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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 7  |  Page : 14-23

Traumatic aneurysms of the intracranial and cervical vessels: A review

1 Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Neuroradiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication3-Mar-2016

Correspondence Address:
Sanjay Behari
Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.178032

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 » Abstract 

Traumatic intracranial aneurysms (TICA) are rare in occurrence, constituting less than 1% of the total cases of intracranial aneurysms. Cervical posttraumatic aneurysms arising from major blood vessels supplying the brain are also extremely rare. Their variable locations, morphological variations and the presence of concomitant head injury makes their diagnosis and treatment a challenge. In this review, we discuss the epidemiology, etiology, classification and management issues related to TICA as well as traumatic neck aneurysms and review the pertinent literature.

Keywords: Head injury; radiology; surgery; traumatic intracranial aneurysm; vascular injury

How to cite this article:
Bhaisora KS, Behari S, Godbole C, Phadke RV. Traumatic aneurysms of the intracranial and cervical vessels: A review. Neurol India 2016;64, Suppl S1:14-23

How to cite this URL:
Bhaisora KS, Behari S, Godbole C, Phadke RV. Traumatic aneurysms of the intracranial and cervical vessels: A review. Neurol India [serial online] 2016 [cited 2023 Feb 1];64, Suppl S1:14-23. Available from: https://www.neurologyindia.com/text.asp?2016/64/7/14/178032

 » Introduction Top

Traumatic aneurysms are rare lesions; they develop as an outpunching or ballooning from the vessel wall following brain or cervical injury. Direct injury to the vessel may cause dissection of the vessel or transmural vessel damage, which results in a contained hematoma or a pseudo-aneurysm. Blunt or penetrating cerebrovascular trauma is increasingly being diagnosed with resulting aneurysm formation in the intracranial and extracranial vasculature.

An intracranial aneurysm that develops after trauma presents a unique challenge both during the diagnostic as well as the treatment phase. Traumatic pseudoaneurysms are usually associated with blunt or shearing forces on the vessel against a fixed surface of the skull base; or, as a direct injury over the convexity of the skull. [1],[2],[3],[4],[5]

The clinical consequences of the presence of an extracranial vessel aneurysm are also poorly understood. These aneurysms are often associated with a high velocity cerebrovascular trauma. Traumatic aneurysms of the extracranial internal carotid artery (ICA) and vertebral artery (VA) have been reported in approximately 15-23% and 4-8% cases of traumatic cerebrovascular injury, respectively. [6]

Traumatic intracranial aneurysms often present with either immediate or delayed intracranial bleed, which may be intraparenchymal in cases of distal aneurysms. Aneurysms, which are in relation to the skull base may present with intracranial nerve palsies, epistaxis, subarachnoid hemorrhage and mass effect. If left untreated, a mortality rate of approximately 30-50% due to the sudden precipitation of hemorrhage, has been quoted in various studies. [7],[8] Extracranial aneurysms usually present with an embolic stroke, recurrent episodes of headache, transient ischemic attacks, and as they progressively grow in size, they may also present with a lump in the neck. Various treatment modalities from open surgery to endovascular occlusion have been used to tackle these rare lesions but due to the paucity of literature, an adequate treatment protocol has not been defined. In this review, we discuss the epidemiology, classification, clinical presentation and treatment modalities of traumatic pseudoaneurysms.


In the available literature, traumatic intracranial aneurysms account for less than 1% of all intracranial aneurysms. 20-30% of all TICA occur in patients younger than 18 years of age. [2],[9] They constitute 30% of all pediatric aneurysms. [9] The true incidence of traumatic intracranial aneurysms is, however, not known, with various studies quoting a variable incidence ranging from 3.2-3.6% to 5.7%, and even 42%. [9] In younger patients, the ratio of male-to-female patients is 1:1; in adults, however, the male patients predominate with the ratio being 17:4. [2],[5] Mao et al., in their recent series of 15 patients with traumatic aneurysms following blunt head trauma reported a 0.64% incidence with the male:female ratio being 11:4. [10] Blunt cerebrovascular trauma may present in 1% of cases admitted with a high speed trauma. [11] Foremen et al., reported 13 cases of extracranial aneurysms after a cerebrovascular trauma with the mean age being 32.4 years and the male:female ratio being 1:3.3. [6]

