Continuing Education Activity

Vertebral artery injuries may result from blunt or penetrating trauma, spontaneous dissection, or surgical complications, and represent a significant cause of stroke in younger patients. These injuries range from subtle vessel wall irregularities to complete transection with hemorrhage. This course reviews the clinical features of vertebral artery injuries, including headache, neck pain, vertigo, and posterior circulation stroke symptoms, such as speech, swallowing, or coordination difficulties. Diagnostic evaluation including modified Denver Screening criteria and computed tomography angiography, which play critical roles in early detection, are also reviewed. Management based on injury grade, location, and clinical presentation is also discussed, ranging from thrombolytic therapy to surgical interventions.

This activity explores the pathophysiology, diagnostic accuracy, and therapeutic decision-making in vertebral artery injury. Participants will gain a deeper understanding of screening criteria, imaging selection, and individualized treatment planning. This activity for healthcare professionals is designed to enhance the learner's competence in identifying vertebral artery injury, performing the recommended evaluation, reducing stroke risk, and implementing an appropriate interprofessional approach in the acute and long-term management of cerebrovascular trauma and dissection.

Objectives:

• Identify the myriad of clinical presentations of vertebral artery injury.
• Apply the modified Denver Screening criteria to recognize patients at high risk for cerebrovascular injury.
• Evaluate the indications for appropriate interventions for vertebral artery injury based on injury grade and clinical status.
• Collaborate with interprofessional teams to ensure timely diagnosis, coordinated care, and improved recovery in cerebrovascular trauma management in patients with vertebral artery injury.

Introduction

Vertebral artery injuries may develop from trauma, spontaneous dissection, or iatrogenic surgical complications. Traumatic causes most often involve blunt force to the head or neck, although penetrating injuries can also occur. Spontaneous dissections result from intrinsic vessel wall weakness, frequently linked to vascular or connective tissue disorders, and often lead to arterial dissection. Minor precipitating events commonly precede spontaneous dissections, including maneuvers that increase neck manipulation. The injury grade can range from subtle vessel wall irregularities to complete transection accompanied by intracranial or extracranial hemorrhage.

Patients frequently present with headache and neck pain during the initial evaluation, although some remain asymptomatic. Vertebral artery injury represents a major cause of stroke and transient ischemic attack, especially among younger patients. Because the vertebral arteries supply the posterior circulation, including the brainstem, cerebellum, and occipital lobes, injury or occlusion commonly produces posterior circulation stroke symptoms. Manifestations may include impaired speech, swallowing difficulty, imbalance, loss of coordination, or visual disturbances. The modified Denver Screening Criteria assist clinicians in identifying patients at elevated risk of cerebrovascular injury, while computed tomography (CT) angiography is the preferred initial diagnostic modality. Management depends on the injury’s location, severity, and symptoms, and may involve fibrinolysis, anticoagulation, antiplatelet therapy, endovascular intervention, or open surgical repair.[1]

Etiology

Vertebral artery injury arises from blunt trauma, penetrating trauma, iatrogenic injury, or spontaneous dissection. In blunt trauma, rapid cervical hyperextension with rotation or lateral flexion, and direct bony impingement from fracture-dislocation or transverse foramen involvement, can produce intimal disruption or intramural hematoma with secondary thrombosis (thromboembolism predominates over hypoperfusion). This matters clinically because ischemic deficits are often delayed after a normal initial examination.[2]

Penetrating trauma to the neck (eg, from a gunshot wound) is a rare but potentially devastating cause of vertebral artery injury with mortality of 15%.[3] Penetrating neck trauma and procedural injury cause direct arterial wall violation, ranging from partial laceration to transection, with immediate hemorrhage or delayed pseudoaneurysm or arteriovenous fistula. Additionally, intraoperative injuries may occur during anterior or posterior surgical approaches and are often associated with anomalous arterial courses.[4]

Spontaneous vertebral artery injuries occur when the structural integrity of the arterial wall is compromised. While this condition may be associated with vascular or connective tissue disorders, eg, fibromuscular dysplasia, Ehlers-Danlos syndrome, and Marfan syndrome, the majority of patients diagnosed with a spontaneous cerebral artery dissection have no known history of the underlying predisposing disease. Most “spontaneous” cases correlate with a mildly traumatic event.[5] Multiple case reports describe various sports, trampoline use, amusement park rides, coughing, sneezing, vomiting, childbirth, sexual intercourse, yoga, scuba diving, and chiropractic neck manipulation, among several other potential triggers. 

