Traumatic

Internal

Carotid

Artery

Occlusion

Case Report—



Koji TODOROKI, Tetsuhiko ASAKURA*, Reizo KANEMARU and Kenichiro TAJITSU Kanemaru Neurological Hospital, Miyazaki; *Department of Neurosurgery, Faculty of Medicine, University of Kagoshima, Kagoshima

Abstract A 20-year-old tomography nal carotid symptoms,

was admitted

but eventually

occlusion severe

male

demonstrated artery occlusion is relatively

head trauma

comatose

he died from

rare,

is recommended.

Key words:

trauma,

delayed

but is serious

and vascular

angiography

immediately

occlusion,

internal

carotid

traumatic

and requires

artery,

Traumatic internal carotid artery (ICA) occlusion is well known but rare. Early diagnosis and treatment are essential because of the high mortality and mor bidity. However, current use of computed tomog raphy (CT) has reduced the use of angiography after trauma, and therefore early diagnosis has be come less frequent. Here, we report a patient with traumatic subarachnoid hemorrhage (SAH) and traumatic ICA occlusion who died of delayed traumatic apoplexy. Report

A 20-year-old male was involved in a dent on July 13, 1989. He was emergency hospital, then transferred 1 hour after the accident. On admission, he was comatose,

motorcycle acci admitted to an to our hospital with anisocoria

(left > right), and demonstrated a decorticate posture. Physical examination revealed multiple cuts and scratches on the face, multiple scratches on the backs of both hands and knees, and a laceration on Received Author's

December present

9, 1991;

address:

Accepted

K. Todoroki, Japan.

M.D.,

April

early

anticoagulants

Introduction

Case

after

a motorcycle

accident.

Initial

computed

traumatic subarachnoid hemorrhage, and the diagnosis of traumatic inter was established by angiography. Conservative management improved his apoplexy. diagnosis

Traumatic

are contraindicated,

arterial

occlusion,

internal

and treatment.

carotid

For patients

and frequent

recanalization,

artery with

follow-up

apoplexy

the right thigh. No neck lesions were observed. Plain skull x-ray films showed no fracture. CT scans showed SAH in the basal cistern, quadri geminal cistern, ambient cistern, interhemispheric fissure, and Sylvian fissure, and hematoma in the fourth, third, and lateral ventricles (Fig. 1A). Right carotid angiograms showed stenosis of the ICA at the level of the atlas, and complete occlusion just distal to the ophthalmic artery (Fig. 2A). Left carot id angiograms visualized the right anterior cerebral artery (ACA) and the right middle cerebral artery (MCA) through the anterior communicating artery (AComA) (Fig. 2B). Right vertebral angiograms showed the right MCA via the posterior communi cating artery (PComA) (Fig. 2C). Angiography did not demonstrate any obvious lesions as the source of the hemorrhage, such as an aneurysm or arterio venous malformation. After admission, he received conservative therapy with steroids, glycerol, dextran, and cerebral metabolism activators. No anticoagulant therapy was given. The next day, the anisocoria and decor ticate posture disappeared, but persistent left hemiplegia developed. Follow-up CT scans on day 4

16, 1992

Department

of Neurosurgery,

Akune-Shimin

Hospital,

Akune,

Kagoshima,

showed cerebral infarction in the right MCA ter ritory, and on day 12 focal hemorrhagic infarction in the same area (Fig. 1B). Angiography was repeated on day 8. Right carotid angiograms revealed partial recanalization of the previously occluded ICA, but stenoses, possibly due to vasospasm or extension of thrombus, at the right M, and right A, portions (Fig. 3A). Left carotid angiograms visualized the right ACA via the AComA, but not the right MCA (Fig. 3B). Right vertebral angiograms visualized the right vertebrobasilar artery and right ICA (Fig. 3C). The angiograms were not very clear due to body move ment, but no aneurysm was observed. The disturbance of consciousness gradually im proved, and on day 25 he opened his eyes, responded to simple orders, and could give his name and age. However, early in the afternoon on day 33 (August 15) he became comatose and developed irregular respiration. CT scans revealed massive hematoma filling the whole cerebral ventricular system with the Fig. 2 A: Right carotid angiograms, showing stenosis of the ICA at the level of the atlas, and com plete occlusion just distal to the ophthalmic artery. B: Left carotid angiogram, visualizing the right ACA and right MCA through the AComA. C: Right vertebral angiogram, showing the right MCA via the PComA.

