Introduction
Head trauma has been cited as the most frequent clinical presentation in the emergency department. According to a 2013 survey by American College of Surgeons, nearly 800 trauma admissions were reported across different healthcare facilities in the United States. Additionally, skull base injuries were seen in one-third of the patients. The reported incidence is even greater in the developing countries or regions of limited healthcare access. Traumatic brain injury (TBI) therefore represents a global health problem contributing to high rates of in-hospital morbidity and mortality.
Etiology
The etiology can be broadly classified into penetrating and nonpenetrating trauma. Nonpenetrating injuries have been identified as the leading causes of skull base fractures with a prevalence of 7%–16%. This usually includes high-velocity trauma including motorized vehicle collisions (MVCs), blunt cerebrovascular injury (BCVI) via falls, and assaults. Penetrating trauma (mostly gunshot wounds) accounts for less than 10% of the cases. , Identification of skull base fractures often prompts assessment of coexisting orbital and facial fractures in addition to intracranial lesions. The extent of potential vascular complications and resulting management depends on the location and pattern of the fracture, which is in turn determined by the mechanism of injury and type of impact.
Skull base anatomy
The skull base is made up of seven bones, the paired frontal and temporal bones, and the unpaired ethmoid, sphenoid, and occipital bones. It is divided into anterior, central, and posterior regions, which form the floor of the anterior, middle, and posterior cranial fossae.
The anterior skull base (ASB), formed by the frontal and ethmoid bones, separates the anterior and inferior frontal lobes and olfactory structures within the anterior cranial fossa from the orbits and the sinonasal cavity. Anterior fossa is bound by important structures: The lateral and anterior borders are formed by the frontal bone and frontal sinus, and floor is formed by the cribriform plates and roof of the ethmoid sinuses. Lesser wing of the sphenoid bone, including the clinoid process, forms the posterior border between the anterior and central skull base. Anterior and posterior ethmoid artery foramina are located in ASB.
The central skull base (CSB), formed by the sphenoid and anterior temporal bones, is closely related to the pituitary gland, cavernous sinuses, and the temporal lobes superiorly, and the sphenoid sinus anteriorly and inferiorly. The anterior border of the CSB is formed by the posterior margin of the lesser wing of the sphenoid bone, clinoid process, and tuberculum sella. The floor is formed by the greater wing and central body of the sphenoid bone, the sphenoid sinus, and the sella. The posterior border between the central and posterior skull base is formed by the superior margin of the petrous ridge of the temporal bone, the basi sphenoid portion of the clivus, and the dorsum sella. Important vascular structure in this par includes the internal carotid artery.
The posterior skull base (PSB) is formed by the posterior temporal bone and the occipital bone. The anterior border is formed by the petrous ridge of the temporal bone superiorly, and the clivus (basi occiput portion) inferiorly. Foramen magnum located in the PSB transmits the vertebral artery.
According to Van Huijzen’s classification, extension lines from the suborbital fissure and the petrooccipital fissure intersect at the apex of the nasopharynx inside, pointing outward to the zygomatic bone and posterior margin of the mastoid process, respectively. The triangular area between the two lines is described as a lateral skull base and includes parapharyngeal space, infratemporal fossa, and pterygopalatine fossa. The lateral skull base houses important neurovascular structures including internal carotid artery, the lateral sinus, and sigmoid that will give the vein jugular, and petrosal sinus.
A 5-year retrospective study of 1606 patients with skull base trauma reported the highest frequency of temporal bone (40%) involvement followed by orbital roof (24.1%), sphenoid (22.6%), occipital (15.4%), ethmoid (10.8%), and clival bone (1.03%).
Blunt cerebrovascular injury classification
The diagnosis of vascular injury in association with skull base trauma is closely tied to the screening criteria used for patient evaluation. This then facilitates and determines the choice of diagnostic modalities and subsequent management. Biffl et al. proposed a grading scale, Denver criteria, to assess blunt cerebrovascular injuries (BCVIs) and subsequent neurological outcomes: grade I (mild intimal injury or irregular intima), grade II (dissection with raised intimal flap/intramural hematoma/intraluminal thrombosis with luminal narrowing >25%), grade III (pseudoaneurysm), grade IV (vessel occlusion/thrombosis), and grade V (vessel transection). This is commonly used for classification of blunt injury in carotid and vertebral arteries. A total of 76 patients presenting with blunt carotid arterial injury were included in the analysis. Grade I injuries were associated with the best prognosis, with two-thirds of cases resolving spontaneously. On the other hand, vascular transection (grade V) was shown to be refractory to any intervention. Based on their findings, Biff et al. recommended endovascular repair for grade II, III, IV, and V lesions in addition to systemic anticoagulation. Isolated heparin therapy was associated with progressing dissections (grade II) and less than 10% of pseudoaneurysms (grade III) healing. Another clinically relevant tool is Memphis criteria.