Epidemiology

Spontaneous Vertebral Artery Injury 

Spontaneous cerebral artery dissections, affecting both carotid and vertebral arteries, account for approximately 20% of strokes in young adults.[5] Vertebral artery dissections occur less frequently than carotid dissections, with an estimated incidence of 1 in 100,000 individuals in population studies. The true incidence may be higher because many cases remain asymptomatic. The average age of affected patients ranges from 44 to 46 years, with no clear racial or gender predominance. A seasonal variation appears to exist, with more cases reported during winter months, although the underlying cause of this pattern remains uncertain.

Traumatic Vertebral Artery Injury

Traumatic vertebral artery injury represents a relatively uncommon condition, documented in fewer than 1% of trauma admissions.[6] The reported incidence continues to rise, primarily due to heightened awareness and more consistent screening in high-risk populations. The modified Denver Screening criteria guide clinicians in identifying individuals at elevated risk for cerebral artery injury. Cervical transverse foramen fractures or facet dislocations accompany vertebral artery injury in approximately 27.5% of cases, with fractures involving the upper cervical spine demonstrating the strongest association.[7] Routine CTA-neck screening identifies BCVI in 0.94% of all blunt trauma patients, and 16% of BCVI cases occur without Denver risk factors, implying that criteria-only screening systematically underestimates incidence and can miss preventable posterior-circulation ischemia.[6]

Injury severity has important epidemiologic implications, with grade IV occlusions comprising 42.1% of lesions, bilateral vertebral artery injury occurring in 12.3%, and an overall stroke risk of 5.32% that increased with injury grade.[8] Iatrogenic vertebral artery injury during cervical spine surgery is infrequent overall (0.08%), with the greatest reported incidence associated with C1 to C2 posterior fixation (1.35%).[9] 

Pathophysiology

The neurologic consequences of injury to the vertebral artery are due to cerebral ischemia from thromboembolism, hypoperfusion, hemorrhage, or a combination of these conditions. In most cases, vertebral artery injury is due to an intimal tear. Exposed subendothelium triggers platelet-rich thrombus formation. This thrombus may cause local occlusion of the vessel, but more commonly, the clot will embolize to the cerebral circulation, resulting in a stroke. Intimal tears may also dissect and create a false lumen that may lead to arterial occlusion.

Partial arterial transection may result in a pseudoaneurysm, which can be a source of emboli or hemorrhage if it ruptures. Partial-thickness injury may also result in an arteriovenous fistula, particularly after penetrating or iatrogenic injury, producing high-flow shunting (steal, venous hypertension) with risk of ischemia or hemorrhage. Complete vertebral artery transections may result in hemorrhage, which may be intracranial or extracranial depending on the location.

Histopathology

Patients with spontaneous vertebral artery dissection have histopathologic findings of intramural hemorrhage with disruption of the intimal planes. Pathologic changes primarily involve the adventitial and medial layers of the vessel. This finding is not as common in patients with a cerebrovascular injury resulting from acute trauma.

History and Physical

Clinical Features

The history can be quite variable depending on whether the vertebral artery injury is spontaneous or due to acute trauma. Many cases thought to be spontaneous have antecedent minor trauma as an associated factor. Spontaneous dissections are more common in patients with connective tissue disorders, but most patients do not have a known history of connective tissue disease. 

The most commonly reported symptoms are head and neck pain, vertigo, and dizziness, but many patients with small dissections may be asymptomatic. In diagnosed cases, the presenting finding is often a transient ischemic attack or acute stroke. The risk of stroke is greatest in the first 2 weeks after the dissection occurs. Young patients presenting with acute stroke should have cerebrovascular dissection considered, especially if their symptoms are associated with a headache or neck pain. Additional clinical manifestations include scalp tenderness, tinnitus, bruits, or even cervical nerve root involvement. Vertebral artery dissection may also lead to lateral medullary infarction (also known as Wallenberg Syndrome), posterior cervical vestibular symptoms, vision loss, or spinal cord ischemia.

New posterior circulation symptoms after cervical spine manipulation, traction, reduction, or cervical spine surgery should be treated as possible vertebral artery injury-related thromboembolism until excluded. Clinical history should actively probe vertebrobasilar symptoms (diplopia, dysarthria, dysphagia, ataxia, gait instability, transient visual disturbance) rather than relying on spontaneous patient reporting.