Mechanism of injury

TICA may result from a variety of trauma to the head with the etiology including road traffic accidents, sports-related injury, direct blunt or penetrating injury to the head or even warfare injury. The most common type of trauma reported in literature is a road traffic accident [Figure 1], [Figure 2], [Figure 3] and [Figure 4]. [2],[6],[12]
Figure 1: ( a and b) Patient 1: A 24-year male patient, following blunt trauma to the neck, developed progressive neck swelling with recurrent transient ischemic attacks. His CT scan and MRI were normal. The internal carotid artery DSA showed a large traumatic aneurysm arising from the proximal internal carotid artery in the neck

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Figure 2: Patient 1: (a-c) Endovascular coiling of the segment of internal carotid artery, proximal, at the point of origin, and distal to the traumatic aneurysm was carried out; and, (d) as there was a good cross flow from the contralateral internal carotid artery with filling of both the anterior and middle cerebral artery on the side of parent vessel occlusion, the patient tolerated the procedure well and had no neurological deficits

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Figure 3: Patient 2: A 25-year old patient, who presented with an intermittently bleeding neck swelling, with a history of remote neck trauma; (a and b) coronal contrast CT scan showing a partially thrombosed internal carotid artery aneurysm in the neck with a calcified rim; (c) contralateral internal carotid artery angiogram with ipsilateral internal carotid artery balloon occlusion test showing a good cross flow from the opposite side; (d) the DSA showing filling of the lumen of the pseudoaneurysm with a rim of thrombus all around; (e) contrast CT showing the laminations of the thrombosed aneurysm; and, (f) the three dimensional CT scan showing the location of the aneurysm in the neck relative to the cervical vertebral bodies

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Figure 4: Patient 2: Following endovascular proximal occlusion of the ipsilateral internal carotid artery, the large aneurysm was surgically excised; (a) the large aneurysm in the neck with skin excoriation seen; (b) the exposed pseudo-capsule of the aneurysm dissected from the soft tissue structures of the neck; (c) the aneurysmal wall was opened and the thrombus evacuated; and, (d) the distal end of the ipsilateral internal carotid artery was also ligated to prevent retrograde bleeding and the aneurysmal wall excised to decrease mass effect

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Blunt head injury frequently occurs in pediatric patients because of the soft cranial bone and more mobile structures in the intracranial compartment relative to adult patients. Due to the higher mobility, the shearing forces cause more injury to the vessels. [9] Mao et al., reported 15 cases of TICA after blunt head injury with the mean age of their patients being 28.7 ± 10.5 years (the age range being 15 to 53 years), which is higher than that reported in literature [10] [Table 1]. Traumatic cerebrovascular injury is defined as blunt traumatic injury to the carotid artery (CA) or vertebral artery (VA) resulting in aneurysm formation, or dissection, occlusion or transection of the parent vessel. Focal dilatation of the wall of CA or VA following blunt trauma is defined as a traumatic aneurysm. Blunt high-speed trauma is the most common mechanism for the formation of an extracranial aneurysm. During a road traffic accident, injury results from rapid deceleration, with the neck hyperextended or flexed as well as rotated. [13] The CA or VA occasionally may suffer iatrogenic injury during neurosurgical or angiographic procedures that involve vessel exposure, passage of hardware near or through the artery, or direct manipulation of the vessel. ICA injury can also occur during anterior cervical approaches and while achieving proximal control of the vessel during surgery for clipping of an aneurysm. The VA can be specifically injured during surgery for craniovertebral junction pathologies and also during cervical spine instrumentation. Endoscopic third ventriculostomy and endoscopic endonasal surgery may also result in a TICA. The overall incidence of iatrogenic injury ranges from 0.3 to 0.5% of the total cases of TICA. [2],[3],[4],[5],[6],[7],[8],[9],[10]
Table 1: Traumatic intracranial aneurysms due to blunt injury recently reported in literature

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Penetrating injuries, which traverse the territory or course of a vessel, or cross midline structures, also have a high propensity to develop aneurysms and is a common cause of TICA in adults. [7],[9],[14] In one series, out of the 109 patients with a stab injury to the head, 74 patients underwent an angiography and 11 (14.9%) patients were detected to be having a TICA. [14] A study reporting on the effects of high-velocity missile injury on 223 patients revealed an aneurysm in 8 (3.6%) patients. [14] All these injuries either caused a direct impact on the artery or resulted in an abnormal stretching of the arterial wall.

