. Metz H. Murrav-Leslie RM. Bannister RG. Bull JWD, Marshall J: Kinking of the internal carotid artery in relation to cerebrovascular disease. Lancer 1: 424, 1961. 9. Cioffi FA, Meduri M, Tomasello F, Bonavita V, Conforti P: Kinking and coiling of the internal carotid artery: clinicalstatistical observations and surgical perspectives. J Neurosurg Sciences 19: 15, 1975.
87
Vannix,
Joergenson,
and Carter
Figure 7. Diagram i/k&rating
surgical management of the kinked /CA. The /CA is sequentially resected and reimplanted onto the common carotid artery over a splint.
10. Najafi H, Javid H, Dye WS, Hunter JA. Julian DC: Kinked internal carotid artery. Arch Surg 89: 134, 1964. 11. Roberts B, Hardesty WH, Helling HE, et al: Studies on extracranial cerebral blood flow. Surgery 56: 826, 1964. 12. Brice JG, Dowsett DJ, Lowe RD: Haemodynamic effects of carotid artery stenosis. Br Med J 2: 1363, 1964. 13. Desai B, Toole JF: Kinks, coils, and carotids: a review. Stroke 6: 649, 1975.
Discussion John E. Connolly (Irvine, CA): Although we have had a strong interest in carotid endarterectomy over the last ten or fifteen years, I can find only two patients on whom we have operated for kinking of the internal carotid, and in both associated arteriosclerotic disease at the bifurcation of the carotid artery really prompted the procedure. However, we have seen coiling of the internal carotid in a number of our arch studies, which we have considered to be just an incidental finding. As the authors have pointed out, we must distinguish between elongation with coiling and elongation with true kinking. Although coiling is not uncommonly seen, the true kinking situation with obstruction of flow is rare. Kinking can be congenital, and we have seen it in studies on children; but we have usually seen it in adults, perhaps because we have little occasion to do arch studies in children. The evidence suggests that coiling, whether it is unilateral or bilateral, rarely results in symptoms unless there is also atherosclerotic occlusive disease in the carotid, vertebral, or basal arteries. True kinking of the internal carotid alone may occasionally cause symptoms of cerebrovascular disease, but other factors such as variation in blood pressure, alteration in neck position, and the presence of extra- or intracranial occlusive disease may contribute significantly to the symptoms noted. Absolute evidence for connection between kinking and symptoms does not exist, but it is suggestive enough to promljt careful consideration of surgery with excision in patientswho have recurrent cerebrovascular symptoms.
aa
Since the surgery usually involves a generous resection of the common carotid, it also requires removal of the most common site of atherosclerotic plaque formation. Therefore, removing the coil or the kink may not be the only reason for improvement. Of the five cases the authors detailed, three had associated atherosclerotic disease. In case I with the coil in the midcarotid and the plaque extending up to the coil, the patient had hemiplegia after the operation without removal of the coil. It is possible to have thrombosis of the carotid after routine carotid endarterectomy without a coil, for reasons that are not always apparent at reoperation. So, I am not positive that the kinking in case I can be incriminated absolutely as a cause of the hemiplegia. The following criteria for operation are suggested when the syndrome of kinked carotid exists: (1) There must be definite central nervous system symptoms. (2) There must be no other arteriographic abnormality. (3) There must be definite reduction in the lumen of at least 40 to 50 per cent of diameter. (4) Head motion or acute rotation of the head should produce the symptoms. These movements of the head should be carried out during arteriography to see the effect of the kinking. (5) Brain scan shows nothing abnormal. (6) There must be no evidence of associated atherosclerotic disease at the bifurcation. Regarding the technic, once one decides the patient requires surgery, we have come completely full circle on our technicagain employing local anesthesia plus Innova+ and Sublimazea. These agents give us a tremendous sense of security, because we can cross-clamp the carotid as long as we want, talk to the patient, and see if there is any neurologic deficit and on this basis decide whether we need to employ a shunt or not, We have been interested in the carotid stump pressure and have used it, but we have had at least a half dozen instances now where a stump pressure greater than 30 mm Hg.was associated with neurologic deficit with trial cross clamping, and in one instance the stump pressure was 70
The American Journal of Surgery
Kinking of Internal Carotid Artery
mm Hg. Quattlebaum has treated 120 cases of kinked carotid, all under local anesthesia. Perhaps Doctor Etheredge would like to comment on his technic of transecting the common carotid and doing the endarterectomy by the eversion technic. Then you can take out as long a piece of the carotid as you like. This might be an ideal way to treat coiling in certain patients., From a technical point of view, since coiling or kinking may be bilateral, one must be very careful with use of the authors’ technic bilaterally, because it could result in removal of both carotid bodies. Patients with both carotid bodies removed are unable to control their COz tension, which can be a tremendous handicap. Max R. Gaspar (Long Beach, CA): I checked with Doctors Movius and Rosental and in our 650 to 706 carotid thromboendarterectomies we can recall only six kinked or coiled internal carotid arteries. Maybe we are missing them. Maybe we are just too conservative in obtaining angiograms on patients. Noting in the authors’ series that eight patients had no bruits, I wonder how they decided in these patients to get an angiogram. Of course, as Doctor Connolly said, we see many coils and kinks on angiography, but most of them are not symptomatic, and it is very hard to have conclusive evidence that they do produce symptoms. The operation can be very difficult. Doctor Vannix is a superb surgeon, and the method he has chosen appears to be very good. The exposure can be difficult. To get way up on the internal carotid artery at the base of the skull is not easy, but without danger you can dissect lateral to the internal carotid, hugging it closely, and get up to the skull. Very often, in fact practically always, there is a little artery that comes from the external carotid which goes to the sternocleidomastoid. We call