Both Memphis ( Table 10.1 ) and Denver criteria ( Table 10.2 ) have been modified to further improve the utility of these tools in diagnostic settings. Overall, introduction of the screening criteria in combination with advanced imaging has significantly improved the sensitivity of BCVI identification.
| Modified memphis criteria |
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| Modified denver criteria |
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Signs and symptoms
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Trauma to the vertebral artery
Neurological compromise following vertebral artery injury can be significant secondary to ensuing ischemic and embolic sequelae. Vertebral artery injury usually presents as dissection with or without pseudoaneurysm formation, luminal stenosis, or an arteriovenous fistula formation. Blunt vertebral artery injuries are associated with 14%–24% morbidity and 8%–18% mortality .
Grade 1 (vessel lumen stenosis <25%) and grade 2 (luminal stenosis between 25% and 50%) injuries are the most common form of blunt vertebral artery (VA) injury. These low-grade injuries in hemodynamically stable patients can be managed by pharmacological treatment, including acetylsalicylic acid or other antiplatelet or anticoagulant. One study, analyzing a similar group of patients, reported radiological improvement (stable/improved/resolved) in 97.4% of low-grade blunt VA injuries after conservative management. Endovascular therapy with stent placement is preferred in selected situations: (1) hemodynamically unstable dissection, (2) recurrent thromboembolic events, and (3) contraindication to anticoagulant therapy. However, there is no general consensus on the practices related to screening, management, and follow-up of VA injuries. Important variables to consider include the duration of the anticoagulation and risk of posterior circulation strokes. In a retrospective study, Scott et al. reported posterior circulation strokes in only 1.7% of the cases. Interestingly, these infarcts were demonstrated by neuroimaging in the acute period of hospitalization (within 4 days of injury) and showed no correlation to the pharmacological treatment. Another study also reported similar findings in Biffl grade V VA injuries with stroke rates unrelated to the presence of emboli or antiplatelet drugs.
High-grade traumatic vertebral artery injury (TVAI) is most difficult to treat and can lead to a potentially fatal posterior circulation stroke. The variable clinical presentation and lack of widely accepted diagnosis and management guidelines make it a clinical challenge. Patients may have a delayed onset of neurological symptoms including headache, hemiplegia, gait ataxia, and/or position-associated dizziness. However, due to compensatory mechanisms, the majority of the cases of TVAI are asymptomatic, therefore making early screening important. Cerebral catheter angiography (CTA) is considered to be the gold standard for TVAI diagnosis. A high sensitivity of 99% and the ability to initiate timely treatment make it the most widely used screening modality. While medical therapy with anticoagulation is aimed at reducing disease progression and thrombotic sequelae, studies have reported complications of stroke (1.8%–3.8%, first or recurrent) and intracranial hemorrhage (0.5%). However, antiplatelet therapy does help prevent in-stent stenosis. Surgical treatments include ligation and vascular reconstruction. Revascularization is performed in cases of no bleeding and small aneurysm. Life-threatening neurological deterioration with uncontrollable hemorrhage warrants an open surgery. Direct open surgery otherwise is not routinely performed due to vertebral artery anatomy and its location within the transverse foramen, limiting exposure and access. There is extensive literature advocating the safety of adopting an endovascular approach. The minimally invasive and effective treatment modality has shown to be associated with good clinical and angiographic outcomes with no stent-related complications and new-onset neurological symptoms during follow-ups. , Common interventions include stent placement, stent-assisted coiling, and vessel occlusion. A study discussed important variables to consider to devise endovascular treatment strategies. Based on their findings, two approaches were proposed depending on the diameter of the parent artery ( D ) and caliber of the neck of the aneurysm ( d ): (1) D > d , exclusive stenting and (2) D < d , combined endovascular tools (stent angioplasty, coils, balloon, liquid glue) to maintain steady blood flow dynamics. This is because an aneurysmal wall is subject to greater stress from blood flow when the parent artery is thinner, thereby increasing the risk of aneurysm rupture, which requires filling in the sac. Randomized clinical trials and long-term follow-up studies are needed to establish conclusive findings about endovascular management of high-grade TVAI.
