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Role of imaging in penetrating vascular injuries of the craniocervical region
*Corresponding author: Sai Swarupa Reddy Vulasala, Department of Internal Medicine, East Carolina University Health Medical Center, Greenville, United States. vulasalaswarupa@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Kee-Sampson JW, Gopireddy DR, Vulasala SS, Stein R, Kumar S, Virarkar M. Role of imaging in penetrating vascular injuries of the craniocervical region. J Clin Imaging Sci 2022;12:63.
Abstract
Penetrating vascular injury has become the topic of interest with increased gun violence in the United States. The radiologist plays a crucial role in establishing and systemizing the signs of vascular injury such as intimal flap, dissection, pseudoaneurysm, rupture, and arteriovenous fistula. Various imaging techniques such as ultrasound Doppler, computed tomographic angiography (CTA), magnetic resonance angiography, and conventional angiography are being employed based on clinical recommendations. Of all the techniques, CTA has been shown to embrace a promising role in identifying vascular injuries with superior sensitivity, specificity, and accuracy. An acquaintance of the imaging features has been shown to improve the approach to trauma patients in clinical settings. This article details the imaging modalities and the features of the head-and-neck penetrating vascular injury.
Keywords
Head trauma
Gunshot imaging
Vascular trauma
Neck vascular imaging
Head-and-neck
INTRODUCTION
Penetrating injury to the craniocervical region constitutes 5–10% of cases presented at the emergency department. By definition, the penetrating injuries of the neck breach the full thickness of the platysma muscle. The severity of head-and-neck vascular injuries may range from minor damage to fatal vascular rupture that may require no intervention to extensive surgery.[1] Penetrating cerebrovascular injury most commonly involves peripheral cortical branches than the proximal vessels of the circle of Willis.[2] At the same time, branches of the external carotid artery are more prone to extravasation or occlusion in the neck and may result in airway compromise.[2] Signs of vascular injury may range from minimal intimal separation and dissection to pseudoaneurysm formation and complete occlusion [Table 1].[3] Arteriovenous fistula (AVF) may also occur in cases where rupture of the artery and vein leads to a connection between the two vascular lumens.
Hard signs of arterial injury | Soft signs of arterial injury |
---|---|
Severe uncontrolled external arterial bleeding | History of extensive bleeding on scene |
Rapidly expanding or pulsatile hematoma | Proximity of trauma to major vessel |
Palpable thrill | Subjective diminished pulse |
Audible bruit | Small non-pulsatile and stablehematoma |
6 P’s (absent or diminished pulse, pallor, paralysis, paresthesia, and poikilothermia) | Injury to the anatomically related nerve |
Neurologic deficit | Abnormal ABI (<0.9) |
Refractory hypotension | Abnormal flow-velocity waveform on Doppler ultrasound |
Delayed capillary refill |
IMAGING OF PENETRATING VASCULAR INJURY TO THE HEAD-AND-NECK
It is critical to be familiar with the range of clinical findings and imaging pitfalls associated with the diagnosis of traumatic craniocervical vascular injury. Conventional angiography, computed tomographic angiography (CTA), and magnetic resonance angiography (MRA) are the major techniques that are being employed in clinical practice. Conventional angiography is the gold standard in detecting vascular injuries.[4] It has the benefit of performing a therapeutic intervention for vascular injury in the same setting. Although the role of conventional angiography has been replaced by the CTA over the past 15 years, there are certain situations where catheter angiography remains the gold standard. Such situations include patients with the computed tomography (CT) artifact from bullet fragments, dental implants, and metals, or hemodynamic instability requiring endovascular intervention. The major disadvantage of conventional angiography is that it is an invasive procedure with the complications such as hematoma, thrombosis, embolization, ischemia, and intimal dissection in 0.16–2% of cases.[4]
There is an emerging application of CTA in all hemodynamically stable patients with penetrating craniocervical trauma who are not candidates for immediate surgical exploration. In any patient with traumatic craniocervical vascular injury, the imaging shall be performed through the arch of aorta to the circle of Willis, as the primary damage may be away from the visualized signs of trauma.[5] It is unvarying in patients with blunt craniocervical vascular injuries. Various criteria, such as Denver and Memphis, were studied in the literature to include the CTA in the clinical workup of blunt craniocervical injuries.[6] Denver and Memphis criteria demonstrated 18– 34% and 16–29% screening yield, respectively, in identifying 80% and 63–84% of the blunt craniocervical vascular trauma, respectively.[7]