Another mechanism for the formation of TICA is the occurrence of skull base fracture. An intracavernous ICA aneurysm is usually associated with a skull base fracture. An infraclinoid CA or a vertebrobasilar artery aneurysm are the most common aneurysms associated with a skull base fracture. The infraclinoid ICA forms the transition zone between the relatively fixed cavernous segment and the relatively mobile supraclinoid segment of ICA. During trauma, movement of this transitional zone against the anterior clinoid process may lead to trauma to the vessel with a subsequent aneurysm formation. [5],[15],[16]

Traumatic aneurysms in the distal circulation are more commonly found in association with the anterior cerebral artery (ACA), and less commonly, with the middle cerebral artery (MCA). These aneurysms form either due to direct injury to the vessel by the associated skull fracture, or by movement of the brain and vessel against a relatively fixed structure like the falx or the tentorium. A skull fracture is the most common cause for a distal MCA aneurysm formation, and movement of the vessel against the rigid falx is the most common cause for a distal ACA aneurysm formation. [5],[10],[17],[18],[19]

Ventureya and Higgins proposed four etiopathological categories that have been found to be responsible for the formation of TICA. These include closed head injury, missile injury, penetrating injury, and iatrogenic injury. [10]


A TICA has been classified into 3 types based on the histopathological findings. The types include the true, false and mixed types of aneurysms. A true aneurysm is characterized by intimal injury with a variable involvement of the internal elastic lamina and media. This produces a weakness in the wall, which in due course of time, aided by intraluminal hemodynamic changes, forms an aneurysm. [5],[7],[20] In false aneurysm, there is transmural injury to the vessel wall with formation of a contained hematoma outside the vessel wall. There is associated false lumen formation that is responsible for the aneurysmal dilation. [12],[15],[21] The 'false' aneurysm is most common posttraumatic aneurysm associated with penetrating injury. [5],[21] The mixed type of aneurysm initially starts as a true aneurysm. It subsequently ruptures and forms a contained hematoma and has a false lumen. [5],[15],[20],[21] Various authors have described the mixed type of aneurysm as a saccular aneurysm associated with dissection of the parent vessel. [11],[22],[23]

Extracranial aneurysms can be of true, false and dissecting type. Extracranial vessels are the most common sites for dissecting aneurysms. In these cases, the intimal injury causes the hematoma to spread inside the vessel wall. The mechanism of injury in the cases having a dissecting aneurysm include a blunt cerebrovascular trauma associated with head injury or an iatrogenic injury such as a diagnostic or therapeutic angiographic intervention, exposure of the cervical ICA during anterior cervical approaches or during proximal control for aneurysm surgery.

As TICA is a rare entity, not enough literature is available regarding the actual incidence of the various histological types of these aneurysms. The histological classification has little significance in the overall management of these aneurysms because an active intervention is required in all patients regardless of the histological type of the aneurysm present.


Traumatic intracranial aneurysms are most commonly found in the anterior circulation with the supraclinoid ICA and the anterior cerebral artery (especially the pericallosal and the callosomarginal segment) being the most common sites reported in literature. [5],[10] Other sites like the vertebrobasilar artery, middle cerebral artery and middle meningeal artery are also reported in literature. [5],[10],[17],[18],[19] Based on their location, Buckingham et al., initially classified these aneurysms into the skull base and peripheral TICAs. [2]

Posttraumatic aneurysm may also be classified, according to their site, as aneurysms that are present on vessels proximal to the circle of Wills and those that occur on vessels distal to the circle of Wills. [5],[24],[25],[26]

