Traumatic aneurysms of the supraclinoid internal carotid artery

Transcription

1 J Neurosurg 57: , 1982 Traumatic aneurysms of the supraclinoid internal carotid artery Report of two cases EUGENIO POZZATI, M.D., GIULIO GAIST, M.D., AND FRANCO SERVADEI, M.D. Division of Neurosurgery, Bellaria Hospital, Bologna, Italy ~t This paper describes two patients with traumatic aneurysms of the supraclinoid internal carotid artery, which occurred after a closed-head injury and without demonstrable basal skull fracture. In the first case, the traumatic origin of the aneurysm was demonstrated by repeat angiograms. The second case documents the formation of a giant, traumatic, true aneurysm of the supraclinoid carotid artery over a period of less than 2 months; there was an associated traumatic partial occlusion of the vessel proximal to the aneurysm. The mechanisms of injury of the supraclinoid carotid artery are discussed. KEY WORDS arterial occlusion giant aneurysm internal carotid artery traumatic cerebral aneurysm head injury M OST traumatic intracranial aneurysms are located on the middle meningeal artery and peripheral branches of the anterior and middle cerebral arteries. 1,3-5,8,9'13,lS,16,1s,2~ Traumatic aneurysms of the intracranial internal carotid artery (ICA) are encountered mainly in its petrous and cavernous portion, 3,24,zs and are often associated with basal skull fractures; the supraclinoid segment is seldom affected. 13,3~ Giant traumatic aneurysms of the intracranial ICA have been reported only twice; 5,22 in both instances, the infra- and supraclinoid portions of the vessel were affected, and there was an associated carotid-cavernous fistula. We present two young patients with traumatic aneurysms of the supraclinoid ICA. Our Case 2 is the first reported instance of a giant, traumatic, true aneurysm of this arterial segment. Case 1 Case Reports This 17-year-old boy was admitted to our hospital 2 hours after being involved in a traffic accident. He was in a stuporous state and had right hemiparesis. Computerized tomography (CT) revealed a left temporal laceration without significant mass effect. Blood was present in the interpeduncular cistern and in the left Sylvian fissure. A left carotid angiogram showed narrowing of the cervical ICA and an intimal irregularity of the supraclinoid segment of the ICA (Fig. 1 left). Skull x-ray films revealed a fracture of the ascending ramus of the left mandible. His condition gradually improved. On the 5th hospital day, paresis of the left sixth nerve was noted. A second left carotid angiogram demonstrated a large aneurysm of the supraclinoid ICA (Fig. 1 right). Right carotid angiography with compression of the left cervical carotid artery showed good cross filling of the left hemisphere. Graded common carotid occlusion was carried out 2 days later. The patient's postoperative course was uneventful. On a follow-up neurological examination 3 years later, the left sixth nerve paresis and the right hemiparesis had completely resolved. Case 2 This 16-year-old boy was admitted to our hospital 3 hours after a motorcycle accident. He was unconscious, responding purposefully to deep pain, and a slight right hemiparesis was present. ACT scan revealed a low-density area in the left temporoparietal region and diffuse subarachnoid bleeding. Blood was also present in the left suprasellar cisterns, and it was 41 8 J. Neurosurg. / Volume 57/September, 1982

2 Traumatic supraclinoid internal carotid aneurysms FIG. 1. Case 1. Left carotid angiograms, lateral view. Left: There is segmental narrowing (arrow) of the supraclinoid internal carotid artery consistent with spasm or local dissection. Right: Five days after the injury, a large aneurysm of the supraclinoid carotid artery was revealed at the site of the narrowing. interpreted as a part of the widespread traumatic subarachnoid hemorrhage. Skull x-ray films were normal. The patient's condition gradually improved, and 3 days later he was awake. A fluent dysphasia was noted, but the right hemiparesis had improved slightly. A control