5 Traumatic Brain Aneurysms
Abstract
Traumatic intracranial aneurysms are rare and account for less than 1% of intracranial aneurysms. They can have a myriad of presentations and are often not initially apparent. Most of these traumatic aneurysms are actually pseudoaneurysms that are formed due to direct or indirect stress on the vessel walls. Various treatment options exist and can be tailored based on the presentation and angioarchitecture of the aneurysm. While there are generally numerous endovascular options, these may be somewhat limited by an inability or reluctance to use antiplatelets as the traumatic nature of the injury often means that most of these patients have concomitant musculoskeletal or internal visceral injuries. There is no consensus on the natural history and behavior of these subsets of aneurysms, and the evidence in the literature is scarce. Therefore, a broad understanding of the various treatment options is essential before treating these aneurysms.
Keywords: cerebral aneurysm, traumatic aneurysm, pseudoa-neurysm, vessel sacrifice, coiling
5.1 Goals
1. Understand the epidemiology and pathophysiology of traumatic intracranial aneurysms (TICAs).
2. Review the literature to understand the various types of TICAs and their clinical presentations.
3. Critically analyze the timing and role of computed tomography angiography (CTA) versus catheter angiogram in diagnosis and management of TICA.
4. Review the literature for various treatment options currently available for the treatment of TICAs.
5.2 Case Example
5.2.1History of Present Illness
A man in his thirties presents to the emergency department (ED) with a severe traumatic head injury after his car collided with a snowplow. He appeared to have sustained severe maxillofacial injuries and lost consciousness en route to the hospital. History was obtained from family. Past medical history: No significant history, including no past history of aneurysms or polycystic kidney disease. Family history: Denies history of cerebral aneurysms. Social history: Has smoked one to two packs of cigarettes/day for at least 15 years.
Neurological examination: Drowsy and confused. Oriented to person only. Severe periorbital edema on the right side and right pupillary size could not be assessed. No other cranial nerve palsy was observed at that time. He was moving all four limbs equally in response to pain. There was no evidence of cerebrospinal fluid (CSF) leakage from his nose or the scalp wound.
Imaging studies: CT scan and subsequent cerebral angiogram revealed extensive subarachnoid hemorrhage and a traumatic wide-necked aneurysm of the clinoidal segment of the internal carotid artery. See ▶ Fig. 5.1 and ▶ Fig. 5.2.
5.2.2 Treatment Plan
The patient was treated with endovascular coiling to occlude the aneurysm as well as the segment of the right internal carotid artery (ICA) that incorporated the aneurysm. The aneurysm neck was deemed too wide and the aneurysm likely too fragile to treat using intrasaccular coils alone (▶ Fig. 5.2a). Stent or flow diverter placement was felt to be suboptimal due to the need for antiplatelet therapy in the setting of the patient’s extensive intracranial blood and concomitant injuries. The patient tolerated the occlusion due to the presence of collateral flow from the contralateral ICA (▶ Fig. 5.3b).
Fig. 5.1 (a,b) Computed tomography (CT) brain showing a comminuted fracture of the right temporal bone, the lateral wall of orbit, and medial wall of orbit extending into the ethmoid sinus. There is severe subarachnoid hemorrhage, predominantly in the basal cisterns and extending into the right Sylvian fissure.
Fig. 5.3 (a) Anteroposterior (AP) view—postcoil-ing images of the right internal carotid artery (ICA) and pseudoaneurysm, showing complete occlusion of the parent artery, (b) AP view-injection from the left ICA showing collateral flow across the anterior communicating artery.
5.2.3 Follow-up
Following the embolization, the patient eventually required decompressive hemicraniectomy for elevated intracranial pressure (ICP) as a result of his traumatic brain injury. However, he did not experience any negative sequelae of the carotid sacrifice. At 2-year follow-up, he was doing well, with intact cognition and only slight weakness and sensory disturbance on the side contralateral to the aneurysm, a neurological deficit felt to be secondary to his initial injury.
5.3 Case Summary
1. What is the pathophysiology of traumatic intracranial aneurysms (TICAs)?
TICAs are rare and account for< 1% of all cerebral aneurysms.1 They are reported to occur in 3.2% of civilian penetrating craniofacial injuries2 and in 42% of patients with gunshot wounds and missile head injuries.3 They are more commonly seen in patients younger than 18 years.1,4,5 This is possibly secondary to higher rates of traffic accidents and other trauma in this age group. The etiology can be variable and can range from seemingly trivial head injury to severe penetrating head injury. They are associated with severe mortality and morbidity when left untreated.6
Histologically, they can be classified into true, false (pseudoa-neurysms), and mixed aneurysms.7 True aneurysms occur either due to direct impact or indirect transmission of force to the vessel wall, leading to an area of focal vessel weakness. Further flow dynamics across this weak wall leads to the formation of an aneurysm with the adventitia intact over it. False aneurysms, otherwise known as pseudoaneurysms, are far more common4,7 and are due to rupture of all three layers of the vessel wall and formation of a contained hematoma. This leads to the formation of a false lumen and persistent flow into the false lumen which creates an aneurysmal dilatation.4,8,9 Pseudoaneurysms are usually associated with penetrating or stab injuries. Mixed aneurysms are true aneurysms that have a contained rupture and subsequently form a pseudoaneurysm. The term “mixed aneurysms” are also occasionally used interchangeably with dissecting aneurysms.10,11
2. What are the common sites of TICAs?
Although TICAs are seen in both the anterior and posterior circulations, they are predominantly found in the anterior circulation and are more frequent in the distal cerebral branches. The most frequent sites are the peripheral branches of the middle cerebral artery (MCA), followed by the branches of the pericallosal artery.12,13 These are usually associated with penetrating injuries, in which the missile impact has scattered numerous fragments of bone or metal in diverging trajectories.8 Pseudoaneurysms can also be associated with closed head injuries and are caused secondary to shearing forces. One common site in children is the pericallosal aneurysm formed by the impact of the pericallosal artery against the falx margin.8,14 TICAs on more proximal intracerebral arteries are commonly located in the supraclinoid ICA.15
The clinical presentation of TICAs can vary based on the location of the aneurysm. Supraclinoid TICAs can present with massive subarachnoid hemorrhage, delayed intracerebral hemorrhage, or progressive cranial neuropathies.4,16,17 The average time from trauma to aneurysmal hemorrhage is approximately 21 days, and these lesions carry a mortality of almost 50%.7,17 Infraclinoidal aneurysms often present as massive or recurrent epistaxis, cranial neuropathies, diabetes insipidus, or headaches.18,19,20,21 Patients with distal branch TICAs usually present with delayed ICH. They can also present with seizures, can be diagnosed incidentally on routine radiographic follow-up, or in the evaluation of patients with growing skull fractures.22,23
3. Do TICAs vary based on the mechanism of injury?
Blunt trauma is a frequent cause of TICAs in children. The cranium is softer and the relatively mobile cerebral content is more prone to shearing forces which may cause greater harm to the delicate vessels.4,24
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