major site in the third ventricle, and acute hydrocephalus (Fig. 1C). Immediate emergent bi lateral ventricular drainage was undertaken. During the operation, fresh blood was discharged from the drainage tube. Postoperative CT scans showed that the hematoma had enlarged, with marked ven tricular enlargement (Fig. 1D). The coma persisted postoperatively, and he died on day 40 (August 22). No autopsy was performed. Discussion

Fig. 1

A: CT scan on admission, showing severe SAH. B: Follow-up CT scan on day 12, showing focal hemorrhagic infarction in the right MCA area. C: Preoperative CT scan on day 33, revealing massive hematoma filling the whole cerebral ventricular system with the major site in the third ventricle, and hydrocephalus. D: Postoperative CT scan, showing enlarged hematoma compared with preoperative CT scan, and marked ventricular enlargement.

Traumatic ICA occlusion has various causes,') in cluding chiropractic manipulation," digital carotid compression, 13) and motor vehicle accidents. Jernigan and Gardner') found that more than half of these patients were involved in motor vehicle ac cidents. Crissey and Bernstein4) described four types of craniocervical injury producing carotid artery in juries: 1) a direct blow to the anteromedial neck in about 50% of cases; 2) a blow to the side of the head causing hyperextension and rotation of the head and neck, resulting in stretching the carotid artery across

carotid obstruction. The lucid interval is especially characteristic. Yamada et al. 18)reported that more than 90% of patients developed symptoms more than 1 hour after trauma, and some patients developed symptoms after 1 week or several months. 1,10,11,19) The initial diagnosis is often delayed because of the low incidence of traumatic ICA occlusion and the lucid interval. Remembering the possibility of this condition during patient management will achieve early diagnosis. In our patient, CT immedi ately after admission demonstrated SAH. Angiography was used to search for any vascular le sion causing the hemorrhage, such as an aneurysm. Accordingly, the right ICA occlusion was detected in an early stage. Conservative treatment or surgical intervention has been recommended, but this is still controver sial. 2,6,8-10,14,15,17-19) Generally, conservative treatment

Fig. 3

A: Right

carotid

recanalization but severe portions. the right right right

stenoses

revealing

at the right

partial

occluded

ICA,

M, and right

A,

B: Left carotid angiogram, showing ACA via the AComA, but not the

MCA.

showing

angiograms,

of the previously

the

C: right

Right

vertebral

vertebrobasilar

angiogram, artery

and

ICA.

the transverse process of the third cervical vertebra or the bony mass of the first and second cervical vertebrae; 3) intraoral trauma causing blunt carotid injury; and 4) basal or other skull fractures resulting in thrombosis of the intrapetrous ICA. In our pa tient, the carotid artery injury may have resulted from rotation and hyperextension of the head, or shearing strains where the ICA leaves the cavernous sinus,") because no wounds, contusions, or ec chymoses were observed on the neck. The prognosis of traumatic ICA occlusion is poor, and the mortality is 30-40%.9'18) Bok et a1.3)reported five deaths among eight patients. The morbidity is also high.',") To improve the outcome, early diagnosis and treatment are required. The following initial findings are characteristic'': 1) a lucid interval; 2) lateral neck hematoma, particu larly in the anterior triangle; 3) Horner's syndrome prior to other neurological deficits (probably because of stretching or compression of the sympathetic ganglia which accompany the ICA); 4) transient ischemic attacks; and 5) monoparesis or hemiparesis in an alert patient or an unconscious trauma patient without abnormalities on head CT, indicating