CT scan taken at this time was similar to the previous one. Ten days after the accident, he was transferred to a rehabilitation unit. Fifteen days later, the patient began to complain of loss of vision in the left eye, and had polyuria and polydipsia. When readmitted to our hospital 10 days later, he was blind in the left eye and the right temporal field was lost. The left optic disc was atrophic, and there was pallor of the right optic disc. ACT scan revealed a round mass with mixed density in the suprasellar region, outlined by a slightly hyperdense rim; after the administration of contrast material, enhancement of the rim and of the periphery of the lesion ("target" sign) was noted (Fig. 2). No calcification was seen. These findings supported the diagnosis of a giant aneurysm. Left common carotid angiography disclosed a traumatic aneurysm of the cervical carotid artery; the petrous and cavernous portions of the artery were normal. Just distal to the ophthalmic artery, the ICA was nearly completely occluded, with the residual lumen filling the part of the aneurysm that was not thrombosed (Fig. 3). Right carotid angiography with compression of the left carotid artery demonstrated good cross filling of the left hemisphere, with the anterior cerebral arteries stretched around the mass (Fig. 4). A direct attack upon an aneurysm of this size was considered a formidable task, and graded ICA occlusion was successfully carried out over the following days. The postoperative course was uneventful. Control CT scan 7 days later demonstrated complete thrombosis of the aneurysm. No further surgical treatment was given. Over the following months, the patient's diabetes insipidus gradually cleared and there Fro. 2. Case 2. Computerized tomography scan with contrast material shows enhancement of both the rim and the periphery of the lesion ("target" sign) representing the lumen of a partially thrombosed giant aneurysm. was marked improvement of the visual field in his right eye. The left eye remains blind. Discussion Traumatic aneurysms of intracranial vessels may be true, false, dissecting, or "mixed." In true aneurysms, intima, elastica, and media are disrupted, and only the adventitia is intact and allowed to expand. False aneurysms are the result of a full-thickness interruption of the arterial wall with formation of a perivascular hematoma, which subsequently develops a fibrous wall. 22 Dissecting aneurysms result from the formation of a false lumen between the intima and J. Neurosurg. / Volume 57 / September,

3 E. Pozzati, G. Gaist and F. Servadei FIG. 3. Case 2. Left common carotid angiograms, lateral (left) and anteroposterior (right) views, revealing a traumatic aneurysm of the cervical internal carotid artery (double arrow) and a partial occlusion of the supraclinoid carotid artery just distal to the ophthalmic artery, with the residual lumen (arrow) filling the nonthrombosed part of the giant aneurysm. FIG. 4. Case 2. Right carotid angiogram showing good cross filling of the left hemisphere. The anterior cerebral arteries are stretched over the giant aneurysm. internal elastica. 2~ "Mixed" aneurysms develop when true aneurysms rupture, with formation of a secondary false aneurysm. TM Trauma to the cerebral vessels may be direct or indirect, occurring in both closed and open head injuries. These aspects are treated elsewhere 5,9,2~ and will not be discussed in detail in this paper. In both our patients, the aneurysm was located on the ICA just distal to the ophthalmic artery. Several factors may contribute to the formation of traumatic aneurysms at this point. It is conceivable that, in the absence of a basal skull fracture, the injury to the ICA may be caused by blunt contusion produced by a severe impingement of the artery on the overlying anterior clinoid process, or by overstretching or sudden torsion of the vessel during brain movements within the calvaria at the moment of trauma.16,27 Both these mechanisms of injury may produce an intimal rent sufficient to initiate a local dissection (see Fig. 1) and related sequelae. 16,27 Following head trauma, an overstretching of the intracranial ICA seems to occur just at the level of the midportion of the artery, between the distal segment of the siphon, which is fixed by the anterior and middle cerebral arteries to the shifting brain, and the proximal carotid artery, which is fixed at the cavernous sinus. TM Furthermore, the blood stream subjects the superior wall of the ICA just distal to the ophthalmic artery to the maximum hemodynamic thrust J. Neurosurg. / Volume 57 / September, 1982

