Craniofacial Trauma and Vascular Injury

Abstract

Cerebrovascular injury is a potentially devastating outcome following craniofacial trauma. Interventional radiologists play an important role in detecting, grading, and treating the different types of vascular injury. Computed tomography angiography plays a significant role in the detection of these injuries. Carotid-cavernous fistulas, extra-axial hematomas, pseudoaneurysms, and arterial lacerations are rare vessel injuries resulting from craniofacial trauma. If left untreated, these injuries can lead to vessel rupture and hemorrhage into surrounding areas. Acute management of these vessel injuries includes early identification with angiography and treatment with endovascular embolization. Endovascular therapy resolves vessel abnormalities and reduces the risk of vessel rupture and associated complications.

Vascular trauma to the skull can result from penetrating and closed-head injuries. These in turn can lead to injury to the craniofacial vasculature from longitudinal stretching, twisting, or shearing forces on the vessels. Prognosis is largely dependent on the extent of injury to the vessel and the collateral supply for that vessel. Initial management of patients presenting with craniofacial trauma includes stabilization of the airway and circulation and treatment of injuries.

The face is primarily supplied by branches of the external carotid artery (ECA), including the lingual, facial, maxillary, and middle meningeal arteries (MMA). These arteries are protected by the soft tissues of the face, but vessels are at risk of injury by blunt trauma while crossing bony structures or direct damage from penetrating injuries. Vascular injuries resulting from craniofacial trauma include lacerations, pseudoaneurysms, carotid-cavernous fistulas (CCFs), extra-axial hematomas, arteriovenous fistulas (AVFs), and arterial dissections. A CCF is an abnormal connection between the cavernous sinus and the carotid artery. Extradural and subdural hematomas can follow injury to the meningeal vasculature. Posttraumatic pseudoaneurysm results when damage to the intimal wall results in a collection of blood around the vessel to form a “false” wall. Finally, arterial dissection results from a tear in the inner arterial wall, followed by blood flow between the layers of the vessel.

Upon presentation with craniofacial trauma, noncontrast computed tomography (CT) is the modality of choice because it is widely available, fast, and sensitive for the detection of bone injuries and hemorrhage. Magnetic resonance imaging is less likely to be used in an acute setting due to its longer acquisition times and inferior bone fracture detectability. ¹ CT angiography (CTA) with its 90 to 100% sensitivity and 93 to 100% specificity is the procedure of choice to screen cervical vascular injuries in asymptomatic neck trauma. ^{2 3} Digital subtraction angiography remains the gold standard in the confirmation and treatment of vascular injury, such as lacerations, pseudoaneurysms, CCFs, and dissections, given its high spatial and temporal resolution capabilities. ⁴

Interventional goals are repair of the inciting injury and stop bleeding in the acute phase, and to eventually reduce morbidity and mortality. Image-guided percutaneous and endovascular procedures are considered first-line treatment. ⁵ Coils, particles, and liquid embolic materials are preferred, where thrombogenic actions provide permanent control of bleeding. ⁶ In most cases, occlusion of the injured ECA and its branches produces minimal complications because the face is highly vascularized with collateral circulation. Regardless, studies have reported distal ischemia, infection, and embolism following endovascular intervention. ⁷ Microvascular surgical procedures can be implemented following failed endovascular intervention.

Lacerations, pseudoaneurysms, CCFs, extra-axial hematomas, AVF, and dissections are potentially fatal complications of craniofacial traumatic injury. For this reason, early detection and management plays a vital role in reducing morbidity and mortality. ⁸ The objective of this article is to provide a clinical overview and management strategies for craniofacial trauma resulting in vascular injuries.

