Blunt cerebrovascular injuries (BCVI) refer to blunt traumatic injury involving either carotid or vertebral artery. In literature the incidence of blunt trauma is 1%. But more recent publications indicate an overall inflation in incidence of BCVI in the in-hospital trauma population and as high as 9% in patients with severe head injury. This frequently leads to underdiagnosis, and failure to timely identify and intervene leading to serious complications and deaths.

We conducted a retrospective patient‐file analysis of data. This study was conducted in SRM Medical College and Hospital, Chengalpattu, Tamil Nadu. We encountered a19-year-old female brought to our Emergency Department with alleged history of road traffic accident, pedestrian got hit by two-wheeler followed by accidental ran over by four-wheeler where patient being the pedestrian at a nearby location and sustained injury to head, left side of chest and abdomen. The patient was brought to the Emergency Room within 10 minutes of the event by ambulance.

On primary survey, airway was patent and on examination right carotid bruit was elicited. In view of midline cervical tenderness, in-line stabilisation was done with hard cervical collar. In breathing, Air entry was reduced on left side of chest with respiratory rate of 28 breaths/ minute and SPO2 of 85 % at room air which improved to 96 % with 15 litres of oxygen. Circulation showed pulse rate of 110 beats/minute and blood pressure of 80/40 mm Hg.In view of left tension pneumothorax needle decompression was done at the left 5^th ICS anterior to mid axillary line followed by ICD placement. On reassessment of primary survey post ICD patient hemodynamically improved with respiratory rate of 20 breaths/minute, SPO2 of 100% with 15 litres of oxygen, Pulse rate of 74 beats/minute and blood pressure of 130/70 mmHg.Disability evaluation revealed a Glasgow Coma Scale (GCS) of 15 where she was alert and oriented to person, place, and time, but amnestic to details of the collision. She was moving all four limbs with power of 5/5 in all extremities with intact sensations. There were left upper quadrant abdominal grazed abrasions with no peritoneal signs. She also had swelling over high parietal region with multiple facial abrasions. After initial airway, breathing and circulation stabilization with IV fluid resuscitation, needle decompression followed by ICD, patient was started on IV analgesics, IV antiepileptics and tetanus vaccine and shifted to ICU for further management.

As per institutional trauma protocol the patient underwent computed tomography (CT) scans head to pelvis with contrast to assess for traumatic injuries. CT scans of the brain, chest and abdomen/pelvis were unremarkable except subgaleal hematoma in the high parietal region(figure1) and mild left pneumothorax and small peripheral lung contusions with ICD in situ (figure 2).

CT whole spine with MRI Screening showed C5 Vertebral fracture, tear drop fracture in the anteroinferior aspect and left lamina fracture along with compression fractures of D2- D6(Figure 3).

assess the improvement in treatment which showed no further worsening of thrombus with no focal neurological deficit. Patient was then started on antiplatelets and shifted to ward.

Significant injuries to the cerebral vessels can occur because of blunt or penetrating trauma to the neck. Blunt cerebrovascular injuries (BCVI) incorporate blunt traumatic injury to carotid or vertebral artery. The incidence of BCVI is 1%^[1]. In recent years, various studies have proposed early screening systems for BCVI, in which approximately 1.1–3% of hospitalized trauma patients are diagnosed with BCVI^[2,8]. This fraction jacked up to 9% in patients with severe head injury^[3,4,5,6]. However, 53-79% of patients are asymptomatic at presentatio ^[1]. Therefore, asymptomatic patients with high-risk injuries require screening. The clinical presentation of BCVI varies widely depending on the affected vessels, the site of injury, the level of injury, and any pre-existing cerebrovascular disease^[8].

The most common mechanism for sustaining BCVI is Motor Vehicle Collision (MVC) associated with high energy trauma^[9,13]. This includes stretch injury and crush injury. Stretch injury occurs due to hyperextension-hyperflexion-rotation mechanisms which stretch the carotid over the lateral processes of the upper spine. Crush injury causes damage to proximal structures such as the petrous portion of the temporal bone around the carotid canal [1,10]. Direct blow to the vessel intraorally or externally also results in BCVI^[1,11]. These shearing forces over the neck cause intimal injury, and these tears can become a nidus for thrombus development [9]. Injuries to either vessel can predispose the patient to an ischemic stroke from obstruction of arterial flow. Clinical characteristics range from imprecise symptoms to definite neurological deficits.

The presenting signs comprises of ipsilateral headache (58% to 92%), neck pain (18% to 46%), pulsatile tinnitus, transient blindness, carotid bruit (12% to 39%), partial horner syndrome (9% to 75%) and the most alarming complication ischemic stroke^[1,12]. However, 53-79% of patients are asymptomatic at presentation^[1,8,12,14]. Prompt and meticulous diagnosis can significantly bring down mortality and morbidity; therefore, early screening of patients even at asymptomatic phase remains crucial.