Direct vertebral arteriovenous fistula may result from penetrating trauma (stab wounds, projectile injury, iatrogenic). The fistulous connection of the injured vertebral artery is usually occluded using detachable endovascular coils, placed proximal and distal to the site of fistula formation. Often, proximal occlusion combined with a retrograde microcatheter from the contralateral vertebral artery is sufficient. Assessment of fistula recurrence is made using long-term follow-up with delayed angiography to ensure no collateral pathways develop.
Carotid-cavernous fistulas
Sphenoid body fractures (seen in 50% of sphenoid fractures), including sellar and clival involvement, are associated with increased risk of carotid injury. Carotid-cavernous (CC) fistula represents a pathologically created direct communication between carotid artery and venous channels in the cavernous sinus, thereby creating a high-flow fistula ( Fig. 10.1 ) . An anatomical–radiographic (Barrow et al.) classification can be used for patient evaluation: (1) type A, high-flow shunts between the internal carotid artery (ICA) and the cavernous sinus, (2) type B, between meningeal branches of the iICA and the cavernous sinus, (3) type C, between meningeal branches of the external carotid artery (ECA) and the cavernous sinus, and (4) type D, between meningeal branches of both ICA and ECA and the cavernous sinus. Further subclassification of traumatic CC fistulas (Barrow type A) can be performed via angiographic evaluation of the opacification of anterior cerebral artery (ACA) and middle cerebral artery (MCA): small-size (opacification of both ACA and MCA), medium-size (opacification of either ACA or MCA), and large-size fistula (opacification of neither ACA nor MCA).
Depending on the type of injury, the onset of symptoms may be within hours (direct shunt) or weeks to months (indirect shunt) after injury. CC fistulas usually present with Dandy’s triad of exophthalmos, bruit, and conjunctival chemosis. Other clinical manifestations include ophthalmoplegia (cranial nerves III, IV, VI), epistaxis, diplopia, and progressive visual loss. , Pathologic mechanisms contributing to visual decline include reversal of venous drainage, arterial flow into the superior ophthalmic vein, increased intraocular venous pressure, and eventually ischemic optic neuropathy. The incidence in untreated CC fistulas can be as high as 89%, thereby warranting an early intervention. Prior studies have reported high morbidity (32%–67%) and mortality (17%–38%).
The gold standard for diagnosis of CC fistulas is four-vessel digital subtraction cerebral angiography. With evolution in the treatment strategies, endovascular embolization is the intervention of choice. Prior to endovascular treatment, management of Barrow type A CC fistulas comprised muscle occlusion and/or carotid artery ligation. In addition to procedural risks, these methods were associated with a high recurrence rate due to collaterals. , There are multiple approaches to endovascular treatment. One group described the transarterial route through the carotid artery. Approaches that could aid better localization of rent in the carotid artery include use of higher magnification rates and use of a microwire for exploration of the carotid artery wall. Following access to fistula, access is maintained using a microcatheter advanced into the cavernous sinus. This is followed by the placement of long coils into the cavernous sinus. One method to prevent coil placement in carotid artery lumen is use of a balloon in carotid-cavernous artery to help distinguish cavernous sinus from ICA. Both coils and detachable balloons can be used for embolization of the fistula. The selection of detachable balloon as an embolic material has shown to be cheaper. However, studies have demonstrated higher failure rates (5%–10%). Additionally, unexpected balloon detachment can lead to embolism and stroke. Therefore, anticipation of embolic materials and understanding of fistula size is crucial to avoid unfavorable outcomes. If direct transarterial approach is not feasible due to inability to advance the microcatheter through the rent in the carotid artery, embolization can be performed via venous access through the inferior petrosal sinus or superior ophthalmic vein. Small patient population–based studies using superior ophthalmic vein have reported no complications. Superior ophthalmic vein can be accessed through direct puncture or ophthalmologic cutdown. , As a last resort, the carotid artery may be sacrificed to occlude the CC fistula.
Traumatic intracranial aneurysms
Traumatic aneurysms of the intracranial arteries are rare, accounting for less than 1% of all cerebral aneurysms. However, in injuries secondary to penetrating trauma, the incidence can be as high as 20%–50%. , Common etiologies include motor vehicle accidents and falls. These include both true aneurysms with all three arterial wall layers or pseudoaneurysms with no wall layers. The risk of rupture of untreated intracranial aneurysms is highest in the first 3 weeks postinjury, with a mortality of 50%. The risk of mortality is even greater with conservative versus surgical treatment.
