Chapter 141 Management of Traumatic Intracranial Aneurysms

Giuseppe Talamonti, Giuseppe D’Aliberti, Massimo Collice ^∗

The injury of intracranial arterial wall may result in immediate hemorrhage, thrombosis, dissection, or development of traumatic intracranial aneurysms (TICAs).¹ Intracranial vasculature results virtually injured in all cases of severe head injury, which explains the almost constant presence of subarachnoid hemorrhage due to lesion of small pial vessels.¹ However, TICAs may develop even following mild or trivial head trauma.² Despite the frequency of head injury, the incidence of TICAs is quite low, accounting for less than 1% of all intracranial aneurysms.²^–⁶ Indeed, the actual rate of TICAs could be underestimated, since nowadays diagnostic angiograms are rarely performed for head injuries^2,^5,⁶ and computed tomography (CT) angiography is not sensitive enough to replace digital subtraction angiography.⁷ TICAs have been reported in patients of any age, but they are more common in the pediatric population.^2,^8,⁹ Moreover, there is a clear male preponderance,² which is presumably related to the greater frequency of head injury in males.⁸

In the last two decades, we managed about 1800 cerebral aneurysms and 1600 severe head injuries (21 missile injuries): we found just 14 TICAs (Figs. 141-1 to 141-4). During the same period, we performed about 8000 brain surgery procedures, which were responsible for just 1 case of iatrogenic aneurysm (Fig. 141-5; also see video). Our series is summarized in Table 141-1.

FIGURE 141-1 A and B, Preoperative angiograms (anteroposterior and lateral views) showing a giant dissecting aneurysm of the right petrous carotid artery. The posterior circulation was supplied by a large trigeminal artery. This patient was referred to us because of multiple episodes of transitory ischemic attack. He had a history of head injury (a car accident occurred 2 years before) with diffuse axonal injury, multiple skull base fractures, and subsequent complete recovery. Treatment consisted of cervical ICA–MCA bypass and aneurysm trapping. C, Postoperative angiogram showing the revascularization of the whole territory of MCA and even of the posterior circulation through the trigeminal artery.

FIGURE 141-2 A, Preoperative angiogram showing a giant aneurysm of the left petrous carotid artery. This patient had a history of head injury (a car accident occurred 6 months before) with a Glasgow Coma Scale (GCS) score of 12 points, subarachnoid hemorrhage, petrous bone fracture, and left palsy of the sixth nerve. The GCS score returned to 15 points in a few days, but Jefferson syndrome became full blown in a couple of months. Treatment consisted of the interposition of a saphenous vein graft between the petrous and the clinoid segments of the carotid artery. Then the injured arterial tract was trapped and removed. Pathologic studies depicted a false aneurysm. B, Postoperative angiograms showing the revascularization obtained through the graft. The arrows point to the proximal and distal anastomoses.

FIGURE 141-3 A, Initial angiogram obtained a few hours following severe head and neck injury due to precipitation. The cervical left ICA was dissected and thrombosed. The left MCA was supplied through the posterior circulation. B, CT scan obtained 7 days later, when the patient acutely deteriorated: a subarachnoid hemorrhage not evident previously is now visible. C, Repeated angiogram obtained 7 days after injury, showing the development of a large aneurysm on the M1 tract of the left MCA. Treatment consisted of bypass between the common carotid artery and the M2 tract followed by aneurysm trapping. D, Postoperative angiogram showing the revascularization of the MCA territories.

FIGURE 141-4 A, Angiogram obtained 15 days after a precipitation injury, when this fully alert patient with multiple craniofacial fractures suddenly deteriorated. Immediately before angiography, a repeated CT scan had revealed a hemorrhage not evident previously. The angiography showed an aneurysm on the A1 segment of the right anterior cerebral artery. B, Intraoperative picture showing a false aneurysm originating from the A1 segment. The lesion appeared larger than expected. Treatment consisted of trapping and excision. Pathologic studies confirmed the false aneurysm. C and D, Postoperative angiograms showing the aneurysm on the right A1 tract was completely excluded and the right A2 segment was supplied through the anterior communicating artery.

FIGURE 141-5 A, Enhanced CT scan obtained 6 years after a neurosurgical procedure, when this young woman experienced multiple generalized seizures. A hyperdense image not evident previously is now visible, and a vascular lesion was suspected. In 1996, this patient had undergone left temporal lobectomy because of hemorrhage due to a giant cavernous angioma; during this procedure, a perforating branch of the ICA was accidentally injured and coagulated. The postoperative course was uneventful, and the patient remained well during the following 6 years. B and C, Preoperative angiograms showing a large aneurysm had developed on the ICA bifurcation. Treatment consisted of clipping during hypothermic cardiac arrest (15 minutes). D and E, Follow-up angiograms showing the aneurysm was excluded and the parent vessel was reconstructed by multiple tangential clips. See also video.