Modified Denver criteria and modified Memphis criteria are used as major screening criteria to identify and distinguish those patients who are at higher risk of BCVI (Table 1 & 2)^{[1,3,6,7,10,11,15]}. However, this remains controversial because of its odd presentations and feasibility. Strokes from blunt carotid artery injuries occur more frequently than those from blunt vertebral artery injuries^[1,18,19]. They tend to develop neurological deficits in a delayed manner with 20% stroke risk in vertebral artery injuries. The untreated stroke risk following BCVI is 10% to 40% and is highest within the first 7 days. The risk of stroke increases with increasing grades of carotid artery injury ranging from 8% in grade 1 to 100% in grade 5 (Table 3 & 4)^{[1,6,10,16,17,20]}.

Table 1: Major Screening Criteria for BCVI – Modified Denver Criteria)

Table 2: Major Screening Criteria for BCVI – Modified Memphis Criteria

Table 3: stroke risk in carotid artery injury)

Table 4: stroke risk in vertebral artery injury

High risk patients identified by screening criteria are subjected to radiological scrutiny. Digital subtraction angiography (DSA) is the gold-standard diagnostic modality to detect BCVI with sensitivity was 47% to 52%^[1,22]. Being invasive, conventional catheter-based four-vessel digital subtraction angiography (DSA) is not routinely performed recently. Duplex ultrasonography, magnetic resonance angiography (MRA), and CT angiogram (CTA) are non-invasive diagnostic imaging modalities^{[1,6,16,17,20,21]}. Duplex Doppler ultrasound has poor specificity and sensitivity. Evaluation of carotid arteries near the skull base and vertebral arteries within the bony vertebral foramen, where most injuries occur cannot be evaluated. Therefore approximately 90% of lesions remain undetected. Hence, use of ultrasound for screening for BCVI is limited [16,17,20-23]. Vessel wall magnetic resonance imaging (MRI) can also assist in the diagnosis with a sensitivity of only 50 to 75% and a specificity of only 47 to 67%.but its impractical in polytrauma cases due to long examination times. Hence not recommended in emergency settings. CTA is another potential alternative in imaging done nowadays, with 16-slice or better scanners it has a sensitivity of 68% to 100% ^{[1,6,20,21,22]}.

The prompt detection and meticulous treatment of BCVIs has been shown to reduce the morbidity and mortality. Both asymptomatic and symptomatic patients should be carefully monitored for development of neurological deficits or further deterioration. Based on CTA findings, BCVI is compared and treated with Biffl scale grading. It can be managed either conservatively or surgically based on symptoms and grading (Table 5). Medical management with antithrombotic therapy is indicated for patients with grade 1 to 4 injuries without neurological deficit. The recommendations are not specific regarding choosing between systemic anticoagulation (e.g. heparin, LMWH) or antiplatelet (e.g. aspirin, clopidogrel) agents, and there does not seem to be a difference in outcomes between these two classes of agents^[19,20]. For anticoagulation, the current regimen includes a heparin infusion started at 10 units/kg/h and titrated to aPTT of 40 to 50 seconds. If antiplatelet therapy is selected, 75 to 325 mg/day of aspirin (or 3 to 5 mg/kg in children) is recommended. In most cases 3 to 6 months of antithrombotic treatment is ideal [1,3,10,20]. Surgical management include ligation, resection, thrombectomy, endovascular stent placement, or transarterial embolization. These options are limited by injury locations that are less accessible such as the carotid canals or vertebral foramen^[10,24,25]. If treated appropriately either medically or surgically, strokes can be reduced from 25.8% to 3.9%^[10].

This case study demonstrated successful conservative management of an asymptomatic BCVI following high energy motor vehicle collision (MVC) with subsequent arterial remodelling. To our knowledge, this is the first case reporting as a medical literature on the clinical presentation and outcome of our patient demonstrated sonographic progression of carotid artery remodelling in a patient following BCVI due to MVC. Blunt cerebrovascular injury has been seriously neglected in clinical practice. Blunt trauma to the neck can lead to immediate or delayed ischemic strokes. A high index of suspicion and the maintenance of standardized evaluation and treatment protocols for patients with possible BCVI will avoid diagnostic delay and may improve the overall outcome by reducing the risk of permanent neurological dysfunction, and even death.