On exam, an expanding cervical hematoma, new bruit/thrill, or otherwise unexplained neurologic change should trigger immediate reassessment and expedited vascular imaging. Physical examination should prioritize ocular motility and nystagmus, cranial nerves, limb coordination, and gait when feasible. Subtle or fluctuating deficits warrant repeat focused examinations and urgent escalation.

Patients presenting with acute trauma should first have a primary and secondary survey and should undergo stabilization following Advanced Trauma Life Support guidelines. Like with spontaneous dissections, some patients may initially have no neurologic findings. Patients with blunt cervical trauma who meet the modified Denver Screening criteria should undergo evaluation for cerebrovascular injury.

Denver Screening criteria include:

• Lateralizing neurologic deficit (not explained by head CT)
• Infarct on head CT
• Nonexpanding cervical hematoma
• Massive epistaxis
• Anisocoria/Horner syndrome
• Glasgow coma scale (GCS) less than 8 without significant CT findings
• Cervical spine fracture
• Basilar skull fracture
• Le Fort II or III facial fractures
• Seatbelt sign above the clavicle
• Cervical bruit/thrill

Evaluation

Vertebral artery injury is frequently clinically silent initially, and posterior circulation ischemia can be delayed; therefore, evaluation in trauma should be screening-driven rather than symptom-driven. In blunt trauma, patients meeting the modified or expanded Denver screening criteria should undergo vascular imaging of the neck because early diagnosis primarily functions as stroke prevention (thrombus on intimal injury with embolization).

Computed tomography angiography (CTA) is the preferred initial diagnostic test for suspected blunt cerebrovascular injury in most contemporary trauma algorithms because it is rapid, widely available, and can be performed alongside CT head and cervical spine imaging to define competing hemorrhage risk and vascular injury severity simultaneously. CTA should include adequate coverage of the cervical vertebral arteries through the skull base. The lesion laterality and any intracranial extension should be evaluated to guide the urgency of antithrombotic initiation and neurointerventional consultation. 

Patients meeting the modified Denver Screening criteria should undergo CTA. Radiographic description should include the Biffl (Denver) grade because the grade summarizes lesion phenotype, predicts remodeling versus persistence, and standardizes interprofessional decision-making.[10] (Please refer to the Table "Denver Radiologic Grading Scale for Blunt Cerebrovascular Injury" in the Staging section for more information). Grade I denotes intimal irregularity or minor dissection (<25%), grade II dissection or intramural hematoma with luminal narrowing, grade III pseudoaneurysm, grade IV occlusion, and grade V transection with extravasation.[11] 

Repeat vascular imaging is usually indicated because low-grade injuries frequently evolve, and initial CTA may overcall spasm or underestimate an evolving lesion. In a landmark cohort using routine follow-up arteriography at 7 to 10 days, repeat imaging altered therapy in a large fraction of grade I and II injuries, supporting early reassessment.[11] Best-practice guidance recommends a follow-up CTA at approximately 7 days to confirm or refute the diagnosis, and repeat imaging around 3 months to guide the duration of therapy and the need for further surveillance.[10]

Digital subtraction arteriography (DSA) remains the reference standard but requires greater contrast volume, is less widely available, and is more invasive. DSA also carries a rare risk of stroke. Clinicians may still select DSA when concurrent endovascular therapy is being considered or when other imaging techniques yield inconclusive or unavailable results. CTA has largely replaced DSA in clinical practice.

Magnetic resonance imaging (MRI) serves as a useful screening tool for vertebral artery injury in patients with blunt spinal cord or vertebral subluxation injuries. Magnetic resonance angiography (MRA) demonstrates similar or slightly lower specificity than CTA for detecting vertebral artery injury and often lacks practicality or accessibility in emergency settings. MRA should not be used as the sole screening method for blunt cerebrovascular injury. Although widely available and least invasive, duplex ultrasonography lacks sufficient evidence to support its use in evaluating vertebral artery injury. Anatomical limitations, particularly bony structures obscuring vascular visualization, significantly reduce ultrasound sensitivity.

Additionally, young patients presenting with acute ischemic stroke should undergo evaluation for possible spontaneous cerebral artery dissection as a contributing cause. CTA is commonly performed after a noncontrast head CT in these cases to confirm or exclude this diagnosis.

Adjunct brain imaging might be indicated to assess for neurologic consequences and treatment safety. Noncontrast head CT is used to identify intracranial hemorrhage that constrains antithrombotic therapy. Brain MRI with diffusion-weighted imaging is useful when posterior circulation ischemia is suspected, but CT is unrevealing, or symptoms are subtle, fluctuating, or delayed.