Those TICAs that are proximal to the circle of Wills include the ones on (a) infraclinoid carotid artery, (b) supraclinoid carotid artery, and (c) vertebrobasilar artery. Those TICAs that are distal to the circle of Willis include the ones on (a) subcortical arteries, and (b) cortical arteries. Mao et al., further classified peripheral TICAs into the perifalx and distal cortical aneurysms. The perifalx aneurysms are located on vessels around the falx cerebri and cerebelli as well as the tentorium, and include TICAs on the distal ACA, posterior cerebral artery and superior cerebellar artery. The distal cortical aneurysms involve cortical branches of the MCA or ACA due to injury caused by depressed or linear fractures. [10]

Clinical presentation

Traumatic aneurysms, like other aneurysms, may present with subarachnoid hemorrhage. The average time from the occurrence of the initial trauma to the precipitation of hemorrhage is approximately 21 days, although a period of as long as 7 years has also been reported before the occurrence of hemorrhage. [5],[7],[25] The pattern of presentation depends upon the site of aneurysm formation. An infraclinoid aneurysm usually presents early with massive epistaxis, progressive cranial nerve palsies or diabetes insipidus. [2],[5],[7],[10],[25] Maurer et al., proposed that the triad of unilateral blindness, cranial base fractures, and recurrent epistaxis aids in the diagnosis of ICA aneurysms situated at the cranial base. [18] Bavinzski et al., reported the prevalence rates of massive epistaxis and unilateral blindness associated with these skull base aneurysms as being 71% and 51%, respectively. [27] The presentation of supraclinoid, distal ACA and distal cortical TICAs is delayed and usually severe in intensity. [28] The supraclinoid TICAs usually present with cranial nerve deficits, sudden severe headache and/or altered sensorium due to the presence of subarachnoid hemorrhage or delayed intracerebral bleed [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], and [Figure 12]. [4],[10],[28] Perifalx aneurysm usually also present with the same clinical manifestations. [4],[10],[25],[28] Distal cortical aneurysms are more likely to be diagnosed before they rupture. These aneurysms are usually associated with skull fractures, with growth of these aneurysms giving rise to a growing skull fracture-like appearance. [29],[30] When presenting with the symptoms of hemorrhage, they usually have an intracerbral bleed. Buckingham et al., reported a series of 11 cases of distal cortical aneurysms associated with blunt head injury; seven (63.6%) of these patients presented with evidence of hemorrhage. Proximal aneurysms most commonly presented with a subarachnoid hemorrhage or an intracerbral bleed; only 20.5% were diagnosed before the hemorrhage occurred. [2]
Figure 5: Patient 3: (a - e) A 33 - year old male, following a road traffic accident, had moderate to severe headache with vomiting and blood in sputum, 14 years ago. (a-e) His coronal contrast CT scan at that time had shown a suprasellar aneurysm

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Figure 6: Patient 3: (a-d) His MR angiogram done 14 years ago had shown an aneurysm arising from the cavernous and paraclinoid segment of left ICA. He underwent endovascular intervention with coiling and obliteration of the left ICA and had an immediate symptomatic improvement

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Figure 7: Patient 3: After 7 years of the endovascular intervention, he sustained another road traffic accident, following which he had profuse epistaxis with unconsciousness. Urgent haemodynamic resuscitation with CT scan was performed. After 4 days, he developed rapid onset, left sided complete visual loss that did not recover; (a and b) The contrast axial CT scan images; and (c and d) the bone windows of axial CT scan showed the recurrence of suprasellar aneurysm with expansile bony erosion in the region

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Figure 8: Patient 3: (a) The left internal carotid artery DSA; and, (b) the enlarged view showed the pseudoaneurysm arising form the cavernous segment and genu with a little collateralization from the ethmoidal branches of external carotid artery. There was hardly any supply to the brain from the left internal carotid artery

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Figure 9: Patient 3: (a) The right carotid angiogram showed the filling of bilateral anterior cerebral arteries from the right side; (b) the anteroposterior; and, (c) lateral images of vertebrobasilar circulation shows a good left sided filling of the middle cerebral artery via the posterior communicating artery from the vertebrobasilar system