Carotid-Cavernous Fistula

CCFs are abnormal shunting of blood between the internal carotid artery (ICA) and/or ECA branches and the cavernous sinus. They are divided into four types: Type A is a direct fistula between intracavernous portion of ICA and the cavernous sinus. Type B is an indirect connection between the meningeal branches of ICA and the cavernous sinus. Type C is an indirect connection between meningeal branches of ECA and cavernous sinus. Type D is a connection between the meningeal branches of ICA, meningeal branches of ECA, and the cavernous sinus. ⁹

Direct CCFs (Type A; Fig. 1 ) most commonly result from a traumatic incident, such as a closed head injury with associated basilar skull fracture. ¹⁰ ICA tears may result from shearing forces or fractured bones that tear the dura around the cavernous sinus, resulting in a fistula. ¹¹ Alternatively, increased intraluminal pressure of the ICA may rupture the vessel wall, resulting in a CCF. ¹² Patients with a direct CCF present with an acute onset of symptoms, including diplopia, proptosis, blurry vision, orbital pain, orbital bruits, and headache. ^{1 12 13 14} Less commonly, patients may present with ophthalmoplegia and intracerebral or subarachnoid hemorrhage. Presentation may be delayed in case of indirect CCF ( Fig. 2 ); symptoms may be subtle and include chemosis, ophthalmoplegia, or decreased visual acuity due to ophthalmic vein congestion. ¹⁵ CTA or MR angiography (MRA) shows an enlarged superior ophthalmic vein, cavernous sinus, and petrosal sinus. ¹ Ocular abnormalities and cavernous sinus enlargement in the setting of a basilar skull fracture should raise suspicion for a CCF.

Fig. 1.

Direct carotid-cavernous fistula following motor vehicle collision. ( a, b ) Left internal carotid artery (ICA) angiography seen on early and delayed arterial phase showing poor intracranial flow and shunting of blood through cavernous sinus anteriorly into superior ophthalmic vein and posteriorly into the inferior petrosal sinus. Post–transvenous embolization, left ICA angiography in lateral ( c ) and anteroposterior views ( d ) showing no filling of the fistula and good intracranial circulation.

Fig. 2.

Indirect carotid-cavernous (CCFs) fistula showing delayed presentation with redness and chemosis of bilateral eyes following motor vehicle collision. ( a, b ) Anteroposterior (AP) and lateral views of right ICA (ophthalmic vein—black arrow) and ( c ) AP view of right external carotid artery angiographies showing fistulous filling of bilateral cavernous sinuses with prominent anterior venous drainage into superior ophthalmic veins. ( d ) Transvenous embolization of bilateral cavernous sinuses through ophthalmic vein showing successful obliteration of the CCF.

Treatment of Carotid-Cavernous Fistula

Direct CCF is the most severe and acute form of traumatic CCF. Initially, a complete physical examination including auscultation for orbital bruit is performed. CTA, CT venography (CTV), and/or MR venography form the initial radiological evaluation. Angiographic indication of the severity of the shunt can be obtained from filling of the anterior and middle cerebral artery on ICA angiography in the arterial phase, and the venous reflux into the cortical vein, which portend impending catastrophe and would require emergent treatment. Endovascular approach to treatment of direct CCF is primarily by transarterial obliteration of the fistula. A complete angiography of ICA and ECA at high frame rate is required to demonstrate the anatomy of the rent from the ICA into cavernous sinus and to exclude any external carotid feeders to the fistula. Vertebral angiography with compression of the carotid artery in the neck will often help demonstrate the distal site of the rent in the ICA, if there is a patent fetal posterior communicating artery to the ICA on the side of the fistula. Sometimes, there can be multiple rents in the ICA. ¹⁶

Direct CCF is best treated by microcatheter cannulation of the CCF from cavernous ICA into the cavernous sinus and embolization using coils. ¹⁷ A balloon assistance helps prevent migration of coils into ICA and to differentiate the location of ICA from the coils within the cavernous sinus. ¹⁸ There are reports of using flow diverters in cavernous ICA to treat direct CCF. This can be done with or without coil deployment in the cavernous sinus either from transarterial or transvenous route. ^{19 20}