it the sling artery because it makes a sling around the glossopharyngeal, and if you cut that artery, it allows you to push the glossopharyngeal medially and to get high on the internal carotid. Passing a shunt in this situation can be rather difficult because, as Doctor Vannix said, these vessels are very thin and can be easily damaged. I can recall one patient who had an intramural hemorrhage and dissection of this portion of the vessel, and it was difficult to handle. Occasionally, this lesion occurs in children. We had such a case in which the pulsation on the side of the neck was alarming. It was corrected by resection of a portion of the common carotid artery. This is very much like Doctor Etheredge’s operation. Doctor Vannix mentioned that completion arteriography occasionally is necessary. We believe it is necessary in every case. I was happy to see he uses a shunt, and I hope he uses it in every carotid thromboendarterectomy. Doctor Vannix mentioned doing flow studies on these patients. Do you do flow studies on these particular patients all the time? Do you do them in all carotid thromboendarterectomies? It is always difficult to be sure that an anatomic lesion seen in an extracranial vessel is the cause of cerebrovascular symptoms, even if the symptoms disappear after the op-
Volume 134,July1977
eration. However, a completed stroke is so devastating that it behooves us to give serious consideration to any possible way to prevent a stroke, even in these kinked and coiled arteries. Samuel N. Etheredge (Oakland, CA): In our original paper on this subject, we warned that you either plan to correct it completely or you leave it alone. If you go halfway, particularly in the patient with atherosclerosis, you may get the vessel half-kinked and half-unkinked as you pull down a little bit, and you may change a coil into a kink. These vessels do not behave like normal arteries. They do not just pull down a little way. You might change what would be a coil into a kink, and this can be devastating. Our series is roughly half that of Doctor Gaspar; statistically we have similar percentages of kinking and coiling. Very few cases were truly symptomatic. Concerning the carotid body, differently from what Doctor Connolly mentioned, we have operated bilaterally many times and have not had any difficulty with our pa. tie& afterwards. To completely mobilize the carotid body, we divide it completely, on purpose, on both sides. That is not taking the carotid body out, but I think the effect would be just about the same. We have had no trouble with this. Richard Carter (closing): In answer to Doctor Gaspar, the backdrop for this series is based upon approximately 312 carotid endarterectomies, an incidence of 4.8 per cent. Central nervous system symptoms suggestive of carotid disease prompted the angiographic workup in all cases. Flow studies have been done on all cases, and intraluminal shunts have been routine. As has been pointed out before, most redundant internal carotid arteries are clinically unimportant unless mechanical blockage by kinking, associated plaque obstruction, or an atheromatous ulceration is present. Arterial kinking without an occlusive plaque may lead to cerebral ischemia and even infarction. To put this subject in perspective, most patients with kinking or redundancy require no surgical treatment whatsoever, but in a small number of patients kinking or buckling usually due to atherosclerosis and often associated with recurrent transient ischemic attacks may benefit from surgical correction. Adequate arteriography is an absolute prerequisitein preoperative selection of these people. Endarterectomy and resection of the redundant segment with reanastomosis appears to be the treatment of choice. Failure to deal with a significant kink at the time of the endarterectomy may lead to a poor result, as Sterling Edwards and others have also pointed out. It was our hope that this presentation would stimulate interest in this subject and help us to more clearly define judicious maximal surgery on the one hand and unjustified heroics on the other. Kinking of the internal carotid artery is not just an anatomic curiosity but may be a potentially lethal condition which presents challenging surgical problems.
89
Dramatic advances in diagnosis and surgical treatment of extracranial occlusive disease have developed since 1954 when Eastcott, Pickering, and Rob [I] reported the first successful carotid reconstruction. The cerebrovascular insufficiency in most cases is due to an underlying atheroma at the carotid bifurcation, which is usually segmental, well localized, and accessible to surgical correction. Although kinking of the internal carotid artery has been recognized for many years, the clinical importance of this phenomenon still remains controversial. The purpose of this report is to emphasize that this lesion is not an anatomic curiosity but a potentially disabling, even fatal condition which represents challenging clinical and technical problems. History
As early as 1898 tortuosity or kinking of the internal carotid artery was noted in four cases by Brown Kelly [2] in the Glasgow Medical Journal. He emphasized the potential danger in these cases of hemorrhage during tonsillectomy or drainage of a peritonsillar abscess. Recognizing the neurologic importance of the kinked internal carotid artery, Riser et al [3] in 1951 advocated arteriopexy by suturing the tortuous artery to the medial margin of the sternocleidomastoid muscle. The first direct surgical resection of a kinked internal carotid artery was reported by Hsu and Kistin [4] in 1956 and was unsuccessful. In 1959 Quattlebaum, Upson, and Neville [5] successfully resected the common carotid artery with end-to-end anastomosis in three patients with kinked internal carotid arteries. In the same year Freeman and Lippitt [6] reported ten additional cases. In 1962 Derrick and Smith [7] suggested that carotid kinking was a more common cause of strokes than previously recognized and recommended transplantation of the internal carotid artery beneath the sternocleidomastoid muscle. (Figure 1.) From the Departments of Surgery, University of Southern California, Los Angeles, and University of California, Irvine, Irvine, California. Reprint requests should be addressed to Robert S. Vannix, MD, Department of Surgery, University of Southern California, Los Angeles, California 90033. Presented at the Forty-EighthAnnual Meeting of the Pacific Coast Surgical Association, Palm Springs, California, February 20-23, 1977.