Laboratory testing supports safe imaging and downstream treatment decisions. Serum creatinine (contrast safety), CBC/platelets, and coagulation studies are appropriate when CTA/DSA and antithrombotic therapy are contemplated, because coagulopathy and thrombocytopenia change risk-benefit decisions even when imaging confirms injury.

Spontaneous Vertebral Artery Injury

In spontaneous vertebral artery injury, evaluation may reasonably extend beyond confirming the index dissection to identify an underlying systemic vasculopathy. Targeted screening for connective tissue disorders is appropriate in patients with recurrent or multivessel dissections, suggestive physical features, or relevant family history, whereas routine genetic testing is not indicated otherwise. Because spontaneous cervical artery dissection is associated with extracervical vascular disease, adjunct testing may include intracranial vascular imaging to screen for coexisting cerebral aneurysms, aortic imaging to assess for aortic root dilation or occult aortopathy, and renovascular evaluation in patients with hypertension or features suggestive of fibromuscular dysplasia.[12]

Treatment / Management

Posterior circulation infarction is the dominant preventable morbidity from vertebral artery injury. Contemporary trauma guidance, therefore, prioritizes early antithrombotic therapy (ATT) when bleeding risk is acceptable, because ATT reduces stroke and mortality in BCVI meta-analysis (stroke OR 0.20; mortality OR 0.17).[1] International best-practice guidance similarly advocates starting antithrombotics “as soon as considered safe,” continuing for at least 3 months, and performing repeat CTA at approximately 7 days and at approximately 3 months to confirm evolution and guide de-escalation or escalation.[10]

Antiplatelet therapy is commonly favored because it targets platelet-rich thrombus at sites of intimal disruption (emboligenic surfaces), while generally imposing less systemic bleeding liability than therapeutic anticoagulation in polytrauma. In a 2024 systematic review and meta-analysis, antiplatelet therapy was associated with lower stroke risk than anticoagulant therapy (OR 0.57) and lower bleeding risk (OR 0.29).[13] In the same meta-analysis, when analyses were restricted to aspirin versus heparin, stroke rates were not significantly different (OR 0.43; p=0.11), reinforcing that agent choice may be less important than prompt, consistent exposure to some effective antithrombotic in eligible patients.

The management challenge is balancing early embolic risk against hemorrhagic progression from concomitant injuries, because intimal disruption can thrombose and embolize within hours (time-sensitive thromboembolism). In patients with BCVI plus traumatic brain injury and/or solid-organ injury, early initiation of aspirin/clopidogrel or low-intensity heparin immediately on diagnosis did not increase worsening TBI (9% versus 10%) or need for delayed operative intervention (7% versus 5%) compared with similar trauma patients without BCVI, while BCVI-related stroke still occurred in 9%.[14] Multicenter data indicate that preventable stroke risk is highest before antithrombotic therapy initiation and during treatment interruptions, with a median initiation time of 27 hours, 64% of strokes occurring before treatment, and interruptions present in 75% of patients with stroke versus 24% without.[15] 

Treatment escalation beyond antithrombotics is appropriate when the lesion has high-risk features (symptomatic ischemia from flow-limiting injury with hypoperfusion, enlarging pseudoaneurysm, or transection/extravasation). Routine stenting for grade II to III BCVI is not recommended, since incremental benefit is uncertain and stents commit patients to long-term antiplatelet therapy.[1] When antithrombotics are feasible, stenting is rarely required and should be reserved for refractory symptoms or clearly enlarging pseudoaneurysms.[16] In penetrating or iatrogenic vertebral artery injury with active hemorrhage, urgent endovascular control (often with embolization) is typically favored, with open ligation/repair as rescue when endovascular therapy is not feasible or fails.[17][18]

Follow-up imaging is indicated because low-grade lesions often evolve within days, changing the need for ongoing antithrombotics or endovascular consultation.[11] A practical approach is repeat CTA at about 7 days to confirm diagnosis and assess progression, with follow-up imaging at about 3 months to document healing and guide discontinuation of antithrombotic therapy, which is continued for at least 3 months in most patients.[10] If imaging shows healing, de-escalate or stop therapy; if persistent or progressive (new pseudoaneurysm, worsening stenosis, new symptoms), then continue ATT, escalate monitoring, and seek specialist input for endovascular treatment options. 