Indirect CCF and cases of failed transarterial embolization of direct CCF are treated by transvenous catheterization of the cavernous sinus and embolization using coils. CTA and CTV will facilitate venous access. A venous roadmap from the venous phase of the ICA angiography will help cannulation of the cavernous sinus with a microcatheter. The venous route often chosen for cavernous access is through inferior petrosal sinus. This can be blindly accessed from internal jugular vein even if the inferior petrosal vein is not seen or distended. ²¹ Venous access can also be performed through other veins such as the superior ophthalmic vein. ^{22 23 24 25 26 27 28 29 30} If the superior ophthalmic vein is dilated, the initial coils are placed at its origin from the cavernous sinus. If the cortical vein is distended, it is chosen for initial coil placement to avoid its distension and potential rupture. Liquid embolic materials can be used if there is persistent filling of the CCF despite coil embolization when angiography is performed through the catheter in the ICA. ^{31 32 33} The liquid embolic materials are injected through the microcatheter placed through the transvenous access for coiling. Alternatively, it can be injected through a second microcatheter at the initial placement of coiling catheter, as once coiling is completed the coiling microcatheter cannot be placed distally in the cavernous sinus. ³⁴

Embolization of meningeal feeders to CCF using particles and liquid embolic agents can be performed if there is persistent filling of indirect CCF. ³⁵ Follow-up angiography is done to demonstrate persistent and complete CCF obliteration.

Intracranial Extra-Axial Hematomas

Traumatic injury to MMA can cause pseudoaneurysms which may thrombose or rupture with subsequent epidural hematoma in up to 70% of cases. ³⁶ Less commonly, MMA rupture results in a subdural, subarachnoid, or intraparenchymal hemorrhage ^{37 38} ( Fig. 3 ). Most often, these hematomas are located in the temporal fossa. Evacuation is recommended when the volume of epidural hematoma (EDH) is more than 30 mL, 15 mm thick, causes a midline shift of 5 mm, or the patient develops neurological decline. If small, they are monitored by imaging for change in size. To reduce the economic burden, effect of added radiation, and risk of sudden clinical deterioration, the MMA can be embolized. ³⁹ Angiography may reveal laceration, pseudoaneurysm, or an AVF. Enlarging EDH can occur up to 30 days after trauma. ^{40 41} Symptomatic chronic subdural hematomas are usually managed by surgical evacuation. But they can recur due to underlying vascular etiology. MMA embolization has been shown to prevent increase in size of the hematoma or promote subsequent spontaneous resolution. ^{42 43 44}

Fig. 3.

Chronic subdural hematoma. A 48-year-old male was found underneath a semi-truck after being struck. On arrival, the patient was hemodynamically stable. ( a ) CT showed a left frontoparietal subdural hematoma. ( b ) Left external carotid artery angiography showing prominent blush in the left high parietal region, which was confirmed on selective left middle meningeal artery posterior division angiography using microcatheter ( c ). ( d ) Post onyx embolization angiography showing obliteration of the vascular blush.

Treatment of Intracranial Extra-Axial Hematomas

Treatment is targeted according to the location of the hematoma. Selective microcatheter angiography of MMA is performed. In case of pseudoaneurysm of MMA, it is selectively embolized using coils, poly vinyl alcohol, or liquid embolic materials. In case of chronic subdural hematoma, collaterals can often be seen in relation to convexity branches of MMA, which are then embolized. Both poly vinyl alcohol and liquid embolic materials have shown good results. ^{39 42 43}

Pseudoaneurysm

Penetrating and high-speed trauma are common causes of pseudoaneurysms. ^{45 46} Though rare in civilian populations, pseudoaneurysms are the most commonly missed extracranial vascular diagnosis in the military following trauma. ⁴⁷ In both populations, penetrating injuries are seen to affect the deeper blood vessels of the head and neck, including the ECA and its branching vessels. ⁴⁷ These injuries can be caused by sharp or blunt objects, including knives, firearms, and high-explosive military munitions. They initially present with severe bleeding and/or airway obstruction, followed by late potential vascular complications. For example, pseudoaneurysms may present days, weeks, or even years following a traumatic craniofacial incident. ⁴⁸ These patients are at greatest risk of spontaneous, life-threatening bleeding, requiring surgical intervention. ^{5 47} Pseudoaneurysms should be on the differential during long-term follow-up in trauma patients and should not be confused for lipomas or cysts. ⁴⁹

Pseudoaneurysms, or pulsating hematoma, result from intimal damage with subsequent hematoma formation inside the adventitia or surrounding tissue. Over time, the clot undergoes fibrotic changes and progressively becomes an arterial outpouching. The wall of the pseudoaneurysm is contained by weak fibrous tissue and clot material, in contrast to true aneurysms which are confined by the three layers of the arterial wall. ⁵⁰ Rupture of these weak “false” walls can result in life-threatening, heavy bleeding.