Alongside the routine interpretation of thin-section axial CTA images, various post-processing techniques including multiplanar reconstruction, volume-rendered images, bone subtraction, and maximum intensity projection (MIP) can aid to identify vascular injuries such as dissections and occlusions. Recently, the material decomposition capability of DECT is being applied to subtract bone through calcium-subtraction techniques. Such images can be utilized to create the MIP images without the confounding bone. The low-energy virtual monoenergetic images (VME) increase the iodine attenuation and thereby improving contrast-noise-ratio and image quality. The deployment of low-energy VME in clinical practice reduces the required volume of contrast and radiation exposure.[8]
A dissection commences as a tear in the tunica intima or directly in the tunica media. Mural hematoma is a hypoechoic area along the vessel wall on color duplex US. However, US sensitivity decreases in dissection cases with low-grade stenosis. The accuracy in identifying craniocervical dissection can be improved using the B-flow US to visualize the intimal flaps and intramural hematoma. The color Doppler US is 95–96% sensitive in the diagnosis of internal carotid artery (ICA) dissection and 75% sensitive in vertebral artery (VA) dissection.[9] Although ultrasound is readily available, it has limited value in case of deeply located injuries. On digital subtraction angiography (DSA), features of vessel dissection include (i) irregular vessel wall, (ii) string sign (flow of contrast distal to stenotic foci), (iii) “string and pearl sign” (focal narrowing and distal dilatation of the vessel), and (iv) pseudoaneurysm formation.[10]
MR imaging has an advantage in detecting minor injuries manifested as a small subintimal hematoma. Acute thrombus on MRI appears as a crescent sign with high-signal intensity, best observed on T2-weighted imaging or T1-weighted fat saturation imaging sequences obtained during the acute phase of dissection.[11] The intimal flap appears as a curvilinear T2 and the intramural hematoma is hyperintense on the T1 fat-suppressed MRI technique. The T1 shortening depends on the methemoglobin level with the hematoma evolution.[12,13] The T2-weighted imaging also shows absent flow-void in patients with dissection. Contrast-enhancement along the peripheral and luminal margins of the artery may be observed.[13]
The sensitivity of CTA in detecting head-and-neck vascular injuries is 72.7% and 98–100%, respectively.[14] CTA guides clinicians in deciding the proper dissection management for good clinical outcomes. The variation in vessel caliber is the hallmark of vascular injury on imaging. The normal artery maintains the constant vessel caliber and consistently rounded cross-section, except on turns, from the proximal to the distal part. The subtle change in vessel caliber but maintained cross-section indicates minimal intimal injury or dissection.[12] Signs of CTA in patients with dissection include expansion of dissected vessel, an abnormal vascular contour, eccentric crescent-shaped thrombus in the periphery, thin ring-shaped enhancement along the vessel wall, and a dissecting aneurysm. Vessel wall hematoma appears hyperattenuating and isoattenuating on unenhanced CT and CTA corrected for window settings. While 55% of traumatic dissections improve on follow-up angiography, 25% of the lesions progress to complete vessel occlusion.[11]
Conventional angiography is the gold standard for diagnosing traumatic intracranial aneurysms (TICA).[15] The TICA can be differentiated from congenital aneurysms by (i) the absence of an aneurysmal neck, (ii) irregular aneurysmal sac, (iii) lesion located at an unusual site, and (iv) delayed filling and emptying of the sac than the adjacent vessels. DSA also assists in screening for TICA in penetrating trauma patients with a sensitivity and specificity of 74–98% and 84–100%, respectively.[15]
The criteria for diagnosing AVF on color Doppler and duplex ultrasound include low to high-resistance flow in the affected artery, high velocity and arterialized waveform in the affected vein, and high-velocity turbulent flow in the fistular area.[16] The AVF demonstrates early opacification of the venous component on conventional CTA and MRA. The DSA aids in visualizing the feeding arteries and elaborating the vascularity map for endovascular management.[16] The arterial steal distal to the fistula can be observed on CTA as the asymmetric enhancement of the venous aspect of the fistula. The arteriovenous combinations associated with high-flow fistulous connections are common or ICA/internal jugular vein, external carotid artery/internal jugular vein, and VA/internal jugular or vertebral vein.
