Endovascular Treatment of Intracranial Posttraumatic Lesions

Assessing arteriovenous fistulas, dissections, and aneurysms.

By Rosana Ceratto, MD; Jorge Chudyk, MD; Carlos Bleise; and Pedro Lylyk, MD

The incidence of cerebrovascular trauma has increased in recent decades, due to a greater amount of car accidents, military confrontations, and urban violence. The improvement of diagnostic and therapeutic procedures allows us to have a better understanding of the pathology and improve treatment.

Many vascular head and neck injuries are immediately lethal. In the surviving patients, the most frequently diagnosed entities are:

  • Arteriovenous fistulas: when the injury compromises both the artery and the vein parallel to the lesion, and no immediate vascular repair is performed; deflected blood flow to the vein may occur through this communication, which is called an arteriovenous fistula.
  • Dissections: the entry of blood from the arterial wall to the intramural hematoma formation; this can be located in relation to the intima (subintimal) or to the adventitia (subadventitial).
  • Pseudoaneurysms: if the vascular injury has no communication with the outside, it produces a hematoma, usually formed by a fibrous capsule that, in time, turns into a pulsatile mass known as a false aneurysm due to the lack of arterial wall as in true aneurysms.


The most frequently observed cases are carotid cavernous fistulas (CCF), although they are a rare complication (0.2%–0.3%) of traumatic brain injury.1

A CCF is any abnormal communication established between the carotid artery and the cavernous sinus causing a pathological arteriovenous shunt, which can manifest in an anterograde way to the orbit, producing a severe ocular condition known as pulsating exophthalmos.

Within this group of fistulas, we can distinguish two different entities:

  • Direct CCF: presents direct communication between the intracavernous internal carotid artery (ICA) and cavernous sinus (Figure 1). These are usually related to severe trauma with basal skull fractures, but have also been associated with direct surgical trauma and rupture of intracavernous carotid aneurysms.
  • Indirect or dural fistulas: these have no posttraumatic etiology.

Direct CCFs

Direct CCFs are posttraumatic abnormal communications between the carotid artery and the cavernous sinus. Trauma is the etiology in 75% of the different carotid cavernous shunts, which have an incidence of 1/10,000 to 1/20,000 in hospital admission. As many as 90% of the patients with direct CCFs may lose vision in the absence of treatment.2

The progressive loss of vision or the identification of cortical drainage veins in the angiogram determines urgent therapy. A detailed four-vessel angiogram including visualization of the circle of Willis pattern with and without carotid compression is mandatory to plan an accurate endovascular treatment. The location of the fistula in the cavernous carotid, presence of arterial dissection with the fistula, and maintenance of the flow in the ophthalmic vein and petrous sinuses must also be determined. Sometimes, a bilateral carotid cavernous shunt is found.

Embolization (Figure 2) allows access to the CCF through direct arterial access via the ICA.3 In patients already treated with surgical clipping of the ICA (Figures 3, 4 and 5), the superior ophthalmic vein can be approached directly or by retrograde venous catheterization through the ipsilateral or contralateral petrosal sinus (Figure 6).


Carotid dissections (Figure 7) have an annual incidence of 2.6/100,000 habitants.4 Information involving vertebral territory is unknown. Although they usually affect young population groups between 30 and 50 years, carotid dissections have also been described in children and older adults.

It is the cause of 2.5% of all ischemic cerebrovascular events, whereas in patients younger than 60 years, it represents 22% of the cases.

The most common site for dissections is the extracranial portion of the cervical vessels.


The origin of carotid dissections is primarily idiopathic, with traumatic injury as the second most common origin.

Many publications have shown the association between minor cervical trauma and significant physical effort with cerebrovascular dissections (25%–41% of cases). It has been described in relation to cough, vomiting, childbirth, weightlifting, pushing vehicles, chiropractic maneuvers of the neck, flexion and extension cervical rockers, prolonged use of the phone with neck flexion, and cervical rotation.


The classic clinical triad of carotid dissection is ipsilateral headache, symptoms or signs of cerebral ischemia, and ipsilateral Horner syndrome. However, the presence of the three symptoms occurs in only 20% of the cases.5 When the dissection affects intracranial vessels, it can also involve subarachnoid hemorrhage, because the vessels across the dura lose the external elastic membrane and have thinner adventitia.

Once the diagnosis is confirmed, carotid dissection is usually treated with intravenous heparin anticoagulation, and 100 mg of aspirin per day is sometimes prescribed.

Oral anticoagulation is prescribed, and frequent cervical Doppler scans are scheduled to evaluate the evolution of the dissection. In patients with multiple traumas, anticoagulation is usually contraindicated due to the increased risk of cerebral bleeding.

