Chief Complaint:

GSW to face

HPI:

31-year-old male presents to the ED by EMS after reportedly being involved in a road rage incident where he was shot in his face. He was the unrestrained driver that then sustained an accident by running into a ditch. He was found by EMS with GCS 15 at the scene and was normotensive with a normal heart rate. He arrived with obvious wounds to his left neck and right cheek. He is able to speak words with discomfort. He denies any vision or hearing changes. He denies neck pain. He is complaining of pain in his face and head. He also complains of dysphagia and dyspnea. Admits to cocaine use today and alcohol last night.
History PMH: Substance abuse PSH: Bilateral knee arthroscopy Alcohol use: Alcohol use Drug use: Cocaine, Marijuana Smoking status: Smoking status for patients 13 years old or older: Current everyday smoker

Pertinent Exam Findings:

Head:1 cm wound posterior to left ear, no expansile or pulsatile hematoma present, minimal oozing; 2cm wound to right cheek with significant associated edema
Eyes:L pupil: reactivity (2mm) R pupil: reactivity (2mm)
ENT, Mouth:Laceration to right cheek, through and through, 3cm. There is 4 cm laceration in the right retromolar/palatoglossal arch soft tissue.
Neck:supple, trachea midline, no bruit/NL carotids, no JVD
Extremities:dry, moves all, normal movement/sensation, normal temperature
Neurological:alert, oriented X 3, CNII-XII intact, follows commands, localizes stimuli, no motor deficits, no sensory deficits, opens eyes – tracks

Imaging Interpretation:

CT MAXILLOFACIAL SINUSES WO Ballistic trajectory extending across the right buccal/masticator space and left carotid/parapharyngeal space with subcutaneous emphysema and blood products. Comminuted ballistic fractures of the right maxillary alveolus involving the posterior-most molar.

CT HEAD: No evidence of acute intracranial process.
CTA HEAD: The left internal carotid artery is reconstituted in the petrous segment likely via retrograde circle of Willis collateral flow. No intracranial large vessel occlusion or hemodynamically significant stenosis. No intracranial arterial injury.
CTA NECK: The left internal carotid artery is injured with occlusion in the upper cervical segment, either vasospasm or thrombosed. No active contrast extravasation is identified.
CERVICAL SPINE: No acute cervical fracture.
CT TRAUMA CHEST W ABD W PEL W: Acute mild L1 compression fracture. No significant height loss nor retropulsed fracture fragment.

ED Course:

Due to the significant amount of blood and secretions, discussed with patient elective need for intubation for airway protection and to obtain imaging. VAscular recommended starting rectal aspirin for left ICA dissection

Vascular Surgery and Nuero Interventional Radiology were consulted.

No further interventions in the ED were recommended and patient was admitted to the ICU intubated

Hospital Course:

Plastic surgery was consulted for face wound and they repaired facial wound and recommended peridex swish and spit 4 times daily x10 days – Patient with GSW to the left neck behind the ear and right cheek. No hard signs of vascular injury

A repeat CTA 2 days later revealed minimal increase and dissection. Patient without neuro deficits after extubation on hospital day 2.

Hospital day 3 discharged from hospital Prescriptions for chlorhexidine, aspirin, and Toradol

Post gunshot wound day 7 ED visit Presents with increased need for pain meds after running out. Started on Augmentin but noted to have no signs of infection on exam.

6 weeks later, outpatient image

CTA NECK Evolution of left internal carotid artery distal cervical segment dissection with interval development

DISCUSSION:

Background:

The left and right common carotid arteries are the major vessels responsible for supplying blood to the head, neck, and brain. The left common carotid artery originates directly from the aortic arch and the right common carotid artery branches off of the brachiocephalic artery. These arteries then divide in the neck to form the external and internal carotid arteries which supply blood to the face and neck, and to the anterior portion of the brain, respectively. A tear or separation in the layers of the carotid arteries can disrupt this critically important blood supply. Subintimal dissections often result in luminal stenosis or occlusion of the vessel whereas subadventitial dissections may result in aneurysm of the arterial wall. As more blood begins to pool in the arterial walls, the normal flow of blood to the head and neck can be slowed down or completely blocked with potentially devastating consequences. This condition can occur spontaneously but most frequently develops after a major or minor traumatic injury to the neck. Those with connective tissue disorders and vascular abnormalities have been noted to be at an increased risk of carotid artery dissection. Epidemiological studies have shown the occurrence of this condition to be approximately two people per 100,000, but the true incidence may be higher as many dissections may be subclinical in nature. Clinically significant carotid dissections are more common in people in their 40s or 50s and is the most frequent cause of cerebrovascular accidents in young and middle-aged patients. Additional risk factors include connective tissue diseases, large vessel pathologies such as fibromuscular dysplasia, and osteogenesis imperfecta. This diagnosis should be considered in any potential stroke patient presenting with neck pain or in trauma patients with neurologic deficits despite a normal head CT.

Diagnosis:

Carotid artery dissections (CAD) should be suspected when history reveals traumatic neck injury due to motor vehicle accidents, gunshot wounds, physical activity or neck manipulation which induces or require extreme neck rotation or extension. However, it is important to remember that dissection may also occur spontaneously. The clinical presentation of carotid artery dissections is characterized by a number of nonspecific symptoms including eye pain, neck pain, weakness or numbness to one side of the body, and trouble speaking or swallowing. Symptoms may occur suddenly or gradually over days.