The pathologic outpouching of vessel walls commonly involves intracavernous ICA, infraclinoid carotid artery, and vertebrobasilar artery. Infraclinoid segment represents the transitional zone between the relatively fixed cavernous and mobile supraclinoid segments of ICA. In distal circulation, anterior cerebral artery (ACA, pericallosal, and callosomarginal segments) and, less frequently, middle cerebral artery (MCA) are involved. Fleischer et al. reported 41 cases of traumatic aneurysms, with distal branches of MCA involved in 50% cases. Traumatic intracranial aneurysms (TICAs) can be classified based on location relative to circle of Willis: proximal to circle of Willis (supraclinoid carotid, infraclinoid carotid, and vertebrobasilar arteries), distal to circle of Willis (subcortical and cortical arteries). Mao et al. further classify TICAs into perifalx and distal cortical aneurysmal. Perifalx aneurysms are located on distal ACA, posterior cerebral artery, and superior cerebellar artery. Distal cortical aneurysms involve cortical branches of MCA or ACA.
Common clinical features include cranial nerve palsies, epistaxis, subarachnoid hemorrhage, and mass effect. Average duration to the onset of hemorrhage from injury is 3 weeks. Clinical presentation can vary depending on the location of the aneurysm. , Infraclinoid ICA aneurysms usually present acutely with epistaxis, progressive cranial nerve palsies, and diabetes insipidus. , Supraclinoid ICA, distal ACA, and distal cortical aneurysm have a delayed onset of severe symptoms. The patient may report sudden onset of headache and/or altered sensorium secondary to subarachnoid hemorrhage. , It is important to look for signs of intracerebral bleed in these cases. Buckingham et al. reported findings from 11 patients presenting with distal cortical aneurysms. Subarachnoid hemorrhage was seen in 63% of the cases, with only 20% of the aneurysms being diagnosed before rupture.
Intracranial aneurysms are a rare complication of skull base trauma. At present, CT scans are more commonly employed as primary investigation tools in closed head injury. This versus cerebral angiography may lead to more intracranial aneurysms being overlooked or misdiagnosed. There is no general consensus on the timing of performing cerebral angiography. While multiple studies have recommended different time frames, clinical presentation and risk of impending hemorrhage are important factors to consider. CT angiography (CTA) has emerged as a noninvasive screening tool for TICAs. However, given the limited sensitivity, some studies suggest use of digital subtraction angiography (DSA) following negative findings on CTA as a necessary confirmation tool. ,
The high risk of aneurysm rupture warrants treatment. Overall, surgical management of TICAs is challenging due to its pathological complexity and close anatomical relations to the skull base. As the mainstay treatment of intracranial aneurysms, clipping is also an important surgical intervention for TICAs. However, for TICAs, it may not always be feasible due to absence of neck, poorly defined wall, and arachnoidal adhesions. These anatomic features present a higher risk of intraoperative rupture of TICAs during clipping. Therefore, it is important to plan ahead of the procedure. Alternative interventions include trapping, excision, and wrapping of the aneurysm. To be noted, studies have shown high prevalence of recurrence and rupture with wrapping. For PICA aneurysms, one option is PICA-PICA bypass and sacrifice of the vertebral artery given adequate flow in the contralateral circulation. Both surgical clipping and endovascular occlusion can be challenging for management of infraclinoid ICA aneurysm. It is helpful to determine the feasibility of proximal ICA ligation or external carotid–internal carotid (EC-IC) bypass before securing ICA. This can be done preoperatively using a balloon test occlusion. Endovascular occlusion can also be performed if anatomy favors coiling. However, TICAs tend to be small with no true arterial wall, leading to risk of rupture. A study assessed the outcomes of endovascular approach in 13 patients presenting with TICAs (MCA = 7, ACA = 2, ICA = 4). Glasgow Outcome Scale (GOS) was determined: five patients with a score of 5, seven patients scored 7, and one patient had 3.