In cases where a pseudoaneurysm (Figure 8) is present in the diseased segment or cerebral ischemia or severe stenosis occurs, treatment of the lesion is indicated.

Surgical techniques with vein patching have fallen into disuse. The current treatment of choice is endovascular therapy with angioplasty and stent placement (Figures 9, 10 and 11).6 When a pseudoaneurysm is diagnosed, angioplasty is indicated in order to repair the vessel by flow diverter stent placement.7 In some of these cases, additional treatment with platinum coils may be necessary.


Traumatic intracranial aneurysms are considered a rare entity, representing < 1% of all aneurysms. They can be produced by a blunt or penetrating trauma and are most frequently described in the pediatric population; symptoms depend on the affected territory.

Early diagnosis of a traumatic aneurysm is a challenge, because it is sometimes not evident in the acute phase, and it may take 2 or 3 weeks until it becomes visible on the CT angiogram,8 which is the method of choice for diagnosis.

Delayed hemorrhage (3 to 4 weeks after trauma) is typical and carries a high mortality rate (about 50%).

Until recently, these were treated by craniotomy and clipping, showing better results than conservative management, but with a mortality rate of approximately 30%. Recent publications showed successful endovascular treatment with low morbidity and no mortality.9-11 For these patients, endovascular approaches have emerged as a valid therapeutic alternative.

This technique avoids craniotomy, brain retraction and dissection, and external manipulation of the vessels during surgery. Thus, other related complications to craniotomy, such as epilepsy or wound infection, are avoided.

The goal of endovascular treatment is to achieve complete occlusion of the aneurysm with preservation of the parent vessel. Platinum microcoils, acrylics (NBCA), polymers (Onyx, Covidien), or flow diverter stents may be used, depending on the location and size of the aneurysm vessel.


Multiple mechanisms of neural injury act in concert in the traumatized brain, including axonal shearing, hemorrhages, and increased intracranial pressure. Consequently, the traumatized brain is especially vulnerable to ischemia after emboli or hemodynamic compromise. The loss of vascular autoregulation in the injured brain reduces the ability to compensate for hypoperfusion.

In conclusion, endovascular treatment for CCF, pseudoaneurysms, and vascular traumatic dissections seems to be a rational and effective way to restore the artery lumen and prevent late hemorrhages or neurological deficits.12

Rosana Ceratto, MD, is an interventional neuroradiologist at ENERI in Buenos Aires, Argentina. She has disclosed that she has no financial interests related to this article.

Jorge Chudyk, MD, is a radiologist at ENERI in Buenos Aires, Argentina. He has disclosed that he has no financial interests related to this article.

Carlos Bleise is a radiologist at ENERI in Buenos Aires, Argentina. He has disclosed that he has no financial interests related to this article.

Pedro Lylyk, MD, is Chairman of ENERI in Buenos Aires, Argentina. He has disclosed that he has no financial interests related to this article.

  1. Fabian TS, Woody JD, Ciraulo DL, et al. Posttraumatic carotid cavernous fistula: frequency analysis of signs, symptoms, and disability after angiographic embolization. J Trauma. 1999;47:275-281.
  2. Das S, Bendok BR, Novakovic RL, et al. Return of vision after transarterial coiling of a carotid cavernous sinus fistula: case report. Surg Neurol. 2006;66:82-85; discussion 85.
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  5. Béjot Y, Daubail B, Debette S, et al. Incidence and outcome of cerebrovascular events related to cervical artery dissection: the Dijon stroke registry. Int J Stroke. 2013 Oct 22. doi: 10.1111/ijs.12154. [Epub ahead of print]
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  8. Uzan M, Cantasdemir M, Seckin MS, et al. Traumatic intracranial carotid tree aneurysms. Neurosurgery. 1998;43:1314-1322.
  9. Cohen, JE, Gomori JM, Segal R, et al. Results of endovascular treatment of traumatic intracranial aneurysms. Neurosurgery. 2008;63:476-486.
  10. Cohen JE, Rajz G, Itshayek E, et al. Endovascular management of traumatic and iatrogenic aneurysms of the pericallosal artery. report of two cases. J Neurosurg. 2005;102:555-557.
  11. Horowitz MB, Kopitnik TA, Landreneau F, et al. Multidisciplinary approach to traumatic intracranial aneurysms secondary to shotgun and handgun wounds. Surg Neurol. 1999;51:31-42.
  12. Cohen JE, Rajz G, Gomori JM, et al. Urgent endovascular stent-graft placement for traumatic penetrating subclavian artery injuries. J Neurol Sci. 2008;272:151-157.

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