Management in ED:

When a patient has sustained blunt or penetrating trauma to the head and/or neck a cervical collar should be placed. Once a diagnosis of CAD is confirmed through imaging, treatment must begin immediately to prevent further ischemic injury and long-lasting neurologic deficits including death. Consultation to vascular surgery or neurology may be indicated for further treatment evaluation or management.

Acute treatment of carotid artery dissection depends on the timing of medication delivery, the location of dissection (extracranial or intracranial), and the dissection mechanism (traumatic or spontaneous). The provider should initially begin evaluation for fibrinolytic therapy with tPA. Requirements for tPA include a three-hour symptom window and an extracranial dissection with evidence of ischemic stroke. For patients who do not meet tPA criteria, antithrombotic therapy should be considered.

Anticoagulation therapy, typically with low-molecular-weight heparin, is often used with severe artery stenosis, vessel occlusion, or pseudoaneurysms. Treatment with antiplatelet therapy is most often used when the patient has a poor prognosis or is predisposed to increased risk of bleeding. Antiplatelet therapy includes aspirin, clopidogrel, or both. Antiplatelets may be considered when anticoagulation therapy is contraindicated, as in spinal cord hematomas, large intracerebral infarcts, or intracranial extension due to the risk of subarachnoid hemorrhage. The 2012 landmark Cervical Artery Dissection in Stroke Study (CADISS) study found no evidence of superiority between anticoagulation and antiplatelet therapy in preventing stroke or death in patients with symptomatic carotid and vertebral artery dissection. Both treatment modalities aim to restore blood flow, prevent further bleeding, and minimize neurologic insult.

Finally, all patients with confirmed carotid artery dissection, fluctuating neurologic state, and new or worsening symptoms should be admitted to telemetry for continued monitoring and further work-up (i.e. MRI).

Prognosis:

Patient outcomes are related to the severity of the associated ischemic stroke or subarachnoid hemorrhage. Poor functional outcome after a cervical artery dissection is associated with a high NIHSS score at onset, arterial occlusion, and older age. Recurrence rate with or without severe neurologic symptoms remains uncertain and available data are inconsistent. There are favorable outcomes for those with spontaneous dissections, with about 75% of patients making adequate recovery. Mortality rates of spontaneous dissections are less than 5%. Traumatic dissections, likely due to mechanisms of injury and worsened disease on presentation, are associated with greater risk of mortality on admission and discharge. In a 2011 retrospective study on twenty-nine patients, 70% had complete symptom resolution and 25% had partial resolution. General consensus indicated that most carotid artery dissections have favorable outcomes, with very low mortality and long-term morbidity rates.

Differential Diagnoses:

• • Ischemic or Hemorrhagic Stroke
  • TIA
  • Subarachnoid Hemorrhage
  • Vertebral Artery Dissection
  • Acute hypoglycemia
  • Retinal Artery/Vein Occlusion
  • Carbon Monoxide Toxicity
  • Tension/Migraine Headache

Clinical Pearls:

• • Carotid artery dissection is a rare but potentially lethal condition that most commonly presents secondary to a traumatic neck injury.
  • Carotid artery dissection is the most common cause of cerebrovascular incidents in young and middle-aged adults, and it can present with a wide array of nonspecific, neurologic symptoms.
  • CTA is the most effective and efficient imaging modality for the diagnosing carotid artery dissection.
  • Fibrinolytic therapy and anticoagulation are the mainstays of carotid artery dissection treatment along with urgent neurology and vascular surgery consultation.

References:

1. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015; 14: 361–367.
2. Ballester J., Thomas D. Evaluation and Management of Cervical Artery Dissection in the Emergency Department. Emergency Medicine Reports; 2016.
3. Cairns, George, and Alex Belshaw. “Successful Management of Internal Carotid Artery Transection Secondary to a Gunshot Wound and Subsequent Malignant MCA Syndrome.” Case Reports in Neurology, S. Karger AG, 25 May 2021, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8216034/.
4. “Carotid Dissection.” Cedars Sinai, https://www.cedars-sinai.org/health-library/diseases-and-conditions/c/carotid-dissection.html. Accessed 7/26/2022.
5. David Zohrabian, MD. “Carotid Artery Dissection Workup: Laboratory Studies, Angiography, Ultrasonography.” Carotid Artery Dissection Workup: Laboratory Studies, Angiography, Ultrasonography, Medscape, 17 Oct. 2021, https://emedicine.medscape.com/article/757906-workup#c7.
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7. Radiopaedia. Internal carotid artery dissection. (https://radiopaedia.org/articles/internal-carotid-artery-dissection-1?lang=us) Accessed 4/7/2022
8. Rao AS, Makaroun MS, Marone LK, Cho JS, Rhee R, Chaer RA. Long-term outcomes of internal carotid artery dissection. J Vasc Surg. 2011 Aug;54(2):370-4; discussion 375. doi: 10.1016/j.jvs.2011.02.059. Epub 2011 May 28. PMID: 21620626.
9. Shea K, Stahmer S. Carotid and vertebral arterial dissections in the emergency department. Emerg Med Pract. 2012 Apr;14(4):1-23; quiz 23-4. PMID: 22567808.
10. Zinkstok S, Vergouwen M, Engelter S, et al. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011; 42: 2515–2520.

Authors

Aaron Wolfe, DO, FACEP

Kirsten Hughes, M4

Mark O’Brien, M4

Carleigh Schley, M3

Justin Evans, MS2

Caitlin Lofton, MS2

Jack Spartz, MD