Traumatic Cerebral Aneurysms Secondary to Penetrating Intracranial Injuries

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CHAPTER 382 Traumatic Cerebral Aneurysms Secondary to Penetrating Intracranial Injuries

Kiarash Golshani, Gavin W. Britz, Alice Yoo, G. Alexander West

Traumatic intracranial aneurysms may be the result of either penetrating or nonpenetrating trauma.¹^–³ Traumatic aneurysms were first described in 1895 by Guibert,⁴ and despite the common occurrence of head trauma, they are rare entities that represent less than 1% of all intracranial aneurysms.⁵^–¹³ The risk of a traumatic intracranial aneurysm developing depends on the mechanism of injury, with aneurysm formation being much less likely after closed head injury than after penetrating trauma. In addition to their occurrence after traditional trauma, traumatic aneurysms have been reported to occur iatrogenically, such as after transsphenoidal surgery,¹⁴^–¹⁸ sinus surgery,^17,¹⁹ ventricular taps,^20,²¹ stereotactic brain biopsy,²² and endoscopic third ventriculostomy.²³

Penetrating trauma can be divided into low-velocity injuries, such as those created by knives, screwdrivers, and shotgun pellets,²⁴ or high-velocity injuries caused by missiles such as bullets and shrapnel. South Africa has provided much of the literature with respect to low-velocity injuries, which are prevalent in this region, with stab wounds to the brain accounting for up to 6% of all trauma admissions.^7,²⁵ The incidence of aneurysm formation after this type of injury may be as high as 10% to 12%.^7,^25,²⁶ Traumatic aneurysms can occur as a result of skull fractures as well (Figs. 382-1 and 382-2). The aneurysm can result directly from depressed bone fragments injuring an underlying vessel or dispersed bone fragments from a penetrating injury (e.g., shrapnel).

FIGURE 382-1 A, Computed tomography (CT) of the head 5 months after traumatic brain injury with a lesion on left frontal pial surface (arrow). B, CT bone windows showing a fracture (arrow) overlying a traumatic aneurysm.

FIGURE 382-2 A, Sagittal computed tomographic angiography showing a largely thrombosed traumatic aneurysm in the left frontal area. B, Cerebral angiogram demonstrating a traumatic distal left middle cerebral artery pial artery aneurysm (arrow).

With respect to missile injuries, conflicts in Lebanon, Iraq, and Iran have demonstrated aneurysm formation in 0.1% to 8% of patients sustaining this type of injury. The incidence is related to velocity, with lower velocity shrapnel injuries having a higher incidence of aneurysm formation than higher velocity bullet injuries.^1,^3,^5,²⁷ The American experience was obtained during the Vietnam War and reported by Ferry and Kempe, who demonstrated only two traumatic aneurysms in 2187 patients with penetrating head trauma, primarily gunshot wounds.²⁷

Despite the rarity of traumatic intracranial aneurysms, they have a mortality rate of 30%.⁵ This outcome is related more to the primary injury than to the aneurysm itself.³ However, it is important to make the diagnosis and offer surgical treatment because secondary insults affect the neurological outcome of patients.

Pathology

In penetrating trauma, the traumatic event disrupts the elements of the vessel wall, which may involve varying amounts of the intima, media, and adventitia.²⁸ Depending on the degree of involvement of the different internal structures, a false aneurysm, true aneurysm, dissection, or fistula may occur. An example of vessel changes with a traumatic aneurysm is shown in Figure 382-3. The findings are from a patient who suffered a severe traumatic brain injury with bilateral skull fractures that required evacuation of a subdural hematoma on the right. A pial artery aneurysm was diagnosed 5 months after the injury (see Figs. 382-1 and 382-2). The aneurysm grew significantly in size and was removed surgically. The aneurysm showed loss of the internal elastic lamina and smooth muscle in the media and an increase in size of the adventitia.

FIGURE 382-3 A, Excised traumatic pial aneurysm showing extension into the dura and an underlying skull fracture. B, Masson trichrome and elastic van Gieson staining of a pial traumatic aneurysm. The stains show loss of the internal elastic lamina, loss of smooth muscle, a very thickened tunica adventitia, and thrombus. C, High-power view showing loss of the internal elastic lamina architecture and changes in the media and adventitia.

Aneurysms are defined as true or false based on histologic findings. True aneurysms demonstrate outpouching of the intima through the media along with fragmentation of the internal elastic membrane, which results in an aneurysm wall consisting of intima separated from the adventitia by fibrous tissue. True aneurysms account for the majority of saccular aneurysms associated with aneurysmal subarachnoid hemorrhage, but they are much less common after trauma. In contrast, false aneurysms, which form the majority of traumatic intracranial aneurysms, are essentially contained hematomas with disruption of all three layers of the vessel wall. Distinction between a true aneurysm and a false one requires histologic analysis, so it is not always possible to distinguish them on angiography. The more inclusive term pseudoaneurysm is often used to describe aneurysms related to trauma.