a2
Incidence and Etiology
By definition, coiling is elongation and redundancy of an internal carotid artery resulting in an exaggerated S-shape curvature or a circular configuration, whereas kinking is angulation of one or more segments of the artery, often associated with stenosis. Coiling is usually ascribed to embryologic causes and is generally asymptomatic, whereas kinking or buckling is predominantly associated with atherosclerosis and may be accompanied with recurrent transient ischemic attacks. Patients with cerebrovascular symptoms who have significant kinking of the internal carotid artery without plaques may require surgical correction, especially if aggravated by head rotation. Precise angiographic definition of coils and kinks is fundamental to determine if surgical correction is indicated. The incidence of coiling or kinking in the general population has been estimated as high as 16 per cent by Metz et al [8] based on a series of 1,000 angiograms. Cioffi et al [9] found this lesion in 10.1 per cent of 1,010 unselected angiograms, while Najafi et al [IO] reported a 5 per cent incidence of kinking in a series of 308 patients undergoing carotid procedures. There were 15 instances of kinking in our series of 312 carotid reconstructions (4.8 per cent). Cerebrovascular insufficiency associated with coils and kinks has been attributed to atherosclerosis and failure of embryologic development of the carotid arterial system. Coiling or looping has been observed in infants and fetuses. Embryologically the internal carotid artery is derived from the third aortic arch and the dorsal aortic root. In the embryo the internal carotid artery is normally kinked, and straightening occurs when the fetal heart and great vessels descend into the mediastinum. Inordinate differential growth of the internal carotid artery and the descending heart may lead to persistence of coiling and kinking which, when present, is bilateral in approximately 50 per cent of cases. Kinking of the internal carotid artery is almost always accompanied by atherosclerosis with subintimal deposits, loss of elasticity, elongation, and even formation of aneurysms. As the vessel elongates, it bows on fixed points at the base of the The American Journal of Surgery
Kinking of Internal Carotid Artery
J
1
Figure 1. A, tortuous Internal cafotld aftery ( tCA ) sutured to stemoc~ekiomastold muscle as advocated by Riser et al [ 31; 8, redundant /CA resected and reanastomosed [41; C, klnked ICA straightened by resecting common cafut/d artery segment [5]; D, relmplantatlon of ICA without resection (Lorkner); and E, segmental resection and reimplantation of /CA.
skull and thoracic inlet, and rotational ischemia is most likely to occur when the head is turned toward the side of the kink. Signs and Symptoms
Roberts et al [II] demonstrated that in man the internal carotid arteries carry about 90 per cent of cerebral blood flow. They further showed that as the head is moved through a normal range of movements, blood flow through the carotid or vertebral arteries may be obstructed. The neutral position of the head is the one most favorable for maximal cerebral flow. However, the presence of atherosclerosis, vertebral artery compression, anomalies of the circle of Willis, and blood pressure variations such as hypovolemia and antihypertensive drugs may make angulation more critical and produce transient ischemic attacks. In view of these facts, clinical and angiographic evaluation of these patients must be a dynamic one. Experimental studies have shown that graded occlusion of the carotid artery does not reduce cerebral blood flow until more than 90 per cent of the lumen has been obstructed [12]. The clinical symptoms associated with atheromatous ulceration, stenosis, or occlusion of the internal carotid artery are well described in the literature. Transient ischemic attack is a focal neurologic deficit due to a temporarily occluded blood supply to a portion of the brain. Although complete and spontaneous recovery usually occurs, a transient ischemic attack frequently precedes frank cerebral infarction. The patient with a kinked internal carotid artery may also present with a transient ischemic attack. Prophylactic surgery directed toward the clinically significant kinked internal carotid artery may prevent a completed stroke. Volume 134, July 1977
Surgical treatment is advisable when atheromatous ulceration, critical stenosis, and/or significant kinking with occlusion is present in the internal carotid artery when associated with appropriate cerebral vascular symptoms. Desai and Toole [13] observed that indisputable evidence for an exact causal connection between kinking of the internal carotid artery and cerebrovascular symptoms is difficult to establish. However, surgical correction should be carefully considered in patients with recurrent cerebrovascular episodes with internal carotid kinking in which other causes have been excluded, particularly in those exhibiting cervical rotational ischemia. Material and Methods This study is based on fifteen patients (12 male, 3 female) with kinking of the internal carotid artery, fourteen of whom were successfully treated within the past twenty-four months. The age range was thirty-one to seventy-five years (mean, 64 years). Preoperative evaluation of all patients included a complete neurologic evaluation, electroencephalogram, skull x-ray fiis, static and dynamic brain scan, cardiac evaluation, and complete extracranial and intracerebral angiography. Computerized axial tomography was obtained in the last seven patients treated. (Table I.) Case Reports
Salient clinical features of the kinked internal carotid artery are illustrated by the following case reports: Case I. A seventy-four year old normotensive diabetic woman without neck bruits had five transient syncopal episodes with visual changes during a six month period. Dynamic brain scan showed a marked decrease flow in the left carotid distribution. Arteriogram showed 70 per cent occlusive plaquing of the origin of the left internal carotid artery, with a tortuous coil above the plaque and retarda83
4 <
g
0,
E
9
b
s
ii
1
z
$
Clinical
71/F
75/F
63/F
58/F
62/F
57/F
74/F
65/F
AT
HL
El3
JB
EB
oc
BK
Note:
FS
CS
LR
CVA
71/F
69/F
60/M
fugax.