The facial, maxillary, and temporal arteries are especially vulnerable to trauma due to their superficial location ^{46 51} ( Fig. 4 ). The most common pseudoaneurysm occurs in the superficial temporal artery (STA) and presents weeks to months following maxillofacial trauma. ⁵² The STA is most vulnerable while traversing the zygomatic arch after exiting the parotid gland. ⁵³ Diagnosis can be made through direct observation of a pulsatile mass in the region of STA. Patients may further present with headache, dizziness, audible pulsations, neurological deficit, or ear discomfort. ^{52 54} Proximal occlusion of the artery will diminish pulses. ⁴⁹ Treatment is required due to risk of hemorrhage, pain, or cosmetic defects. Treatment options include surgical resection, ligation, intravascular sclerosis, endovascular coil embolization, ultrasound-guided compression, or percutaneous thrombin embolization. ^{46 47 52 53 55 56 57 58} Needle biopsy should be avoided due to risk of bleeding.

Fig. 4.

Left facial A pseudoaneurysm (black arrow) following stab injury seen on CTA ( a ) and left common carotid artery angiography of the neck ( b ). ( c , d ) Postembolization angiography showing coils beyond and proximal to the aneurysmal neck to prevent reflux filling from collaterals.

Though vascular injuries are rare secondary to condylar fractures, pseudoaneurysms of the ECA and maxillary artery have been reported due to their anatomical proximity to the mandibular condyle. ⁵⁹ The maxillary artery travels through the parotid gland, crosses between the ramus and sphenomandibular ligament, and enters the mandible. For this reason, maxillary artery pseudoaneurysms usually result from high-velocity maxillofacial trauma, though there is one report of a maxillary artery pseudoaneurysm that occurred secondary to a stab wound. ^{60 61 62} Pseudoaneurysms of extracranial vessels, such as the maxillary artery, may present with painful pulsatile swelling in the periauricular or mandibular region. ^{59 63} Patients may also present with facial paralysis or bruit within the mass. ⁶⁰

The lingual artery originates in the neck and travels to supply the tongue and regions surrounding the submandibular and sublingual salivary glands. The mandible forms a bony protection around the lingual artery, thereby preventing most forms of trauma. Pseudoaneurysms of the lingual artery are at risk of spontaneous rupture, causing oral or nasal bleeding, and often present secondary to mandibular fractures. ^{5 64} Due to its bony surroundings, the lingual artery is difficult to image using CTA due to dental artifact. ⁵ In the case of lingual artery pseudoaneurysm, MRA may substitute for CTA. Treatments involve endovascular embolization or thrombin injection, though surgical approaches are also available. ^{65 66 67}

Patients with skull fractures involving the MMA groove can result in vascular lesions including active contrast extravasation (71%) and pseudoaneurysm (29%) on angiography ⁶⁸ and are associated with a high mortality rate. ⁶⁹ The MMA branches off the maxillary artery in the infratemporal fossa and courses through the foramen spinosum into the middle cranial fossa. Radiographically, traumatic MMA pseudoaneurysm can have an irregular wall with signs of dissection and generally is located distally with slow filling and emptying. ⁶⁹