4 Traumatic supraclinoid internal carotid aneurysms Posttraumatic occlusion of the supraclinoid carotid artery occurs rarely. 2 In our Case 2, the almost complete thrombosis of the supraclinoid ICA proximal to the giant aneurysm was caused most likely by an embolus migrating from the traumatic aneurysm in the cervical carotid artery. In this circumstance, the partial occlusion of the vessel probably saved the aneurysm from rupture, promoting massive intraluminal thrombosis. Other mechanisms may be proposed. Prolonged spasm of the damaged artery may have promoted the partial thrombosis by slowing down the blood flow, 2 or compression produced by the bulk of the aneurysm upon the vessel might have partially occluded the artery? 5,29 In intracranial arteries, the strength of the arterial wall is in the internal lamina elastica rather than in the adventitia. As postulated by Shaw and Alvord 27 and confirmed by our Case 2, the intimal and medial tear may produce aneurysm formation in addition to the occlusion of the lumen by a dissecting aneurysm or thrombus formation. Case 2 provides some information regarding the mechanics of growth of giant aneurysms, and demonstrates that these lesions may reach a giant size in a short period of time. There are three possible mechanisms that may be responsible for enlargement of the aneurysms: 1) progressive expansion of an original small aneurysm due to continuous dilatation produced by the jet of the blood stream; 2) the recurrence of peripheral hemorrhages from a richly vascularized wall; '~ and 3) repeated intramural, intrathrombotic hemorrhages from tiny blood vessels without endothelial lining which are formed in the organized thrombus. 29 The formation of a giant aneurysm is deemed to be slow and insidious, spanning a period of years. 7,'9 Only Fried and Yballe 11 described the rapid formation of a giant aneurysm from a hematoma in communication with an intracranial aneurysm of originally moderate size. Although histopathological examination is lacking, we believe that our Case 2 documents how an aneurysm may enlarge very rapidly by simple distension of the aneurysmal wall. Even if it is not known for certain that in Case 2 a saccular aneurysm was not present before the accident, our reasons for considering this aneurysm to be of traumatic origin are the young age of the patient and the accidental and severe nature of the trauma. Sometimes the outer margin of giant aneurysms shows an intense enhancement on CT scan with administration of contrast material. 6,17,26 Byrd, et al, 6 believed that the enhancement of the rim in a giant aneurysm represents enhancement of the adventitia as well as the circulating contrast material within the vasa vasorum of the aneurysmal wall. On this basis, it is reasonable to assume that our Case 2 represents a true rather than false traumatic aneurysm, the enhanced rim being the distended adventitia of the vessel and not the fibrous wall of a perivascular hematoma. The direct attack upon traumatic aneurysms of the supraclinoid ICA within a few days of injury is considered technically difficult, and it may be catastrophic due to both the deep location and the fragility of the lesion hidden below the anterior clinoid process. '3,3~ According to Yonas and Dujovny, 3~ these are the reasons why extracranial carotid occlusion, with or without a bypass procedure, seems to be the treatment of choice in the early management of these aneurysms. Acknowledgment The authors are grateful to Mr. P. Mantovani for preparing the