Amaurosir
31/M
WW
MM
fugar.
Amaurosis
71/F
hemlpareslr.
Mental
hemiparesis.
left
Translent
heml-
hemI.
Left
arm
= cerebravascular
rotation.
Syncope
accident;
on head
Right hemlparesls. Apharla.
monopares1r.
Syncope.
syncope. Poor coord#nation.
paresIs.
rtght
Transient pare*,*.
fugax.
Gait mstablllty. Syn. cope. Amaurow
Aphasia.
Right
deterloratlo”.
Syncope.
Gart tnstablllty.
Right
fugax.
hemipareris.
Amaurosls
Left
fugax.
Tranrtent
amaurosir
Residual
hemi-
paresis.
rrght
aprax\a.
Transient
loratlo”.
Men-
Poor
left arm.
DB
tal detc
cow&nation.
Amaurosls.
Monoplegla
car&d.
left
carotid.
No
No
= electrocardlogmm:
bruits.
No
No
Bruit
murmur.
Notmotensive.
heart
No bruits.
brult5.
No
Bruit
murmur.
carotid.
Normotensive.
heart
left
BP 180/84.
murmur.
Basal heart
left
BP 150/80.
bruits. No “l”r”l”rs.
Normotensive.
carotid.
Bruit
rys-
murmur.
Aortlc
right
Normotenswe.
tolic
t,d.
Bruit
caro-
No heart
left caro-
Bruit
neck
murmur. Normotenslve.
tld.
Bruit
BP 176/300.
left
BP 150/80.
brwts.
No
Bruit
hyperten-
510”. No
Lablle
bruits
Normotenwe.
carotid.
BP 156/90.
left
No
murmurs.
bruits.
heart
No
bruits.
No
Internal
Signs
of the
Normotenslve.
Kinking
EKG
with
episodes.
Symptoms
in 15 Patients
5 syncopal
Data
60/M
Sex
Age(w)/
I
RH
EL
Care
TABLE
ICA
Artery
Enlarged “onrpeclf-
ventricle.
scar.
normal.
ventricular
normal
normal.
EKG
carotrd
normal.
= Internal
EKG
old posscar.
EKG: terior
Hypertensmn.
EKG
normal.
olemia.
Hypercholester-
EKG
Ischemla.
EKG:
normal.
Drabetes.
EKG
hne abnormal.
enlargement. EKG: border-
Left
History of hypertension. AngIna.
Left calf claudication. EKG: LVH
EKG
largement.
scar. Cardiac
old posterior
EKG: en-
old myo-
normal.
Diabetes.
EKG
cardlal
EKG:
of anemia.
normal.
History
EKG
ic abnormalltles.
EKG:
left
Diabetes.
Associated Findings
Carotid
artery;
Flow
done
left
BP = blood
Normal
“orm21.
rschemia.
Preop
Normal
Portop
pressure;
Postop
cerebral
hemlspheilc
Ischemla.
Left
Normal.
Normal.
Normal
Normal
Not
left
cerebrum.
normal.
normal.
Preoo
Flow
decreased
oosterlor
Flow
Normal.
normal.
clearing
infarct.
nghtpost-
parletal 1975:
of defect.
Oct.
error
1975:
tld dlstributlo”.
Sept.
de.
I” left caro-
normal.
creased
Scan
Flow Study
Brain Scan and
LVH
atherosclerotic
ICA. angle
kinks
ICA.
= left
angled ICA. ventricular
right
2 acute
both orrg,”
plaque
80%
left
ICA.
carotlds.
Co11
occfus~ve
ICA.
hypertrophy.
kinks
orlgl”
C2 level. Internal Left ICA.
ICAs.
of both
right
ICA
atherosclerotic ICA.