Laceration

Penetrating injuries to the head and neck commonly occur secondary to a high-velocity gunshot wound or a lower velocity stab wound. They may also be seen following motor vehicular accidents. Injuries to the face may involve the facial nerve which is more superficially located ⁷⁰ and deeper injuries frequently involve the vascular structures including the ECA. ⁷¹ For anatomical purposes, it is useful to divide the neck region into three zones. Zone 1 extends from the clavicle to the cricoid cartilage, Zone 2 from the cricoid cartilage to the angle of mandible, and Zone 3 from the angle of mandible to the base of the skull. Although Zone 2 injuries are more common, ⁷² Zone 1 injuries are more dangerous and carry a high mortality. ⁷³ Mortality rate following a penetrating trauma to the neck region ranges from 3 to 6%; however, when the vascular structures are involved the mortality increases significantly. ^{74 75} Neck exploration may prove to be negative in up to 15% of cases. ⁷⁵ Lacerations of the face and neck vessels can cause massive bleeding with high mortality rate. ECA branches are the third least common vessels to be involved in the head and neck region ( Figs. 5 and 6 ).

Fig. 5.

Patient with history of gunshot wound to the right side of the mandible with persistent bleeding; angiography showed lacerated right proximal internal maxillary artery (black arrow) ( a ) which was successfully embolized using coils ( d ). Also seen is the right internal carotid artery (ICA) dissection (chevron arrow) ( a ), and intracranial circulation being filled through left ICA ( b ) and left vertebral artery ( c ) through patent circle of Willis.

Fig. 6.

Right lingual artery laceration. A 23-year-old male who presented after motor vehicle collision suffering multiple injuries. ( a, b ) Selective right lingual artery angiography in lateral view showing laceration with active contrast extravasation. ( c, d ) Post–glue embolization of the laceration showing no contrast extravasation.

Dissection

Following blunt trauma, dissection of the ECA and its branches can occur, which may not be detected on CTA and these injuries are often missed as symptoms may be overlooked due to the related head injury. This can prove fatal. ^{76 77}

External Carotid-Jugular Arteriovenous Fistula

AVF following trauma to the neck region is a rare but serious complication. There are reports of AVF between the ECA and the internal jugular vein following traumatic events such as blast injury or even cannulation of the internal jugular vein. ^{78 79 80} They may present with pulsatile swelling and bruit in the affected area. They can be successfully imaged using Doppler or CTA ( Fig. 7 ).

Fig. 7.

Left occipital arteriovenous fistula (AVF) in a 48-year-old male with stab wound to the neck. A left common carotid artery angiography showing AVF fed by muscular branch from the left occipital artery ( a ), which was successfully embolized using micro coils ( b ).

Treatment of Pseudoaneurysm, Laceration, Dissection, and AVF

CTA usually gives an idea of the involved vessel. Once the patient is stabilized hemodynamically, an angiography is performed. If active leak is identified and the traumatized vessel is small with good collateral circulation, the vessel can be sacrificed. This can be performed using coils, gelfoam, or liquid embolic materials. Gelfoam as pledgelets is used for medium to large vessels, while gelfoam slurry is used for small to medium size vessels. Gelfoam gives temporary tamponade and has been proven to be effective. Coils including fibered coils allow tamponade of the leak in large vessel. However, coils may not attain complete obliteration and may require subsequent embolization with gelfoam or liquid embolic materials such as N-Butyl 2-cyano acrylate or ethylene vinyl alcohol copolymer (Onyx). Endovascular embolization can access surgically inaccessible vessels relatively rapidly. ^{78 81 82 83 84 85 86}

Conclusion

Clinical presentation following blunt and penetrating craniofacial injuries is variable and is dependent on the type of vascular trauma present. Vascular injury resulting from craniofacial trauma includes pseudoaneurysms, CCFs, extra-axial hematoma, and arterial dissections. The goal of treatment is early prevention of hemorrhage through occlusion of the parental vessel or repair of the deficit. To date, digital subtraction angiography is the gold standard for identification of traumatic neurovascular injury, though CTA is usually the first-line imaging modality used at presentation. Treatment of vascular trauma is primarily achieved through endovascular procedures, because it is less invasive compared with microvascular surgery. Interventional radiological procedures in craniofacial trauma are evolving with modern techniques, newer materials, and equipment, and have been supporting the trauma team for rapid control of bleeding in surgically difficult to access vessels.