Despite the multiple studies and recommendations on the role of CTA in evaluating vascular injury, there are a few limitations to its application in certain circumstances. Bullets, metallic objects, and dental amalgams may cause streak artifacts that obscure blood vessels’ visualization. The entirety of the vessel cannot be studied in the case of arteries enclosed in a bony canal such as ICA as it traverses the skull base or the VA through the foramen transversarium.[12] CT angiography requires a higher amount of contrast material than conventional angiography. In addition, it is limited by the lower spatial resolution and the fact that intervention cannot be performed simultaneously.
PENETRATING INJURIES TO THE HEAD
Penetrating brain injuries (PBI) are life-threatening, with gunshot wounds being the most common cause (12%) [Figures 1-9].[17] Around 80% of such injuries traverse the skull.[18] Because of higher mortality rates, the actual incidence of intracranial vascular injuries is unclear. The arterial injuries happen secondary to shock waves or cavitation from the kinetic energy transfer of the penetrating object.[19] The AVF (86%) is the most common imaging sign in PBI, followed by the pseudoaneurysm (12%), occlusion (2.4%), and transection (2.4%).[14] Risk factors of intracranial vascular injury include bi-hemispheric trajectory, entry wound located over the fronto-baso-parietal area, trajectory adjacent to the circle of Willis, and intraventricular hemorrhage (IVH) and IVH score, and subarachnoid hemorrhage (SAH) and SAH score.[20] The trajectory path in proximity to the circle of Willis (within 2 cm of the suprasellar cistern) comprises the most crucial risk factor for arterial injury.[20,21] Complications secondary to intracranial vascular injuries may lead to hemorrhage, ischemia, and neurological damage, constituting the primary cause of vegetation or death.[22]
The imaging workup of penetrating head injury depends on the type of injury [Table 2].[57-62] MRI is not routinely recommended in gunshot wounds due to the probability of remnant metal in the body. The DSA is the standard imaging modality to evaluate the intracranial vascular injury. However, the significant limitations are that it is expensive, requires intense labor, and is challenging in situations with limited qualified personnel.[20] DSA can be justified in case of highly probable arterial injury, and such probability is determined based on several CT imaging signs such as IVH score (Modified Hijdra score) and SAH score (Modified Graeb score).[21] In addition, DSA may be considered if the CTA is inconclusive or compromised by the metal artifact.[23] The non-invasive CTA has substituted DSA, with a reported sensitivity and specificity of 73% and 94%, respectively.[24]
Dissections are frequently observed in the proximal portion to the M1 section of the middle cerebral artery, VA, and basilar artery.[25,26] Findings of arterial dissection on imaging include intramural hematoma, double lumen, aneurysmal dilatation, saccular aneurysm, pearl and string sign, occlusion, and stenosis.[13] Visualizing and differentiating dissection flaps from atherosclerosis or vasculitis on CTA are challenging. In such situations, MRI aids in diagnosis through an enhanced signal-to-noise ratio in conjunction with blood flow, cerebrospinal fluid, and fat suppression techniques. The double lumen sign is more appreciable on MRA compared to CTA. TICAs are observed in 3–42% of patients who survived PBI.[20] The pseudoaneurysms are more prevalent in the branches of vertebral and anterior cerebral arteries compared to the ICA or circle of Willis.[27,28] CTA is 100% sensitive and specific in patients with TICA.[24] Identifying extraluminal contrast on CTA, described as a “spot sign,” highly suggests active hemorrhage due to TICA.[17] The higher SAH score is considered the sole risk factor in patients with TICA.[20]
Injury to the dural venous sinus (DVS) is associated with an increased morbidity and mortality (20–41%).[29] The pattern of injury can vary from compression, occlusion, and fistula formation. The compression is secondary to the adjacent blood product accumulation which may result in an increased intracranial hypertension. The presentation of DVS compression is similar to DVS thrombosis and can be distinguished on a CT venogram. Criteria for DVS compression include hematoma extension beyond the sinus or the visualization of extra-axial gas within the hematoma that is compressing the sinus. Whereas DVS thrombosis can be identified through (i) delta sign, (ii) extended hematoma into adjacent sinus, and (iii) enlarged DVS compared to adjacent venous sinuses. Penetrating DVS injuries pose a high risk of DVS thrombosis in 23–41% of patients.[30,31] The DVS thrombosis appears as a tubular-shaped hyperattenuation on CT examination. The “empty-delta sign” or luminal-filling defect is seen on contrast-enhanced CT or MR imaging. The DECT techniques, iodine material decomposition, and quantification can be used to differentiate the iodine flux artifact in the normal sinus and the iodine load in the thrombosed sinus. Calcium-subtraction techniques improve the conspicuity of thrombus through bone subtraction.