European Society for Vascular Surgery Management Guidelines

The 2025 European Society for Vascular Surgery (ESVS) vascular trauma guidelines use a 4-tier morphologic grading system for cervical arterial trauma: ESVS Grade 1 denotes a partial wall injury with normal external wall contour (typically minor intimal injury/dissection), ESVS Grade 2 denotes a complete wall injury with abnormal external wall contour and contained bleeding (commonly a pseudoaneurysm), ESVS Grade 3 denotes a complete wall injury with uncontained hemorrhage (active extravasation/expanding hematoma), and ESVS Grade X denotes occlusion.

For blunt extracranial vertebral artery injury without active hemorrhage (Grades 1, 2, or X), ESVS recommends single antiplatelet therapy as first-line and emphasizes initiating antithrombotics promptly with a high threshold for withholding therapy in polytrauma. Grade 2 pseudoaneurysms are usually managed medically with selective endovascular treatment reserved for enlarging pseudoaneurysm, hemorrhage, or recurrent ischemic events despite antithrombotics, whereas Grade 3 injuries require emergency endovascular embolization when feasible, with surgical ligation as a fallback if endovascular control is not possible. Delayed endovascular treatment may be considered for patients with blunt vertebral artery injury who develop neurological symptoms or demonstrate an enlarging pseudoaneurysm.[19] 

Spontaneous Vertebral Artery Injury

For vertebral artery dissection presenting with acute ischemic stroke, management is following contemporary stroke pathways, with antithrombotics typically for 3 to 6 months and reperfusion (IV thrombolysis or thrombectomy) when eligible. The intracranial vertebral artery dissection with subarachnoid hemorrhage warrants early endovascular or surgical consideration.[12][20]

Intraoperative Vertebral Artery Injury

Intraoperative management of iatrogenic vertebral artery injury begins with immediate hemostatic tamponade and hemodynamic resuscitation. Once bleeding is controlled, urgent angiography is performed to define the lesion and assess collateral circulation. This information guides definitive management, including primary repair, vessel sacrifice, or endovascular reconstruction. Serial postoperative vascular imaging is required to detect delayed complications, eg, pseudoaneurysm or arteriovenous fistula formation.[18]

Differential Diagnosis

Differential diagnoses that should be considered when evaluating vertebral artery injuries include:

• Cervical spine fracture 

• Cervical strain

• Emergent management of subarachnoid hemorrhage

• Migraine headache

• Hemorrhagic stroke

• Tension headache

• Vasculitis affecting the vertebrobasilar circulation

• Vertebrobasilar atherothrombotic disease

Staging

Table

Table. Denver Radiologic Grading Scale for Blunt Cerebrovascular Injury.

Prognosis

Stroke prevalence is 5.32%, but grade III to IV lesions are approximately 10%, and bilateral injury 33.2%.[8] In cervical spine trauma, the posterior circulation stroke risk after vertebral artery injury is 9%.[21] Stroke occurred in 9.8% of BCVI patients treated with antithrombotic therapy compared with 33.6% of untreated BCVI patients. Mortality followed a similar pattern: among 330 patients, death occurred in 16.6% of those receiving antithrombotic therapy versus 40.4% of those not treated.[1]

Lower-grade BCVI resolves more often and earlier, whereas higher-grade BCVI persists, guiding the duration of therapy and repeat imaging.[1] Grade IV occlusion recanalizes in 36% overall and 57% after cervical spine intervention, so reimaging is warranted when management could change.[22]

Complications

Complications of vertebral artery injury can be severe and evolve rapidly, reflecting both the vascular disruption and the secondary neurological consequences. Patients may develop posterior circulation ischemia due to reduced blood flow to the brainstem, cerebellum, and occipital lobes, which can manifest as dizziness, ataxia, diplopia, dysarthria, or altered consciousness. Arterial dissection may lead to thrombus formation with distal embolization, while complete occlusion can precipitate infarction with long-term neurological deficits. Expanding hematomas may compress adjacent neural structures, causing neck pain, radiculopathy, or myelopathy.

More critical complications include subarachnoid hemorrhage, basilar artery thrombosis, and brainstem infarction, all carrying significant morbidity and potential mortality. Delayed recognition may allow progressive vascular compromise or the formation of pseudoaneurysms, which increase the risk of rupture. Because these complications can be subtle at onset, clinicians must maintain vigilance and promptly initiate imaging, monitoring, and coordinated interprofessional management to minimize long-term disability.