Plaqu-
with right
klnkrng narrowing
kink
left
with
C2
or-
Two
ICA.
proximal
ICAs.
left
& clot
right
plaque Tight
Kinking
Tortuoslty
W-shaped
plaques
Kinking
significant
right
loop
of
1976:
left ICA with plaque origr”
plaqulng
ICA.
stenosis
and
plaque
& mlnimal
kinks both left ICA.
Co11 left
wth
Atheromatous
ICA.
Kink
Redundant Ing orjgi”
atherosclerotic
2 rrght
right
95% origin occlusion kinkrng. Ulcerative
ICA.
ICA.
2 sites.
lgin right ICA wrth 360” level. Kink of left ICA.
Ulcerated
ICA.
to right. left
June unchanged.
C2 level+tlght-
of left
atherosclerorls.
kInking
Mammal
Sharp
ICA
klnkr
hyperextension
right
head rot&o”
ened wtth
36O”co1l
angle
C2
1975:
3 cm an-
left
Left
orlgln
normal.
% occlusion
r,ght
80+
ICA
clot.
poststenotx
right
contalmng
level with eurysm
stenosrs
ICA
Sept.
& kInkIng
C3 level & re-
right
plaque.
elongation
wlthout
1974:
carotid
h,gh grade
ICAs
April
flow.
loop
orlgl”s--left
Complete
carotid
0ccIus1~e.
Internal
Internal
tarded
left
60-70%
Plaquing
Angiogram car&d
segmental
segmental
ICA.
rioht
segmental
plantation
cc/mi”. Segmental
left
ICA.
resectlo”
200 and ream
Flow
resectjon ICA.
and
and ream-
[CA. right ICA. endarterectomy
resection
lmplantatlo”
wth
plantation Left carotid
Segmental
resectton
and
and relm-
Flow
endarterectomy segmental
carotid
120
and
110
and
100
and
150
and
ream-
Flow wth ICA.
left ICA. cc/ml”.
reimplantation
wth
Left
Flow
resectto” ICA. resection
plantation Flow 250+
Flow
resectlo”
i20 ccfmi”. _ Segmental resection
olantatio”
cc/min. Segmental
ICA.
resectlo”
endarterectomv segmental
carotid
reimplqntation
wth
Left
cc/mm.
Flow
endarterectomy reimplantatlo”
wth
cc/min. Left carotid
ICA.
resection
125
reimFlow
with
re-
reimplanpatch
endarterectomy relmplantatron
with
carotid
ccjrmn. Left
with Vein cc/mm.
ICA.
with
120
end-
no
de-
No
and reim-
endarterectomy
left
segmental
carotid
relmplantatro”
wth
Right
cc/ml”.
pfantatlo”
ICA. 200
resection
graft. Segmental
right Flow
tatron
resection
ICA.
Segmental
resection
plantation
ICA
Flow
with
endarterectomy
anastomosis.
carot,d
with
angiogram:
reoperatlo” lntraop
aneurysm
Stat
postop
endarterectomy. Immediate
segmental
Left
cc/nun.
to-end
Resected
flap.
clotting.
CVA.
resectlo”.
Left
Treatment
7th.
CVA.
improvement
recovery
Complete
Complete
Complete
Complete
Complete
Complete
Complete
Complete
recovery.
recovery.
recovery.
recovery
recovery.
recovery.
recovery
recovery
Continued imorovement presurglcal CVA.
Unchanged.
10th.
nerve
from
from
12th.
dysfunc-
and aphasia.
recovery.
9th,
recovery
presurglcat
Continued
Complete
Comolete
Complete
tion:
craneal
hemiparesis
Transient
Right
Results
$
L
_z
2
d
Kinking of Internal Carotid Artery
tion of blood flow. (Figure 2.) Left carotid endarterectomy without carotid resection was performed. In the immediate postoperative period the patient had transient recovery and then developed right hemiparesis. Angiogram indicated no evidence of an intimal flap, and at reoperation thrombectomy of the clotted coiled artery was performed. Comment. This patient illustrates the necessity of simultaneously correcting both the occluding intimal plaque and the coiled carotid artery. The decrease in left hemispheric perfusion was due to the coil and not the occlusive plaque. Case II. A sixty year old normotensive man without neck bruits had sudden left arm monoparesis with transient amaurosis. Retrograde arch study showed elongation and kinking of both internal carotid arteries with no evidence of plaque or clot formation. (Figure 3, left.) Seventeen months later the symptoms recurred with persistent weakness in the left arm. Brain scan suggested an infarct in the right posterior parietal region. Repeat scan one month later indicated almost complete clearing. Angiography showed high grade stenosis of the right internal carotid artery with poststenotic aneurysm formation and intraluminal clot. (Figure 3, right.) At surgery, a 3 X 2 cm aneurysm was resected and the internal carotid artery was reconstructed by end-to-end anastomosis, establishing a flow of 150 ml per minute. The patient recovered satisfactorily. Repeat angiography nine months later showed the right internal carotid artery to be normal with the left internal carotid still kinked and elongated. Comment. This patient illustrates that kinking can cause cerebral symptoms of the carotid type that may lead to a completed stroke. Furthermore, kinking may also produce poststenotic aneurysm and clot formation. An important technical consideration is the ease of resecting and reimplanting a kinked internal carotid artery compared with resecting an aneurysm with reanastomosis at the base of the skull. Case III. A seventy-one
year old normotensive woman with a left carotid bruit had a right transient hemiparesis with partial aphasia and amaurosis. Brain scan was normal Retrograde arch study showed 80 per cent occlusion of the left internal carotid origin with two acutely angled kinks above the plaque. (Figure 4.) At surgery, a carotid endarterectomy and segmental resection with reimplantation of the left internal carotid artery was performed without sequelae. Comment. This amplifies the importance of recognizing the coexistence of atherosclerotic changes with marked kinking. Endarterectomy weakens the wall further at the site of the kink and tends to accentuate the angulation. It is manditory to treat both problems at the time of surgical correction. Case IV. A thirty-one year old normotensive man without cervical bruits was chasing a fly ball and suddenly fell with a left hemiparesis and visual aberrations. Brain scan was normal. Retrograde arch study showed the right internal carotid artery had a 360’ coil which tightened with
Volume 134, July 1977
Figure 2. Case 1.Illustration of plague in /CA with a complete loop and confirmatory arteriogram.
