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 plane⁹ 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 trauma^42–44 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

Diagnosis

The most common cause of subarachnoid hemorrhage is trauma, so the diagnosis of a traumatic intracranial aneurysm requires a high index of suspicion. Making the diagnosis is important because patients with multiple episodes of hemorrhage or neurological insults do poorly.⁴⁸ Computed tomography is usually the first investigation, and it may demonstrate nonspecific hemorrhages, infarctions, and skull base fractures. Penetrating trauma is often associated with intracranial hemorrhage, and after missile injuries, concomitant intracerebral hemorrhage is found in 39% to 80% of patients,³⁵ with 26% having subdural hemorrhages.³ In low-velocity penetrating injuries, de Trevou and van Dellen demonstrated that 50% of patients had evidence of an intracerebral hemorrhage.²⁶

Cerebral angiography is the “gold standard” and should be performed in all cases of penetrating trauma.^7,55,56 Angiography is particularly important in patients with orbitopterional injuries, penetrating fragments, and subarachnoid, intracerebral, or subdural hemorrhage.^3,5,26,57 In penetrating trauma, traumatic aneurysms may be visualized on angiography as early as 2 hours after the injury, but the majority of aneurysms are angiographically apparent in 2 to 3 weeks, with a mean of 20 days (median, 13 days).⁵ Therefore, it has been suggested that the first angiogram should be performed at the beginning of the second week after injury.⁷ In patients in whom there is a higher probability of a traumatic aneurysm being present or developing (e.g., those with stab wounds), angiography shortly after admission should be considered. Computed tomographic angiography can also be performed as a screening study and may reveal an unsuspected aneurysm. The timing of angiography is important, and it is not unusual for the first angiogram to be negative in patients with penetrating trauma.^1,31,58 Twenty percent of traumatic aneurysms are multiple, and each individual aneurysm may regress, enlarge, or form in delayed fashion.³⁶ Therefore, most authors agree that a follow-up angiogram should be obtained even if the initial one was negative. The second angiogram should be performed at least 2 to 3 weeks after injury, and it could be argued that a third angiogram should be obtained 6 weeks after injury. Traumatic internal carotid artery aneurysms occur relatively frequently in children (5% to 39% of pediatric intracranial aneurysms) and have a propensity to bleed weeks after the initial trauma. Blood in the basilar cisterns after closed head trauma in children should prompt both immediate and delayed angiographic evaluation.⁵⁹

Treatment

Treatment of a traumatic aneurysm depends on the location, type of vascular injury, and signs and symptoms. In a patient with a large, life-threatening intracerebral hemorrhage, rapid removal of the hematoma is required, and the vascular injury needs to be dealt with. The outcome is generally worse after secondary brain insults, so it is important to diagnose a traumatic aneurysm early; treatment of these aneurysms may be complicated.

Surgery has been the traditional method of therapy, with ligation of the carotid artery in the neck historically used for traumatic aneurysms involving the intracranial internal carotid artery.⁶⁰ Some traumatic intracranial aneurysms have been documented to disappear on repeated angiograms,^1,36 with Amirjamshidi and coworkers reporting that 19.4% of the aneurysms in their patients disappeared.⁶¹ This finding has not been supported by all authors, and most recommend that once a traumatic aneurysm has been diagnosed, therapy should be instituted. The principle of managing a saccular aneurysm is to exclude the aneurysmal bulge from the circulation by clipping or coiling, with preservation of the parent vessel and its branches. Traumatic aneurysms, however, are mostly false aneurysms, so this approach is not often possible; successful clipping has been reported, but it is unusual.^23,62,63 Therefore, with traumatic aneurysms, preoperative planning must include the possibility of excising the involved vessel, as well as the high probability of rupture intraoperatively.

In very distal vessels, the likelihood of an ischemic event after resection of the aneurysm is low, and these aneurysms are often excised with no complications.^3,5,64 In more proximal vessels, preparation for a vascular bypass should be considered, and the surgical approach should allow access to the superficial temporal artery, the saphenous vein, or both. In addition to a vascular bypass, an interposition graft with the superficial temporal artery can be placed.⁶⁵ Some aneurysms may not be amenable to either resection or bypass; in such cases, wrapping with Dacron mesh or muslin may be performed.

Endovascular techniques have advanced over the past 3 decades, and intravascular embolization and occlusion now play a larger role in the management of intracranial traumatic arterial injuries.^66–69 Endovascular therapy has not been a mainstay of treatment of traumatic aneurysms in the peripheral vascular tree because of the high incidence of false aneurysms and the risk for rupture. Recently, however, coils have been successfully placed in traumatic aneurysms.^69,70

Endovascular therapy has become more important for vascular injuries involving the skull base.⁷¹ Traumatic aneurysms involving the skull base are difficult to access and control surgically. With carotid injuries, options include endovascular occlusion of the carotid artery at the skull base, a bypass graft, or rarely, direct repair of the vessel. Stenting may play an important role in the future; however, the need for antiplatelet therapy after stent placement limits the use of this treatment modality in the setting of trauma. Before carotid occlusion, the collateral circulation needs to be evaluated by balloon test occlusion. Adequate collateral circulation is defined as symmetrical angiographic filling of both hemispheres. Awake patients are also examined continuously for neurological deficits. In patients with evidence of adequate cross-flow and collateral flow based on transcranial Doppler studies, angiography, and balloon test occlusion, simple endovascular occlusion can be performed.^53,72 Patients who deteriorate clinically or whose middle cerebral artery transcranial Doppler velocity decreases by 60% have inadequate collateral flow.⁷³ In these patients, alternative therapies have to be considered, including direct surgical repair or endovascular treatment of the carotid artery in the skull base, as well as the cavernous sinus, but such treatment has had variable success.^74–76 Most authors would advocate an extracranial-to-intracranial bypass.⁵³ A saphenous vein bypass graft can be used, with sacrifice of the internal carotid artery surgically.⁶⁵ In some patients, both endovascular and surgical techniques can be used simultaneously to achieve optimal results.⁶⁵

Intracranial dissections pose the risk of both hemorrhage and stroke. To prevent these complications, medical, surgical, and endovascular methods have been described. Medical therapy consists of anticoagulation with either antiplatelet therapy or warfarin (Coumadin) to prevent thrombotic and embolic complications, but it carries a risk for intracranial hemorrhage. Endovascular therapy now offers the alternatives of angioplasty and stent deployment to restore vessel patency. This method is based on using a balloon to dilate the restriction and then stenting back the intimal flap.

Conclusion

Traumatic intracranial aneurysms are a rare but important surgical problem in patients with penetrating intracranial trauma. Because secondary neurological insults can impair recovery, traumatic vascular injuries should be considered in all cases of penetrating injury. Angiography is required to make the diagnosis, and the test should be repeated even if the first angiogram is negative because traumatic vascular injuries can develop in delayed fashion. Surgery is still the mainstay of treatment, but endovascular therapy is becoming an important aspect of care in patients with traumatic vascular injuries, particularly those involving the skull base. Furthermore, endovascular techniques are continuing to evolve rapidly and offer versatility and safety as an alternative to open surgery for the treatment of traumatic intracranial aneurysms.