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Figure 10: Patient 3: Due to the good cross flow, and in view of visual loss, surgical decompression of the aneurysm was done after proximal ligation of the left internal carotid artery in the neck; (a) left Sylvian dissection; (b and c) optic nerve and distal internal carotid artery is seen. The aneurysm is bulging the cavernous sinus wall and pressing on the optic nerve (arrow); and (d) the anterior clinoid is being drilled

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Figure 11: Patient 3: The operative steps continued; (a) the outer shell of anterior clinoid is being removed; (b) the dura is covering the aneurysm which was extending to cavernous and paraclinoidal regions; (c) the aneurysm is decompressed and packed with muscle and its wall plicated; and, (d) the distal internal carotid artery is also clipped proximal to its posterior communicating artery branch to trap the aneurysm

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Figure 12: Patient 3: Follow up DSA; (a and b) Right internal carotid artery angiogram showing a good cross flow to the left side. The remnant of aneurysm is seen; (c) left internal carotid artery angiogram showing the adequately trapped artery with non-filling of the aneurysm; (d and e) the posterior circulation is adequately filling the left internal carotid artery circulation through the posterior communicating arteries

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Mao et al., in their series of 15 patients with a posttraumatic aneurysm had 9 patients with an aneurysm on the infraclinoid ICA and 5 patients with an aneurysm on the supraclinoid ICA. Epistaxis and ophthalmic manifestations were the most common presenting complaints, which were present in 7 patients each. One patient had an aneurysm in the perifalx region of ACA, and this patients presented with a delayed intracerbral bleed. [10]

Extracranial aneurysms may present with headache, neck pain, transient ischemic attacks (TIAs), ischemic stroke, pulsatile tinnitus and cranial nerve palsies. Many patients may, however, be asymptomatic. As the size of these aneurysms increases, they may also present as a neck mass [Figure 13], [Figure 14], [Figure 15] and [Figure 16]. Various studies have shown that, when left untreated, 50% of these aneurysms present with stroke. [6] Saccular extracranial aneurysms tend to have a greater incidence of embolic stroke than fusiform aneurysms due the increased stasis of blood within these aneurysms. Foreman et al., in their series of 13 patients with 26 traumatic aneurysms (9 saccular, 17 fusiform), reported that 3 (23.1%) patients presented with an ischemic stroke. Rupture of an extracranial aneurysm is a rare event. [6] Akiyama et al., reported the rupture of an extracranial ICA aneurysm of size 4 cm, that was managed by endovascular stenting. Horner's syndrome may also be an associated finding in these patient with an extracranial ICA injury. [31]
Figure 13: Patient 4: A 16-year old child following trauma, presented with recurrent epistaxis and dysphagia; (a-f) axial contrast MRI showing a large partially thrombosed aneurysm in the infratemporal region

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Figure 14: Patient 4: (a and b) MR angiogram showing the large aneurysm in the internal carotid artery with mass effect

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Figure 15: Patient 4: (a) Contralateral internal carotid artery injection showing non-filling of anterior cerebral artery and no cross flow; and (b and c) the internal carotid artery ipsilateral to the aneurysm being compressed due to the large aneurysm in the infratemporal region

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Figure 16: Patient 4: (a and b) The posterior circulation is adequately supporting the brain ipsilateral to the side of the internal carotid artery aneurysm; (c) proximal internal carotid artery endovascular occlusion on the side of the aneurysm was performed

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The diagnosis of TICA requires maintaining a high index of suspicion. In the pre- computed tomographic (CT) scan era, when angiography was the primary investigation performed for facilitating the diagnosis of head injured patients, TICAs were more promptly diagnosed. At present, as CT scan images are being utilized as the primary investigation of choice in head injured patients, there are more chances that TICA might be overlooked. [19] In all patients with head injury, postoperative patients with delayed neurological deterioration, those who have had a delayed hemorrhage, those with an unexplained major arterial bleed during evacuation of a hematoma, and those who have sustained penetrating head and neck injuries, may need to be further evaluated for the presence of a TICA. [5],[9],[28]