1. Walls RM, Hockberger RS, Gausche-Hill M. Rosen’s emergency medicine: concepts and clinical practice2018.
2. Y. Kim, W. Biffl et al., 2020. Evaluation and management of blunt cerebrovascular injury: a practice management guideline from the Eastern Association for the Surgery of Trauma., J. Trauma Acute Care Surg., 88 (6) (2020), pp. 875-887.
3. Brommeland, E. Helseth et al., 2018. Best practice guidelines for blunt cerebrovascular injury (BCVI)., Scand. J. Trauma Resuscitation Emerg. Med., 26 (1) (2018), p. 90.
4. Weber CD, Lefering R, Kobbe P, et al., 2017.Blunt cerebrovascular artery injury and stroke in severely injured patients: an international multicenter analysis. World J Surg. 2017; 30:15.
5. Esnault P, Cardinale M, Boret H, et al.,2017. Blunt cerebrovascular injuries in severe traumatic brain injury: incidence, risk factors, and evolution. J Neurosurg. 2017; 127:16–22.
6. Brommeland, T., Helseth, E., Aarhus, M. et al. Best practice guidelines for blunt cerebrovascular injury (BCVI). Scand J Trauma Resusc Emerg Med 26, 90 (2018). https://doi.org/10.1186/s13049-018-0559-1.
7. Xizhu Huang, Xianglei Kong et al.,2024, A case report of endovascular treatment with blunt cerebrovascular injury., Int J Surg Case Rep. 2024 Oct 22;125:110488. doi: 10.1016/j.ijscr.2024.110488.
8. Biffl WL, Ray CE, Jr., Moore EE, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg 2002; 235:699-706; discussion -7.
9. Brittany A Wash, W Douglas Gregorie et al., 2018. Deconstructing Dissections: A Case Report and Review of Blunt Cerebrovascular Injury of the Neck., Case Rep Emerg Med. 2018 Aug 8; 2018:6120781. doi: 10.1155/2018/6120781.
10. Hacking C, Sharma R, Spires R, et al. last revised in Aug 2024. Blunt cerebrovascular injury. Reference article, Radiopaedia.org, https://doi.org/10.53347/rID-41631.
11. Kay Hon, Denise Roach et al., 2022. A case report of blunt intraoral cerebrovascular injury in a child following intraoral trauma: The pen is mightier than the sword., Trauma Case Reports Volume 37, February 2022, 100567.
12. Miller P. R., Fabian T. C., Croce M. A., et al. 2002. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Annals of Surgery. 2002;236(3):386–395. doi: 10.1097/00000658-200209000-00015.
13. C. Burlew, J.J. Sumislawski, et al. 2018. Time to stroke: a Western Trauma Association multicenter study of blunt cerebrovascular injuries.,J. Trauma Acute Care Surg., 85 (5) (2018), pp. 858-866, 10.1097/ta.0000000000001989.
14. Y. So, A. Sawhney, et al. 2022 Wang Current concepts in imaging diagnosis and screening of blunt cerebrovascular injuries Tomography, 8 (1) (2022), pp. 402-413, 10.3390/tomography8010033.
15. Chong Zheng, Derui Kong et al. 2023. Experience and lessons learned from blunt cerebrovascular injuries: A case report.,Heliyon Volume 9, Issue 3, March 2023, e13968.
16. Abdullah Al-Harthy , Alreem Al-Hinai et al. 2011. Blunt Cerebrovascular Injuries, A review of the literature., Sultan Qaboos Univ Med J . 2011 Oct 25;11(4):448–454.
17. Dennis Hundersmarck 1,3, Willem-Bart M Slooff et al. 2019. Blunt cerebrovascular injury: incidence and long-term follow-up ., Eur J Trauma Emerg Surg . 2019 Jun 13;47(1):161–170. doi: 10.1007/s00068-019-01171-9
18. Stein DM, Boswell S, Sliker CW, et al. Blunt cerebrovascular injuries: does treatment always matter? J Trauma. 2009; 66:132–44.
19. Crawford JD, Allan KM, Patel KU, et al. The natural history of indeterminate blunt cerebrovascular injury. JAMA Surg. 2015;150:841–7.Return to ref 20 in article
20. Simon Sarkisian, Zachary Sletten et al. 2021. Blunt Cerebrovascular Injury: ED Presentations, Evaluation, and Management., Emdocs episode 18.
21. Carrie P. Marder and Kathleen R. Fink et al. 2016. Blunt Cerebrovascular Injury., Radiology Key, Fastest Radiology Insight Engine 7.1
22. Emmett KP, Fabian TC, DiCocco JM, et al. Improving the screening criteria for blunt cerebrovascular injury: the appropriate role for computed tomography angiography. J Trauma. 2011; 70:1058–63.
23. Nagpal P, Policeni BA, Bathla G, et al. Blunt cerebrovascular injuries: advances in screening, imaging, and management trends. AJNR Am J Neuroradiol. 2017; 75:543–9.
24. Orlowski HLP, Kansagra AP, Sipe AL, Miller-Thomas MM, Vo KD, Goyal MS. Utility of CT angiography in screening for traumatic cerebrovascular injury. Clin Neurol Neurosurg. 2018; 172:27–30.
25. Bejjani GK, Monsein LH, Laird JR, Satler LF, Starnes BW, Aulisi EF. Treatment of symptomatic cervical carotid dissections with endovascular stents. Neurosurgery. 1999;44:755–60. doi: 10.1097/00006123-199904000-00037.