head rotation to the right and with hyperextension. (Figure 5.) CAT scan showed nothing abnormal. Resection of a segment of the right internal carotid artery with reimplantation and a vein patch graft at the site of maximum coiling was performed. Postoperative flow was 250 ml per minute and recovery was uneventful. Comment. This case is unique because it demonstrates that a coil may cause major cerebral vascular symptoms even in a young person. It also shows that the angiogram can be used dynamically to demonstrate positional narrowing of the coiled or kinked artery. Coiling or kinking may be present without any associated atherosclerosis. Case V. A seventy-one year old normotensive woman without carotid bruits was admitted with a persistent right hemiplegia. Brain scan showed a reduction of flow to the left cerebral hemisphere. Retrograde arch study showed tortuosity, elongation, and an acutely angulated left internal carotid artery at two sites without atherosclerotic ulceration or occlusion. (Figure 6.) Segmental resection and reimplantation of the left internal carotid artery was done five weeks later. There was no associated atherosclerosis although a recent clot was present. Postoperative flow was 125 ml per minute and she made continued improvement from the antecedent cerebrovascular accident. Comment. This case illustrates that a cerebral infarction can occur from a kinked carotid artery in the absence of atherosclerosis. SurgicalTreatment
Meticulous anesthetic and surgical technics are mandatory for the successful treatment of cerebrovascular disease. The coiled or kinked internal carotid artery presents special technical problems. The artery wall in the
85
Vannix, Joergenson, and Carter
Figure 3. Drawings and angiograms showing: Left, elongation and kinking of right /CA without plaque. Right, stenosis with poststenotic aneurysm and intraluminal clot.
Figure 4. Retrograde arch study showing two critical kinks above plaque formation.
66
coiled or kinked segment is very thin and can be disrupted with minimal dissection. Furthermore, the artery must be mobilized from its bifurcation to the base of the skull and. all fibrous bands completely severed. If adequate mobilization is not completed, accentuation of the kink may result after resection of proximal internal carotid artery and reanastomosis. A tension-free anastomosis is axiomatic. Straightening of a coil after arterectomy may leave a residual twist requiring patch graft angioplasty. After mobilization of the artery and heparinization are completed, an arteriotomy is done on the distal common carotid and for a short distance onto the origin of the internal carotid. (Figure 7.) A shunt is passed distally into the internal carotid artery and then proximally into the common carotid and flow is reestablished. An obliquely resected segment of the internal carotid artery of appropriate length is excised so that the anastomotic lumen will be maximal. The sectioned internal carotid artery is sutured end-to-end to the common carotid artery. The internal shunt is important not only because of poor collateral circulation, which is frequently found in this lesion, but also because the splint facilitates ease of anastomosis. The internal shunt is removed through the arteriotomy in the common carotid artery. End-to-end internal carotid anastomosis is technically difficult because of its thin wall and narrow lumen. Completion arteriography is helpful in the problem case.
The American Journal of Surgery
Kinking of Internal Carotid Artery
Figure 6. Atthogram showing critical kinking of fhe left /CA withouf plaque resulfing in cerebra/ infarction.
Figure 5. Arteriogram illustrating a 360 ’ coil of the right /CA without plaquing which led to a stroke.
artery and cerebrovascular symptoms is sometimes difficult to establish, it is our belief that a more aggressive surgical approach may be warranted in this potentially disabling and even fatal condition.