photographs. References 1. Acosta C, Williams PE Jr, Clark K: Traumatic aneurysms of the cerebral vessels. J Nenrosnrg 36: , Ajir F, Tibbetts JC: Post-traumatic occlusion of the supraclinoid internal carotid artery. Neurosurgery 9: , Araki C, Handa H, Handa J, et al: Traumatic aneurysm of the intracranial extradural portion of the internal carotid artery. Report of a case. J Neurosurg 23:64-67, Asari S, Nakamura S, Yamada O, et al: Traumatic aneurysm of peripheral cerebral arteries. Report of two cases. J Neurosurg 46: , Benoit BG, Wortzman G: Traumatic cerebral aneurysms. Clinical features and natural history. J Neurol Neurosurg Psychiatry 36: , Byrd SE, Bentson JR, Winter J: Giant intracranial aneurysms simulating brain neoplasms on computed tomography. J Comput Assist Tomogr 2: , Cuatico W, Cook AW, Tyshchenko V, et al: Massive enlargement of intracranial aneurysms following carotid ligation. Arch Neurol 17: , Drake CG: Subdural haematoma from arterial rupture. J Neurosurg 18: , Fleischer AS, Patton JM, Tindall GT: Cerebral aneurysms of traumatic origin. Surg Neurol 4: , Fodstad H, Liliequist B, Wirell S, et al: Giant serpentine intracranial aneurysm after carotid ligation. Case report. J Neurosurg 49: , Fried LC, Yballe A: Rapid formation of giant aneurysm: case report. J Neurol Neurosurg Psychiatry 35: , Gibo H, Lenkey C, Rhoton AL Jr: Microsurgical anatomy of the supraclinoid portion of the internal carotid artery. J Neurosurg 55: , Hirsch JF, David M, Sachs M: Les anrvrysmes artrriels traumatiques intracraniens. Neurochirurgie 8: , Jacques S, Shelden CH, Rogers DT Jr, et al: Posttraumatic bilateral middle cerebral artery occlu:ion. Case report. J Neurosurg 42: , Laun A: Traumatic aneurysms, in Pia HW, Langmaid C, Zierski J (eds): Cerebral Aneurysms. Advances in Diagnosis and Therapy. Berlin/Heidelberg/New York: Springer-Verlag, 1979, pp Laurent JP, Cheek WR, Mims T, et al: Traumatic intracranial aneurysm in an infant: case report and review of the literature. Neurosurgery 9: , 1981 J. Neurosurg. / Volume 57/September,

5 E. Pozzati, G. Gaist and F. Servadei 17. Lavyne MH, Kleefteld J, Davis KR, et ah Giant intracranial aneurysms of the anterior circulation: clinical characteristics and diagnosis by computed tomography. Neurosnrgery 3: , Menezes AH, Graf C J: True traumatic aneurysm of anterior cerebral artery. Case report. J Neurosurg 40: , Morley TP, Barr HWK: Giant intracranial aneurysms: diagnosis, course and management. Clin Neurosurg 16:73-94, Parkinson D, West M: Traumatic intracranial aneurysms. 3 Neurosurg 52:11-20, Paul GA, Shaw CM, Wray LM: True traumatic aneurysm of the vertebral artery. Case report. 3 Neurosnrg 53: , Reddy SVR, Sundt TM Jr: Giant traumatic false aneurysm of the internal carotid artery associated with a carotid-cavernous fistula. Case report..i Neurosurg 55: , Sadar ES, Jane JA, Lewis LW, et ah Traumatic aneurysms of the intracranial circulation. Surg Gyneeoi Obstet 137:59-67, Salar G, Mingrino S: Traumatic intracranial internal carotid aneurysm due to gunshot wound. Case report.,1 Neurosurg 49: , Sarwar M, Batnitzky S, Schechter MM: Tumorous aneurysms. Neuroradiology 12:79 97, Schubiger O, Valavanis A, Hayek J: Computed tomography in cerebral aneurysms with special emphasis on giant intracranial aneurysms. 3 Comput Assist Tomogr 4:24-32, Shaw CM, Alvord EC Jr: Injury of the basilar artery associated with closed head trauma. 3 Neurol Neurosurg Psychiatry 35: , Teal JS, Bergeron RT, Rumbaugh CL, et ah Aneurysm of the petrous or cavernous portions of the internal carotid artery associated with nonpenetrating head trauma. J Neurosurg 38: , Terao H, Muraoka I: Giant aneurysm of the middle cerebral artery containing an important blood channel. Case report. J Neurosurg 37: , i Yonas H, Dujovny M: "True" traumatic aneurysm of the intracranial internal carotid artery: case report. Neurosurgery 7: , 1980 Manuscript received March 3, Address reprint requests to: Eugenio Pozzati, M.D., Divisione di Neurochirurgia, Ospedale Bellaria, Bologna, Italy. 422 J. Neurosurg. / Volume 57 / September, 1982