The conventional cerebral angiography is the 'gold standard' investigation for the diagnosis of TICA but due the rarity of cases detected, the exact timing of when to perform the angiography, is a matter of debate. Various studies have quoted that patient with a history of blunt trauma and presenting with recurrent epistaxis, vision loss or progressive cranial nerve palsies, should undergo a cerebral angiography as soon as possible. [5],[10],[19] Patients with penetrating injury require especial attention, with various studies in literature recommending the performance of a routine angiography after 2 weeks. [5],[15],[19],[21] It is believed that post-traumatic aneurysms takes some time to develop so angiography should be delayed until the start of the second week after the occurrence of trauma. [19] Asari et al., found that the mean duration before the precipitation of hemorrhage from a peripheral traumatic aneurysm was 21 days (range 5 days-10 years) after the injury. [24] Haddad et al., recommended an immediate angiography for all cases of missile injury with no exit wound in whom there was an associated intracerbral hematoma. [32] Trevou et al., recommended cerebral angiography soon after admission in patients who sustained a penetrating injury, and patients with vasospasm, or presenting with the characteristic 'vessel cut off' sign on angiography, should undergo a second angiogram. [33] More recent literature has shown that patients with an initial negative angiography have shown the growth of the aneurysm on a subsequent angiography. Most authors have, therefore, recommended a delayed angiogram after 2 weeks of sustaining the traumatic injury. [5],[15],[19],[20],[21]

The criteria for performing a digital subtraction angiography (DSA) following penetrating head injury and closed head injury have been elucidated. [1] DSA should be d in patients in whom the following conditions exist: (a) Penetrating injury through the pterional/orbitofrontal region; (b) known cerebral vessel injury with or without a pseudo-aneurysm seen at initial exploration; (c) a blast injury with the Glasgow Coma Scale (GCS) score being <8; (d) the transcranial evidence of vasospasm; and, (e) a spontaneous, unexplained decrease in the partial pressure of brain tissue oxygen level.

On angiography, characteristic angiographic features may help in differentiating a post-traumatic aneurysm from a congenital aneurysm. These include the absence of the aneurysmal neck or a poorly defined neck, an unusual site of occurrence (a peripheral, non-branching site), an irregular contoured aneurysmal sac, as well as delayed filling and emptying of the aneurysmal sac with the contrast agent filling the adjacent cerebral vessels. A cerebral aneurysm presenting with significant morphological changes in a short period of time may also point towards the presence of a traumatic aneurysm.

Digital subtraction angiography has obvious limitations in terms of time, cost, availability and the risk associated with the procedure. With development of the multidetector CT angiography and its availability in trauma centers, this modality of investigation is increasingly being used for the screening of traumatic aneurysms with the sensitivity and specificity rates of detection of a TICA being in the range of 74-97.7% and 84-100%, respectively.

Magnetic resonance angiography (MRA) with time of flight (TOF) sequence may also be done for a rapid scanning with high resolution and is often used as a screening tool for detection of traumatic aneurysms in high-risk cases with nearly 90% accuracy.


The goal of treatment is to exclude the aneurysm from circulation to prevent its rupture. The management of a traumatic aneurysm should be done emergently after establishing its diagnosis. If left untreated, an approximately 41% mortality rate has been reported in literature, in comparison to the 18% mortality rate in the surgically treated group. [3],[5],[10],[19] Due to the atypical characteristics of these aneurysms, treatment directed towards each patient should be individualized. Surgical clipping is the treatment of choice, if feasible, as it ensures a definitive exclusion of the aneurysm from the circulation. The mass effect produced by the aneurysm on the surrounding structures can also be reduced by evacuation of the hematoma. Levy et al., suggested that a TICA has a higher propensity to rupture than a congenital aneurysm during surgical clipping due to absence of neck, a poorly defined wall and associated arachnoidal adhesions in the former. Thus, clipping without sacrificing the parent artery can be difficult in some cases. [34] Trapping, excision and wrapping of the aneurysm are viable options in the cases where clipping with preserving of the parent artery is proving to be a difficult procedure. In comparison to a peripheral aneurysm, the management of an ICA aneurysm is difficult especially if it is located in the infraclinoidal segment. Securing these aneurysms is a technical challenge both during their surgical clipping or endovascular occlusion, as aneurysms in this part of the ICA segment are usually wide-necked and giant. A preoperative evaluation for the cross flow with balloon test occlusion should be done to determine the feasibility of direct ICA proximal ligation or for the requirement of an external carotid-internal carotid (EC-IC) bypass before trapping the ICA.