Dural AV-fistula (dAVF) between the dural sinus and middle meningeal artery is seen in 2% of trauma cases.[25] It is extraparenchymal and located in the arachnoid or dural membrane. Radiographically, prominent vessel clusters can be noticed near the dural sinus. CTA demonstrates high attenuation secondary to hemorrhage. The dAVF has increased death rate and requires a thorough angiographic evaluation.[13] Carotid-cavernous fistula (CCF) is a type of dAVF that is observed between the cavernous sinus and ICA.[25] It can be identified in 0.2% of traumatic brain injuries and 4% of basilar skull fractures.[32] On imaging, CCF can be classified into four types Barrow Type A-B, depending on the arterial and venous component of the fistula [Table 3].[33] Although CT and MRI aid in identifying CCF, a definitive diagnosis can be attained through DSA. Enlargement of the cavernous sinus, superior ophthalmic veins and extraocular muscles, proptosis, and reticulation of orbital fat are the imaging findings of CCF.[23] MRA may show enhanced flow-related signals in the superior ophthalmic veins and cavernous sinus and the absent flow-related signs in the ICA.[23] Abnormal enhancement of small vessels can be noticed around the cavernous sinus on CTA/MRA.
Sign | US | CT |
---|---|---|
Intimal flap | Thin echogenic structures floating within the vessel lumen may cause turbulence or irregular flow on CFD; thrombosis is seen as an echogenic material on B-mode US and has absent flow on PWD and CFD. | Hypoattenuating linear or curvilinear defect arising from the vessel wall into the contrast-enhanced lumen. |
Dissection | Hyperechoic mobile intimal flap, dividing the vessel into true and false lumens, can be seen on US. True lumen expands during systolic and compresses during diastolic phase of vascular supply. While false lumen is opposite. Velocity of true lumen is faster than false lumen on CFD. | Enlarged vessel with eccentric or narrowed vessel lumen; A linear hypoattenuation area (represent dissection flap) may be seen projecting into the vessel lumen; If associated with false luminal thrombosis, a crescentic focal narrowing of the vessel can be observed. |
Pseudoaneurysm | Anechoic or hypoechoic image with moving echoes on B-mode US; May swell during systole; Typical swirling motion causing Yon-Yang sign on CFD; To-and-fro flow pattern may be observed. | Round, well-defined, outpouching hypoattenuating lesion from the adjacent artery; organized extraluminal collection of contrast through a disrupted vessel wall in all phases; Does not enlarge on delayed imaging. |
Rupture | Hyperechoic irregular or fountain-like-jet or round spot in arterial and delayed phases of contrast-enhanced ultrasound can be noticed. | Irregular blush of contrast outside the vessel lumen; Arterial bleed: Iso -or hyper attenuated blood pool on arterial phase and subsequently enhancing attenuation on portal venous or delayed phase images. Venous bleed: Enhanced attenuation on portal venous phase that expand further on delayed phase images. |
Arteriovenous fistula | Anechoic and anfractuous structure between the vein and artery on B-mode; Color mosaic (aliasing) on CFD due to multiple flow velocities in the fistular blood stream. High systolic and diastolic velocities on PWD. | Early and equal enhancement of major vein compared to the artery and asymmetric early filling of involved vein compared to uninvolved veins is observed. |
PENETRATING INJURIES TO THE NECK