Vertebral artery injury-related posterior circulation infarction typically reflects thromboembolism after intimal injury (mural thrombus, distal embolization). In a Western Trauma Association cohort, among strokes not present on admission, the median time to stroke detection was 48 hours, and 61% occurred within 72 hours, supporting rapid diagnosis and expedited antithrombotic initiation once bleeding risk permits.[23] Stroke risk is grade-dependent: meta-analysis showed overall stroke risk 5.32%, higher with Denver grade III (9.8%) and IV (10.9%) versus grade I (1.9%) and II (3.0%), and substantially higher with bilateral vertebral artery injury (33.2%), prioritizing high-grade or bilateral lesions for early therapy and closer monitoring.[8]

Vertebral artery injury can complicate into hemorrhage, pseudoaneurysm, or vertebro-vertebral arteriovenous fistula, converting a “contained” injury into an urgent lesion requiring definitive control. Iatrogenic vertebral artery injury in cervical spine surgery is linked to hemorrhage and pseudoaneurysm/AVF, so delayed neurologic change or unexpected bleeding warrants urgent vascular imaging and escalation.[18] Penetrating extracranial vertebral artery injury has a frequent pseudoaneurysm (18.5%) and AVF (16.9%), and may present with exsanguinating hemorrhage despite minimal neurologic symptoms.[3] 

A 2020 study on the natural history of BCVI showed that most of the BCVI evolution occurs within 30 days; beyond 90 days, improvement was not seen, and late progression was uncommon (1.4%), arguing against prolonged routine imaging after early stability.[24]

Antiplatelet or anticoagulant therapy reduces ischemic complications but carries a risk of hemorrhagic progression, particularly in patients with concomitant intracranial, solid-organ, or spinal injuries. Therefore, treatment is typically initiated once the critical bleeding risk is controlled. Endovascular intervention introduces additional risks, including access-site complications, thromboembolism, and mandatory antiplatelet exposure, which may amplify bleeding risk. 

Deterrence and Patient Education

Deterrence and patient education surrounding vertebral artery injury focus on reducing risk through awareness, early recognition, and proactive management of contributing factors. Patients benefit from clear instructions on avoiding high-risk neck movements, unsafe manipulation, or trauma-prone activities when predisposing conditions, eg, cervical instability or degenerative disease, exist. Education regarding the warning signs of posterior circulation compromise (eg, sudden vertigo, diplopia, severe occipital headache, imbalance, or focal neurological changes) supports timely reporting and rapid evaluation, which can significantly improve outcomes.

Clinicians reinforce deterrence by emphasizing adherence to follow-up imaging, activity modifications, and prescribed therapies that stabilize the cervical spine or reduce vascular risk. Individuals should understand the importance of controlling hypertension, quitting smoking, and managing atherosclerotic risk factors, as these measures reduce the likelihood of complications, eg, dissection or thromboembolism. Collaborative education delivered consistently by physicians, advanced practitioners, nurses, and rehabilitation specialists strengthens patient engagement, enhances safety, and reduces the probability of recurrent or worsening vascular injury.

Enhancing Healthcare Team Outcomes

Vertebral artery injury, whether traumatic or spontaneous, represents a significant cause of stroke, particularly in younger patients. Clinical presentation varies, ranging from headache and neck pain to acute ischemic stroke with posterior circulation deficits. Diagnosis relies on clinical assessment guided by the modified Denver Screening criteria and imaging, with CT angiography serving as the preferred initial modality. Management depends on symptomatology and injury grade, including systemic thrombolysis, catheter-directed thrombolysis, anticoagulation, antiplatelet therapy, endovascular intervention, or open surgical repair. Prognosis varies, with the vertebral artery injury carrying a risk for stroke and mortality, which rises further with concomitant brain injury, older age, arterial occlusion, and higher stroke scores at presentation.

Effective management requires a coordinated interprofessional team including physicians, advanced practitioners, vascular surgeons, radiologists, pharmacists, and nursing staff. Physicians assess patients, determine treatment strategies, and oversee intervention. Pharmacists verify dosing, perform medication reconciliation, and advise on thrombolytic, anticoagulant, or antiplatelet therapy. Radiologists, interventional neurologists, neurosurgeons and vascular surgeons execute endovascular or operative interventions, while nurses provide bedside care, medication administration, and patient monitoring. Clear communication and collaborative decision-making among team members enhance patient-centered care, optimize outcomes, improve safety, and ensure efficient workflow across the continuum of care.

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Disclosure: Leslie Simon declares no relevant financial relationships with ineligible companies.

Disclosure: Aussama Nassar declares no relevant financial relationships with ineligible companies.

Disclosure: Michael Mohseni declares no relevant financial relationships with ineligible companies.