Endovascular techniques are being increasingly used in the management of TICAs. Endovascular techniques have the advantage of avoiding a prolonged anesthesia, in minimizing manipulation of vessels and in allowing an immediate angiographic control. [3],[5],[10],[19],[35] The major disadvantage of the endovascular techniques in addressing the posttraumatic aneurysms lies in the requirement of antiplatelet therapy especially if a stent is used, as often, these patients have the risk of active bleeding. [36]

Posttraumatic aneurysms can occur even after trivial trauma but the morbidity and mortality associated with this entity is as high as 50% with a high incidence of rupture of upto 67%. [3],[5],[10],[19.37],[38] An early surgical exclusion of these aneurysm can reduce the mortality rate to approximately 18%. [5],[10],[19] There is not much literature available regarding the outcome of surgical clipping versus endovascular occlusion for these aneurysms.

Cohen et al., reported on 13 cases of TICA in their series. Twelve patients were treated with an endovascular approach and in one patient, trapping of the aneurysm with an EC-IC bypass was done. Five patients achieved a Glasgow Outcome Scale (GOS) score of 5; seven reached a GOS score of 4; and one patient stabilized with a GOS score of 3. [3] Wang et al., presented their series of 12 patients of TICA, of which 10 patients had an aneurysm of ICA (4 at the cavernous segment and 6 at the supraclinoid segment). An ACA and anterior communicating artery aneurysm were present in 1 patient each, respectively. All patients underwent surgical occlusion (9 clipping and 3 trapping); postoperatively, 9 patients showed an excellent outcome, 2 patient had a poor outcome and 1 patient died due to the development of a cerebral infarct. [36]

Management of extracranial traumatic aneurysms has not been clearly defined. Management strategies vary from surgical intervention, endovascular stenting, to a close follow-up (with anticoagulant administration). Endovascular stenting can be done if the aneurysm size increases (>15mm) at follow up imaging [Figure 17] and [Figure 18]. Starting of antiplatelet therapy reduces the risk of an embolic stroke. Foreman et al., reported on 13 cases of an extracranial traumatic aneurysm, in which no patient suffered from an ischemic stroke after the starting of antiplatelet therapy and only those patients underwent an endovascular stenting in whom there was evidence of increasing size of the aneurysm at follow up. [6] Extracranial aneurysms, if they increase in size during the follow up, should be treated before they attain a significant size because once they become exceedingly large, preservation of the parent vessel may become difficult.
Figure 17: Patient 5: A 16-year old boy sustained neck trauma when he was 8 years old; (a) he was having progressively enlarging pulsatile neck swelling since then; and (b and c) internal carotid angiogram showed the large aneurysm arising from the internal carotid artery in the neck

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Figure 18: Patient 5: (a) The contralateral internal carotid angiogram showed no cross flow from the contralateral side; (c and d) therefore, endovascular stenting was performed maintaining the patency of the vessel while obliterating the neck of the aneurysm

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 » Conclusions Top

Development of TICA following head injury is a rare entity but should be considered both in patients who have sustained either a closed head injury or a penetrating head injury. The timing of angiography has not been clearly defined in literature so a judicious used of angiography is needed in order to diagnose these patients. Missing of a TICA or a delay in its management may result in a high rebleeding and mortality rate. Its management is difficult due to the variability in the aneurysmal characteristics and the presence of concomitant head injury. The choice of surgical clipping, endovascular occlusion, or a parent vessel trapping with or without a vascular bypass, needs to be individualized based on the particular characteristics of the traumatic aneurysm present.

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 » References Top

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18]

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