TABLE 141-1 Treatment Modalities in 15 Traumatic Aneurysms (1989-2009)

Pathology

Basing on the pathology and the mechanism of formation, four types of TICAs have been described: true, false (or pseudoaneurysms), mixed, and dissecting.^2,^4,^5,¹⁰^–¹⁵ True TICAs consist of localized dilatation of the artery with an expanded lumen lined by stretched remnants of the arterial wall: in these cases, only the adventitia is intact and represents the single layer of the aneurysm sac.^2,^8,^10,^14,¹⁵ This would be the main difference between a true TICA and a common saccular aneurysm, which has a wall consisting of both intima and adventitia.^10,¹⁴ Other authors⁴ think true TICAs originate from the outpouching of the intima through a fragmented media, resulting in an aneurysm wall consisting of intima separated from adventitia by fibrous tissue. False TICAs originate from the rupture of all arterial layers with perivascular hematoma formation and organization.⁸ These lesions consist of encapsulated hematoma in communication with the lumen of the ruptured vessel, and sometimes, the surrounding structures contribute to the aneurysm wall formation.^5,¹⁰ Mixed TICAs derive from contained post-traumatic rupture of true aneurysms with local hematoma formation, false lumen development, and production of secondary false aneurysms.^4,^5,^8,¹⁰ Dissecting TICAs originate when trauma provokes the splitting of the arterial wall layers with blood entering through intimal tears inside the arterial wall and forming a false lumen between the intima and the elastica.^5,¹⁰ In such conditions, aneurysm outpouching may easily occur and arterial dissection may evolve to dissecting aneurysm. Dissecting aneurysms also may break and become false aneurysms. The term mixed aneurysm has also often been used to describe saccular aneurysms associated with dissection of the parent vessels.²

A fifth type of TICA might be represented by the arteriovenous aneurysm. Indeed, this term has often been improperly used to indicate the common arteriovenous malformations, but in this context it refers to a lesion that develops when an artery breaks into a collateral vein, such as in case of a false aneurysm that involves an adjacent vein. This type of lesion is well described in abdominal and thoracic surgery, but it is quite rare in neurosurgery with the exception of the well-known carotidocavernous fistulas. These arteriovenous lesions are not considered in this chapter.

Although false aneurysms have been considered the most frequent TICAs,^2,^4,^5,⁸ indeed the relative incidence of the four histologic types is not known.^1,² Furthermore, the term pseudoaneurysm, which should refer only to false aneurysm, is often used as a synonym of TICA.⁴ However, all types of TICAs carry a high hemorrhagic risk, and their distinction is often impossible on angiography. Therefore, the aforementioned classification is academically relevant but of little benefit in clinical practice, because intervention is required regardless the type.^2,^4,⁵

Physiopathology

Both penetrating and nonpenetrating injuries may be responsible for TICA formation.^3,¹⁰ TICAs are most frequently reported following blunt injuries.^1,^2,¹⁶ As for penetrating wounds, low-velocity penetrations (from stab or shotgun wounds) are more risky than high-velocity penetrations (from bullet wounds):^2,^4,⁵ 14.9% versus 3.6%, respectively.^17,¹⁸ The prevalence of blunt trauma could be explained by penetrating injuries more likely being responsible for complete arterial disruption with immediate hemorrhage and without subsequent aneurysm formation. When projectile injuries are responsible of TICAs, these are always false aneurysms with complete lesion of the arterial wall.^1,¹⁹

The main mechanisms of TICA formation are direct injury to the vessel or stretching of the vessel by adjacent forces.² The mechanisms are different in penetrating and in nonpenetrating injuries. In the first case, the proximity of the missile track to the location of the TICA indicates that this is the result of direct contact to the vessel by the missile, shrapnel, or secondary bone fragments.^1,^4,⁵ This could result in arterial laceration or avulsion of perforating branches or produce enough shearing forces to cause a rent in the arterial wall.^1,^17,²⁰ Penetrating fragments around the face or pterion have the high probability to produce TICAs: 65% of these aneurysms are reported in association with facial, orbital, basifrontal, or pterional injury.^1,¹⁹^–²¹ But in case of nonpenetrating injuries, there is a frequent association (60%-90% of cases) between TICA development and presence of skull fractures.^1,^10,²² Otherwise, the arterial disruption triggering TICA formation may result from differential motion between the brain and the skull during acceleration/deceleration.^1,^2,⁸

TICAs are frequently reported in the peripheral vascular tree, and the anterior circulation is more commonly involved with infratentorial TICAs representing less than 5% of the total.^2,^5,^6,^10,¹⁶ The location of TICAs closely depends on the mechanism of injury.² Intrapetrous and/or infraclinoid carotid artery, as well as basilar artery, aneurysms are usually related to skull base fractures, and para- and supraclinoid carotid artery aneurysms may result from fractures of the anterior clinoid process or stretching of the artery across the process during the impact. Otherwise, injury to the paraclinoid carotid artery may originate by the stretching of the artery at the level of the transitional zone between the relatively fixed intracavernous segment and the relatively mobile cisternal segment,^2,^15,²³ pericallosal artery aneurysms may develop from the injury of the artery against the falx edge,^2,^9,²⁴ posterior cerebral artery aneurysms may be the result of trauma against the tentorium,² and cortical artery aneurysms are usually associated with cranial vault fractures.^2,^5,^24,²⁵ TICAs of the meningeal artery are infrequently reported, which is curious considering the intimate relationships of this vessel with the vault bone.^6,¹⁰