Traumatic aneurysms occur distally in the vascular tree, in contrast to the proximal bifurcation site of saccular aneurysms. This peripheral location reflects the underlying mechanism of injury. The anterior circulation is most often affected, with the peripheral branches of the middle cerebral artery being the most frequent site, followed by branches of the pericallosal vessels.³

In penetrating injuries, the velocity of the projectile correlates inversely with aneurysm formation; that is, the lower the velocity, the more likely for aneurysm formation to occur. For example, traumatic aneurysms are 14 times more likely with shrapnel injuries than with bullet injuries, which are of higher velocity.³ Shotgun^29,³⁰ and low-caliber^29,^31,³² wounds also have a higher incidence of traumatic aneurysm formation than do injuries cased by high-velocity missiles. Bullets with higher velocity and thus greater kinetic injury are more likely to rupture a vessel than merely damage the wall.³ Further support for this theory is the very high incidence of traumatic aneurysms after stab wounds to the brain in the South African experience.^7,^25,²⁶ Traumatic aneurysms have also been associated with skull fractures, and in this type of penetrating trauma it has been postulated that momentary herniation of the cerebral cortex and vessel through the fracture results in aneurysm formation.³³ Figures 382-1 to 382-3 demonstrate an example of a distal middle cerebral artery pial artery aneurysm underlying a skull fracture.

Traumatic fistulas are abnormal connections between the intracranial arterial and venous circulation that can occur after severe or even relatively minor nonpenetrating trauma. Occasionally, they result from penetrating trauma, with the most common location being the cavernous sinus with the formation of a carotid–cavernous fistula—an acquired communication between the intracranial carotid artery and the cavernous sinus.³⁴ This communication may occur at the time of trauma or in delayed fashion if a false aneurysm is created that ruptures later. Dural fistulas may also occur after penetrating trauma. In this type of fistula, the abnormal communication between the intracranial arterial and venous circulation lies within the dura.³⁵ These dural fistulas may involve the cavernous sinus and other venous sinuses, including the transverse and sigmoid sinuses.³⁶^–³⁹

Much less common is the formation of dissecting aneurysms after nonpenetrating trauma. They may occur at the skull base and involve the internal carotid artery and vertebrobasilar system. Dissecting aneurysms occur when injury to one or more of the arterial layers allows blood to force its way between the vessel layers along a dissection plane ⁹ and create an intimal flap.⁴⁰ This intimal flap may act as a nidus for embolic material or may occlude the arterial lumen. Occasionally, dissections originate within the media or adventitia, and in this situation, rupture may occur through the adventitia, with resultant subarachnoid hemorrhage or pseudoaneurysm formation.⁴¹ Dissections are more common after nonpenetrating trauma⁴²^–⁴⁴ and may occur spontaneously.^45,⁴⁶ Dissections with pseudoaneurysm formation of the carotid artery can occur as a result of fractures of the skull base or clinoid secondary to traction on the artery at the dural ring.

Clinical Findings

The initial signs and symptoms in patients with head injuries, regardless of whether they have traumatic intracranial aneurysms, are largely related to the primary brain injury, with the initial Glasgow Coma Scale score being a good predictor of outcome.^3,⁴⁷ Secondary manifestations are related to the location and type of the vascular injury. In aneurysms involving the peripheral vascular tree, there is delayed neurological deterioration, usually within 3 weeks of the injury.⁷ Because most traumatic aneurysms are false aneurysms, intracranial hemorrhage is often the reason for this deterioration, but cerebral edema from the initial coexisting hemorrhage or stroke may be responsible. Patients with multiple episodes of hemorrhage tend to do poorly,⁴⁸ so it is best to have a high index of suspicion for traumatic aneurysms and make the diagnosis before its overt clinical manifestations appear.

In patients with aneurysms involving the infraclinoid internal carotid artery, severe and life-threatening epistaxis can be the initial event if the arterial injury communicates with a sphenoidal sinus fracture.^31,⁴⁹^–⁵³ Aneurysms in this location may also be manifested as a bruit, chemosis, exophthalmos, visual loss, and cranial neuropathies referable to the cavernous sinus and formation of a carotid-cavernous fistula.^15,^49,⁵⁰ The extent of these symptoms largely depends on the magnitude of the arterial injury and the adequacy of venous drainage.³⁵

Dural fistulas are often manifested in delayed fashion, with pulsatile tinnitus or headaches being the only features. A less common finding is neurological deterioration secondary to an embolic stroke, which occurs with dissecting aneurysms involving the intracranial vessels, or a mass effect secondary to an enlarging unruptured pseudoaneurysm, particularly in children.⁵⁴