Summary
Observations of a series of fifteen surgically treated coiled and kinked internal carotid arteries are reported. The kinked internal carotid artery may be clinically significant and can cause cerebral infarction, even in the absence of atherosclerosis. Each patient must be thoroughly investigated and evaluated individually. One must distinguish simple tortuosity without blood flow obstruction from critical kinking of the internal carotid artery. If a patient with angiographic confirmation is symptomatic and other causes are eliminated, surgical correction should be carefully considered, especially if rotational cerebral ischemia is present. The surgical treatment of choice is resection of the redundant internal carotid artery with reimplantation and thromboendarterectomy of any associated plaque. Kinking of the internal carotid artery may lead to aneurysm formation requiring a difficult surgical resection. Although the evidence for a precise causal relationship between kinking of the internal carotid Volume 134, July 1977
References 1. Eastcott HHG, Pickering FW, Rob CG: Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancef 2: 994, 1954. 2. Edington GH: Tortuositv of both internal carotid arteries. 6r A& J-2: 1526, 1901. 3. Riser MM, Geraud J, Ducoudray J, Ribaut L: Dolicho-internal carotid with vertiainous svndrome. Rev Neural 85: 10, 1951. 4. Hsu I, Kistin AD:‘Buckling of the great vessels. Arch Intern A&d 98: 712. 1956. 5. Quattlebaum JK Jr, Upson ET, Neville RL: Stroke associated with elongation and kinking of the internal carotid artery. Ann Surg 150: 824, 1959. 6. Freeman TR, Lippitt WH: Carotid artery syndrome due to kinking: Surgical treatment in forty-four cases. J A-ledAssoc Georgia 48: 573. 1959. 7. Derrick JR. Smith T: Carotid kinkina as a cause of cerebral insufficiency. Circulation 25: 849: 1962. 8. Metz H. Murrav-Leslie RM. Bannister RG. Bull JWD, Marshall J: Kinking of the internal carotid artery in relation to cerebrovascular disease. Lancer 1: 424, 1961. 9. Cioffi FA, Meduri M, Tomasello F, Bonavita V, Conforti P: Kinking and coiling of the internal carotid artery: clinicalstatistical observations and surgical perspectives. J Neurosurg Sciences 19: 15, 1975.
87
Vannix,
Joergenson,
and Carter
Figure 7. Diagram i/k&rating
surgical management of the kinked /CA. The /CA is sequentially resected and reimplanted onto the common carotid artery over a splint.
10. Najafi H, Javid H, Dye WS, Hunter JA. Julian DC: Kinked internal carotid artery. Arch Surg 89: 134, 1964. 11. Roberts B, Hardesty WH, Helling HE, et al: Studies on extracranial cerebral blood flow. Surgery 56: 826, 1964. 12. Brice JG, Dowsett DJ, Lowe RD: Haemodynamic effects of carotid artery stenosis. Br Med J 2: 1363, 1964. 13. Desai B, Toole JF: Kinks, coils, and carotids: a review. Stroke 6: 649, 1975.
Discussion John E. Connolly (Irvine, CA): Although we have had a strong interest in carotid endarterectomy over the last ten or fifteen years, I can find only two patients on whom we have operated for kinking of the internal carotid, and in both associated arteriosclerotic disease at the bifurcation of the carotid artery really prompted the procedure. However, we have seen coiling of the internal carotid in a number of our arch studies, which we have considered to be just an incidental finding. As the authors have pointed out, we must distinguish between elongation with coiling and elongation with true kinking. Although coiling is not uncommonly seen, the true kinking situation with obstruction of flow is rare. Kinking can be congenital, and we have seen it in studies on children; but we have usually seen it in adults, perhaps because we have little occasion to do arch studies in children. The evidence suggests that coiling, whether it is unilateral or bilateral, rarely results in symptoms unless there is also atherosclerotic occlusive disease in the carotid, vertebral, or basal arteries. True kinking of the internal carotid alone may occasionally cause symptoms of cerebrovascular disease, but other factors such as variation in blood pressure, alteration in neck position, and the presence of extra- or intracranial occlusive disease may contribute significantly to the symptoms noted. Absolute evidence for connection between kinking and symptoms does not exist, but it is suggestive enough to promljt careful consideration of surgery with excision in patientswho have recurrent cerebrovascular symptoms.
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Since the surgery usually involves a generous resection of the common carotid, it also requires removal of the most common site of atherosclerotic plaque formation. Therefore, removing the coil or the kink may not be the only reason for improvement. Of the five cases the authors detailed, three had associated atherosclerotic disease. In case I with the coil in the midcarotid and the plaque extending up to the coil, the patient had hemiplegia after the operation without removal of the coil. It is possible to have thrombosis of the carotid after routine carotid endarterectomy without a coil, for reasons that are not always apparent at reoperation. So, I am not positive that the kinking in case I can be incriminated absolutely as a cause of the hemiplegia. The following criteria for operation are suggested when the syndrome of kinked carotid exists: (1) There must be definite central nervous system symptoms. (2) There must be no other arteriographic abnormality. (3) There must be definite reduction in the lumen of at least 40 to 50 per cent of diameter. (4) Head motion or acute rotation of the head should produce the symptoms. These movements of the head should be carried out during arteriography to see the effect of the kinking. (5) Brain scan shows nothing abnormal. (6) There must be no evidence of associated atherosclerotic disease at the bifurcation. Regarding the technic, once one decides the patient requires surgery, we have come completely full circle on our technicagain employing local anesthesia plus Innova+ and Sublimazea. These agents give us a tremendous sense of security, because we can cross-clamp the carotid as long as we want, talk to the patient, and see if there is any neurologic deficit and on this basis decide whether we need to employ a shunt or not, We have been interested in the carotid stump pressure and have used it, but we have had at least a half dozen instances now where a stump pressure greater than 30 mm Hg.was associated with neurologic deficit with trial cross clamping, and in one instance the stump pressure was 70
