Traumatic bilateral carotid and vertebral artery dissection.

Sir,

BL is a 23-year-old right-hand dominant woman transferred to our trauma center after a car accident. She had cervical transverse process fractures, right caudate head and basal ganglia infarction, left mandibular fracture and a left temporal lobe contusion. She had left hemiparesis. Computed tomography (CT) angiogram of the head and neck and subsequent cervical angiogram confirmed severe dissection and stenosis of the right internal carotid artery (ICA) and M1, M2 bifurcation, a focal area of dissection within the left ICA, and bilateral vertebral artery (VA) dissections [Figure 1].

Figure 1

(a) Three-dimensional reconstruction of angiogram showing bilateral dissections of the internal carotid artery (arrows). (b and c) Digital subtraction angiogram images of right (b) and left (c) vertebral artery dissections (arrows)

She was anti-coagulated with a therapeutic heparin infusion and bridged to warfarin (dosed to achieve an international normalized ratio between 2 and 3), treated for her other injuries and subsequently discharged to rehabilitation. She ambulates independently 32 months post-injury despite some residual left-sided weakness and her dysarthria has resolved and is only maintained now on aspirin 81 mg daily having completed a year of warfarin therapy. Repeat CT of the head and neck at 32 months reveals persistent, but non-occlusive dissection of bilateral carotid arteries [Figures 2 and 3].

Figure 2

Computed tomographic evaluation of the neck at 32 months post-injury reveals persistent right internal carotid artery non-obstructing dissection (magnified view)

Figure 3

Computed tomographic evaluation of the neck at 32 months post-injury reveals persistent left internal carotid artery non-obstructing dissection (magnified view)

The incidence of traumatic cervical artery dissection (TCAD) may be 0.86% for ICA and 0.53% for VA traumatic dissections,[1] up to 10-20% if all trauma patients are screened.[2] In 25% of cases, two or more arteries may be involved simultaneously,[3] although, we have not found previous reports of four-vessel involvement. Manifestations include pain, headache, facial hemorrhage, cervical bruit, Horner's syndrome, transient brain ischemia or even acute infarction on brain imaging.[13]

CT angiography has superior sensitivity than duplex Doppler ultrasound for diagnosis.[4] Magnetic resonance angiography has been used, but the gold standard remains arteriography.[5] Delay in diagnosis greater than 48 h significantly worsens outcomes.[6] Treatment is by anti-coagulation. Recent evidence suggests that systemic antithrombotic therapy is equivalent to antiplatelet therapy in a comparison of stroke risk and injury healing rates.[7] Recently, endovascular interventions including stenting have been successful in treating TCADs.[8]