Trauma to the middle meningeal artery
Temporal bone fractures are commonly associated with complication of middle meningeal artery (MMA) lesions. Common clinical presentations of MMA lesion include the formation of an epidural or subdural hematoma. It is important to note that while MMA rupture classical presents as epidural hemorrhage, this pathology can be multifactorial and occur secondary to lesions involving middle meningeal vein, diploic veins, and venous sinuses. Fishpool et al. reported important anatomical observations of MMA vasculature at the level of greater wing of sphenoid bone and foramen spinosum. Investigation of 29 cadaveric specimens revealed that dural venous sinuses accompany MMA throughout its course forming a plexiform arrangement around the artery caudal to the foramen spinosum. The authors therefore postulated that epidural hemorrhage was less likely due to an exclusive MMA lesion. Clinical presentation can be divided into three phases: consciousness, lucid interval, and rapid neurological deterioration.
Pseudoaneurysms as previously described commonly involve carotid arteries. However, skull base trauma can also lead to rare MMA pseudoaneurysms. Around 70%–90% of cases occur secondary to fractures of temporal bone. The pathogenesis involves a tear in the MMA, which is in turn sealed by a clot. This is followed by recanalization and formation of a false lumen. The resulting pseudoaneurysm enlarges over time and can lead to epidural hematoma if ruptured . Very rarely, traumatic pseudoaneurysm of MMA (TPMMA) can also present as intraparenchymal hemorrhage (IPH). While the exact pathogenesis remains unclear, a study hypothesized that progressive thinning of dura secondary to TPMMA enlargement may contribute to delayed IPH. Less than 10 cases have been reported in literature. , There are two case reports presenting findings of acute IPH secondary to ruptured TPMMA. In both cases, there was a dural defect secondary to dual contact with ruptured TPMMA. , Sudden and abrupt neurological deterioration in a patient with temporal bone fracture should raise a strong suspicion for TPMMA. This manifestation usually occurs following a latent period of 10–21 days from the initial injury. Studies have also reported clinical presentation of intractable epistaxis secondary to arterial wall weakening and adjacent bony erosion. ,
Middle meningeal arteriovenous fistulas (MMAVFs) are rare and likely underreported lesions occurring between middle meningeal artery and neighboring veins (diploic vein, meningeal vein, cortical vein) or dural venous sinuses (petrosal sinus) . Freckmann et al. investigated 446 angiograms of patients presenting with trauma. In this population, the incidence of MMAVFs was 1.8%. These lesions pose a high risk of intracranial hemorrhage and may explain manifestations of nonaneurysmal SAH. Sakata et al. reported findings of diffuse, basal SAH preceded by a progressively enlarging MMAVF with dilated intracranial venous drainage. This was postulated to occur secondary to formation and rupture of a venous aneurysm.
Initial screening modality is computed tomography (CT). It is important to mention that since routine arteriography has now largely been replaced by CT in the initial management, a large proportion of lesions go misdiagnosed. Therefore, there has been an increase in the number of cases presenting with delayed intracranial hemorrhage following skull base trauma. Main treatment modalities for TPMMA include surgical excision, endovascular treatment with detachable coils, and N -butyl-cyanoacrylate. Selective embolization of the parent artery has several advantages: better localization and visualization of the feeding vessels, greater access to distal vessels, rapid turnover, and preservation of ECA branches. ,
For management of MMAVFs there is no comprehensive comparison of prognosis following conservative versus surgical intervention. The natural history of the lesion is therefore unclear. However, some studies have reported successful outcomes following endovascular obliteration. Liquid embolic agents (onyx) and more dilute preparations (e.g., n-BCA) have been proposed depending on several anatomic considerations: location and size of fistula, degree of vessel tortuosity, and feasibility of navigation.
Venous epidural hematomas
As previously described, most epidural hematomas result from the MMA lesion ( Fig. 10.2 ) . Less frequently, epidural hematoma (EDH) can also originate from rupture of arachnoid granulations, diploic emissary veins, and dural sinuses. They have been described as bifrontal (detach first third of sagittal sinus), biparietal or vertex, and bioccipital (detach posterior third of sagittal longitudinal sinus) EDH . Presence of adequate collateral venous drainage is associated with lower mortality in anterior superior sagittal sinus (SSS, 17%) versus central and posterior lesions (50%). , Goal of intervention is to decompress neural structures and arrest bleeding. The closer the EDH is located to the midline, the slower the bleeding. On exposure, the external surface of dura presents with diffuse bleeding, making it difficult to locate the bleeding source. Surgical management of venous sinus–related EDH is traditionally a craniotomy and evacuation of the clot. This has been well described for transverse sinus. , However, this poses a greater risk of damage to sinus and limited visibility to identify the bleeding spot. Hence, multiple studies have reported using a strip of bone overlying the sinus. In this technique, strip craniotomy, clot is then progressively resected from the periphery. ,