The American Journal of Surgery
Kinking of Internal Carotid Artery
mm Hg. Quattlebaum has treated 120 cases of kinked carotid, all under local anesthesia. Perhaps Doctor Etheredge would like to comment on his technic of transecting the common carotid and doing the endarterectomy by the eversion technic. Then you can take out as long a piece of the carotid as you like. This might be an ideal way to treat coiling in certain patients., From a technical point of view, since coiling or kinking may be bilateral, one must be very careful with use of the authors’ technic bilaterally, because it could result in removal of both carotid bodies. Patients with both carotid bodies removed are unable to control their COz tension, which can be a tremendous handicap. Max R. Gaspar (Long Beach, CA): I checked with Doctors Movius and Rosental and in our 650 to 706 carotid thromboendarterectomies we can recall only six kinked or coiled internal carotid arteries. Maybe we are missing them. Maybe we are just too conservative in obtaining angiograms on patients. Noting in the authors’ series that eight patients had no bruits, I wonder how they decided in these patients to get an angiogram. Of course, as Doctor Connolly said, we see many coils and kinks on angiography, but most of them are not symptomatic, and it is very hard to have conclusive evidence that they do produce symptoms. The operation can be very difficult. Doctor Vannix is a superb surgeon, and the method he has chosen appears to be very good. The exposure can be difficult. To get way up on the internal carotid artery at the base of the skull is not easy, but without danger you can dissect lateral to the internal carotid, hugging it closely, and get up to the skull. Very often, in fact practically always, there is a little artery that comes from the external carotid which goes to the sternocleidomastoid. We call it the sling artery because it makes a sling around the glossopharyngeal, and if you cut that artery, it allows you to push the glossopharyngeal medially and to get high on the internal carotid. Passing a shunt in this situation can be rather difficult because, as Doctor Vannix said, these vessels are very thin and can be easily damaged. I can recall one patient who had an intramural hemorrhage and dissection of this portion of the vessel, and it was difficult to handle. Occasionally, this lesion occurs in children. We had such a case in which the pulsation on the side of the neck was alarming. It was corrected by resection of a portion of the common carotid artery. This is very much like Doctor Etheredge’s operation. Doctor Vannix mentioned that completion arteriography occasionally is necessary. We believe it is necessary in every case. I was happy to see he uses a shunt, and I hope he uses it in every carotid thromboendarterectomy. Doctor Vannix mentioned doing flow studies on these patients. Do you do flow studies on these particular patients all the time? Do you do them in all carotid thromboendarterectomies? It is always difficult to be sure that an anatomic lesion seen in an extracranial vessel is the cause of cerebrovascular symptoms, even if the symptoms disappear after the op-
Volume 134,July1977
eration. However, a completed stroke is so devastating that it behooves us to give serious consideration to any possible way to prevent a stroke, even in these kinked and coiled arteries. Samuel N. Etheredge (Oakland, CA): In our original paper on this subject, we warned that you either plan to correct it completely or you leave it alone. If you go halfway, particularly in the patient with atherosclerosis, you may get the vessel half-kinked and half-unkinked as you pull down a little bit, and you may change a coil into a kink. These vessels do not behave like normal arteries. They do not just pull down a little way. You might change what would be a coil into a kink, and this can be devastating. Our series is roughly half that of Doctor Gaspar; statistically we have similar percentages of kinking and coiling. Very few cases were truly symptomatic. Concerning the carotid body, differently from what Doctor Connolly mentioned, we have operated bilaterally many times and have not had any difficulty with our pa. tie& afterwards. To completely mobilize the carotid body, we divide it completely, on purpose, on both sides. That is not taking the carotid body out, but I think the effect would be just about the same. We have had no trouble with this. Richard Carter (closing): In answer to Doctor Gaspar, the backdrop for this series is based upon approximately 312 carotid endarterectomies, an incidence of 4.8 per cent. Central nervous system symptoms suggestive of carotid disease prompted the angiographic workup in all cases. Flow studies have been done on all cases, and intraluminal shunts have been routine. As has been pointed out before, most redundant internal carotid arteries are clinically unimportant unless mechanical blockage by kinking, associated plaque obstruction, or an atheromatous ulceration is present. Arterial kinking without an occlusive plaque may lead to cerebral ischemia and even infarction. To put this subject in perspective, most patients with kinking or redundancy require no surgical treatment whatsoever, but in a small number of patients kinking or buckling usually due to atherosclerosis and often associated with recurrent transient ischemic attacks may benefit from surgical correction. Adequate arteriography is an absolute prerequisitein preoperative selection of these people. Endarterectomy and resection of the redundant segment with reanastomosis appears to be the treatment of choice. Failure to deal with a significant kink at the time of the endarterectomy may lead to a poor result, as Sterling Edwards and others have also pointed out. It was our hope that this presentation would stimulate interest in this subject and help us to more clearly define judicious maximal surgery on the one hand and unjustified heroics on the other. Kinking of the internal carotid artery is not just an anatomic curiosity but may be a potentially lethal condition which presents challenging surgical problems.
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