Penetrating neck injuries, by definition, involve the entire thickness of the platysma. They account for 1% of trauma encounters in the United States and are associated with a 2–10% of mortality rate and 5% of morbidity rate.[4] Penetrating injuries are due to firearms, stab wounds, and shotguns in approximately 45%, 40%, and 4%, respectively [Figures 10-19].[34,35] The tight and complex neck space anatomy predisposes a more significant potential for vascular, aerodigestive, neurologic, and endocrine injuries. Around 15–25% of penetrating neck injuries involve arteries, resulting in poor clinical outcomes due to neurological sequelae such as stroke or rapid exsanguination.[4,33-39] Roon et al. and Monson et al. divided the neck into three zones [Figure 20 and Table 4] to facilitate the injury assessment.[33-35] Around 47% of the neck injuries are reported in Zone 2, which can be explored efficiently with surgery.[40] There are several limitations to the zone-based approach; (i) Exclusion of posterior neck injuries, (ii) limited correlation between the location of the external wound and internal injury,[41,42] and (iii) situations where the injury is in more than one zone, and (iv) in patients with multiple sites of injury.[43]
Region of body | Adult “k” coefficient |
---|---|
Head-and-neck | 0.0031 |
Head | 0.0021 |
Neck | 0.0059 |
Chest | 0.014 |
Abdomen and pelvis | 0.015 |
Trunk | 0.015 |
The US Doppler is a useful diagnostic modality in stable patients with soft signs and provides anatomic and hemodynamic information about the damaged vessel. However, it is restricted to be used only in Zone II neck injuries.[44] All the limitations of conventional angiography and US Doppler and the advent of CTA lead to the consequent “no-zone approach.” The no-zone approach depends on patient resuscitation, triage (based on hard and soft signs), CTA use in patients with soft signs, and observation in asymptomatic individuals.[45-48] The Western Trauma Association recommended CTA in all patients with penetrating neck injury irrespective of zones while considering Zone II injuries.[49] Among patients with a vascular penetrating neck injury, Ibraheem et al. reported the sensitivity and specificity of CTA in patients with hard signs as 83–90% and 100%, respectively.[50] While in stable patients with soft signs, the sensitivity and specificity were reported to be 89.5–100% and 61–100%, respectively.[50] Irrespective of hard or soft signs, Ibraheem et al. reported the sensitivity of CTA as 94–100% and specificity as 97– 100% in hemodynamically stable patients.[50]
Carotid artery involvement can be observed in 80% of neck injuries, ensuing in a 15% of stroke rate and 22% of mortality.[36,51-53] Cerebral infarctions are the leading cause of death, constituting 80% of the cases, followed by uncontrolled hemorrhage.[43,54] Partial or complete vessel occlusion, which is observed in 36% of patients with penetrating trauma, is the most common carotid artery injury.[36] Vertebral arteries and venous structures involve 43% and 20% of vascular neck injuries.[53,55,56] The laceration to V2 and V3 segments of the VA is usually noticed in patients with cervical spinal fracture, as the artery travels through the transverse foramen of the cervical vertebral bodies.[5] Injury to V3 and V4 arterial segments is commonly observed without association with cervical spine fractures.[5] Therefore, neck injuries prompt immediate medical care by physicians.
CONCLUSION
Penetrating vascular injuries are a severe and common presentation in the emergency department. They should be addressed early due to their increased morbidity and mortality. The various imaging modalities and the corresponding signs of injury guide the clinicians in proper and prompt patient management. The CTA retains a critical role in the acute setting due to its high sensitivity, fewer contraindications, rapid image acquisition, and availability in most institutions.
Declaration of patient consent
Patient’s consent not required as there are no patients in this study.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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