(anticoagulants, etc.) is suitable where the collateral circulation is well developed, but thrombectomy or external carotid-internal carotid bypass should be considered where the collateral circulation is poor. Patients with well-developed collateral circulation but repeated transient ischemic attacks may require ICA ligation or balloon occlusion.") Surgical treat ment should be performed before irreversible ischemic changes occur in the brain. Accordingly, an early diagnosis is also necessary in these cases. Con servative treatment for patients with serious in tracranial lesions, as in our case, should not include anticoagulants because of the possibility of hemor rhage, for example from a traumatic aneurysm. Recanalization of traumatic ICA occlusion has oc curred in Bergquist et a!.,2) and Willer and Bradac,'2) and our cases. Therefore, mild symptoms due to ICA occlusion indicate conservative treatment with monitoring by angiography. In our patient, angiography was repeated after establishing the diagnosis of traumatic SAH. The second angiograms revealed no noticeable lesions other than severe stenoses at the right M1 and Al portions. The neurological symptoms gradually improved, so no further angiogram was taken. He died of delayed traumatic apoplexy on day 40 after the injury. Angiography showed no aneurysm, but traumatic aneurysm due to vascular damage is the most likely cause of the delayed traumatic apoplexy. Thus, more frequent follow-up angiography is recommended. The recent development of noninvasive magnetic resonance angiography may allow easier diagnosis and follow-up of traumatic ICA occlusion, which will lead to an increase in such cases in the future.

ing

References

non-penetrating

Emerg

1)

2)

3)

4)

5)

Beatty RA: Dissecting hematoma of the internal carotid artery following chiropractic cervical manipulation. J Trauma 17: 248-249, 1977 Bergquist BJ, Boone SC, Whaley RA: Traumatic dissection of the internal carotid artery treated by EC-IC anastomosis. Stroke 12: 73-76, 1981 Bok APL, Kieck CF, de Villiers JC: Head injury asso ciated with carotid occlusion due to blunt cervical trauma. S Afr J Surg 22: 43-50, 1984 Crissey MM, Bernstein EF: Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 75: 543-549, 1974 Davis JM, Jimmerman RA: Injury of the carotid and vertebral arteries. Neuroradiology 25: 55-69, 1983

6) Dragon R, Saranchak H, Lakin P, Strauch G: Blunt injuries to the carotid and vertebral arteries. Am J Surg 141: 497-500, 1981 7)

8)

9)

10)

11)

Jernigan WR, Gardner WC: Carotid artery injuries due to closed cervical trauma. J Trauma 11: 429-435, 1971 Kaufmann HH, Lind TA, Clark DS: Non penetrating trauma to the carotid artery with sec ondary thrombosis and embolism. Treatment by thrombolysin. Acta Neurochir (Wien) 37: 219-244, 1977 Krajewski LP, Hertzer NR: Blunt carotid artery trauma. Report of two cases and review of the literature. Ann Surg 191: 341-346, 1980 Little JM, May J, Vanderfield GK, Lamond S: Traumatic thrombosis of the internal carotid artery. Lancet 1: 926-930, 1969 Mooney RP, Bessen HA: Delayed hemiparesis follow

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6: 341-345,

artery

trauma.

Am

J

1988

Miiller H, Bradac GB: Bilateral occlusion of the ex tracranial internal carotid artery secondary to closed neck injury. Neurochirurgia (Stuttg) 27: 53-55, 1984 Nelson DA, Mahru MM: Death following digital carotid artery occlusion. Arch Neurol (Chicago) 8: 640-643, 1963 Perry MO, Snyder WH, Thal ER: Carotid artery in juries caused by blunt trauma. Ann Surg 192: 74-77, 1980 Popowich L: Blunt carotid artery trauma associated with maxillofacial injuries: Report of three cases. J Oral Maxillofac Surg 42: 462-465, 1984 Sedzimir CB: Head injury as a cause of internal carotid thrombosis. J Neurol Neurosurg Psychiat 18: 293-296, 1955 Towne JB, Neis DD, Smith JW: Thrombosis of the internal carotid artery following blunt cervical trauma. Arch Surg 104: 565-568, 1972 Yamada S, Kindt GW, Youmans JR: Carotid artery occlusion due to nonpenetrating injury. J Trauma 7: 333-342, 1967 Zelenock GB, Kazmers A, Whitehouse WM, Graham LM, Erlandson EE, Cronenwett JL, Lindenauer SM, Stanley JC: Extracranial internal carotid artery dissec tions: Non iatrogenic traumatic lesions. Arch Surg 117: 425-432, 1982

Address reprint requests to: K. Todoroki, ment of Neurosurgery, Akune-Shimin Akasegawa,

Akune,

Kagoshima

M.D., Depart Hospital, 4513

899-16,

Japan.

Traumatic internal carotid artery occlusion--case report.

A 20-year-old male was admitted comatose immediately after a motorcycle accident. Initial computed tomography demonstrated traumatic subarachnoid hemo...
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